The DOI matches its Crossref record; 159 of the 159 references it cites were found in a registry or an index.
THE MANY ROLES OF c-Myc IN APOPTOSIS
Abstract
▪ Abstract The proto-oncogene c-myc encodes a transcription factor c-Myc, which is of great importance in controlling cell growth and vitality. The quantity of c-Myc is carefully controlled by many mechanisms, and its actions to induce and repress genes are modulated by interactions with other regulatory proteins. Understanding the kinetic and quantitative relationships that determine how and what genes c-Myc regulates is essential to understanding how Myc is involved in apoptosis. Reduction of c-myc expression and its inappropriate expression can be associated with cellular apoptosis. This review outlines the nature and regulation of the c-myc gene and of c-Myc and presents the systems and conditions in which Myc-related apoptotic events occur. Hypotheses of the mechanisms by which expression and repression of c-myc lead to apoptosis are discussed.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Research indicates that approximately 70% of human cancers involve dysregulated MYC expression.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [515]
Citations
Cites
Induction of apoptosis in fibroblasts by c-myc protein
Evan, G. I., Wyllie, A. H., Gilbert, C. S., Littlewood, T. D., Land, H., Brooks, M. W., Waters, C. M., Penn, L. Z., & Hancock, D. C. (1992) · Cell · doi:10.1016/0092-8674(92)90123-t · Cited by 2,941
Thymocyte apoptosis induced by p53-dependent and independent pathways
Clarke, A. R., Purdie, C. A., Harrison, D. J., Morris, R. G., Bird, C. C., Hooper, M. L., & Wyllie, A. H. (1993) · Nature · doi:10.1038/362849a0 · Cited by 2,271
Wild-type p53 induces apoptosis of myeloid leukaemic cells that is inhibited by interleukin-6
Yonish-Rouach, E., Resnftzky, D., Lotem, J., Sachs, L., Kimchi, A., & Oren, M. (1991) · Nature · doi:10.1038/352345a0 · Cited by 2,079
c-Myc transactivation of LDH-A : Implications for tumor metabolism and growth
Shim, H., Dolde, C., Lewis, B. C., Wu, C.-S., Dang, G., Jungmann, R. A., Dalla-Favera, R., & Dang, C. V. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.13.6658 · Cited by 1,092
Askew, D. S., Ashmun, R. A., Simmons, B. C., & Cleveland, J. L. (1991) · PubMed · Cited by 867
Marcu, K. B., Bossone, S., & Patel, A. J. (1992) · Annual Review of Biochemistry · doi:10.1146/annurev.bi.61.070192.004113 · Cited by 802
A c-jun dominant negative mutant protects sympathetic neurons against programmed cell death
Ham, J., Babij, C., Whitfield, J. R., Pfarr, C. M., Lallemand, D., Yaniv, M., & Rubin, L. L. (1995) · Neuron · doi:10.1016/0896-6273(95)90331-3 · Cited by 795
Proteins of the Myc Network: Essential Regulators of Cell Growth and Differentiation
Arsenian‐Henriksson, M., & Lüscher, B. (1996) · Advances in cancer research · doi:10.1016/s0065-230x(08)60353-x · Cited by 781
Littlewood, T. D., Hancock, D. C., Danielian, P. S., Parker, M. G., & Evan, G. I. (1995) · Nucleic Acids Research · doi:10.1093/nar/23.10.1686 · Cited by 780
Reactive oxygen species and programmed cell death
Jacobson, M. D. (1996) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(96)20008-8 · Cited by 754
Flagged first, then by citations
Research works printed but not linked: 55
- Lemaitre JM, 1996, Adv. Cancer Res., 70, 96
- Shrivastava A, 1995, Curr. Top. Microbiol. Immunol., 194, 273
- Plet A, 1992, Oncogene, 7, 1847
- Eastman-Reks SB, 1986, Cancer Res., 46, 2457
- Rhee K, 1995, Cancer Res., 55, 4188
- Thompson EA, 1991, Cancer Res., 51, 5551
- Medh RD, 1997, Cancer Res.
- Ayala-Torres S, 1997, Mol. Cell. Biol.
- Dean M, 1988, Curr. Top. Microbiol. Immunol., 141, 216
- Cory S, 1987, Oncogene Res., 1, 61
- Askew DS, 1991, Oncogene, 6, 1915
- Kimura S, 1995, Cancer Res., 55, 1379
- Ohta H, 1995, Cancer Res., 55, 691
- Davidoff AN, 1993, Anticancer Res., 13, 1167
- Samid D, 1992, Cancer Res., 52, 1988
- Sumitani K, 1997, Anticancer Res., 17, 865
- Zhao X, 1995, Sci. China-Ser. B, 38, 580
- Fornari FA, 1994, Cell Growth Differ., 5, 723
- Van Waardenburg RC, 1996, Anticancer Res., 16, 1963
- Cerutti J, 1996, Clin. Cancer Res., 2, 119
- Heufelder AE, 1995, Invest. Ophthalmol. Visual Sci., 36, 1420
- Williams SA, 1996, Leukemia, 10, 1980
- Watson PH, 1991, Cancer Res., 51, 3996
- Loke SL, 1988, Curr. Topics Microbiol. Immunol., 141, 282
- Chiarugi V, 1996, Tumori, 82, 205
- Lotem J, 1996, Leukemia, 10, 925
- 10.1016/S0065-230X(08)60353-X · DOI
- Koskinen PJ, 1993, Semin. Cancer Biol., 4, 3
- Onclercq R, 1989, Oncogene Res., 4, 293
- Nishikura K, 1990, Oncogene, 5, 981
- Shiota G, 1995, Res. Commun. Mol. Pathol. Pharmacol., 90, 17
- Amundadottir LT, 1996, Oncogene, 13, 757
- Hundley JE, 1997, Cancer Res., 57, 600
- Morgenbesser SD, 1994, Semin. Cancer Biol., 5, 21
- Green DR, 1992, Semin. Immunol., 4, 379
- Wang Y, 1993, Cell Growth Differ., 4, 467
- Sakamuro D, 1995, Oncogene, 11, 2411
- Hsu B, 1995, Oncogene, 11, 175
- Czaja MJ, 1996, Am. J. Physiol., 270, G60
- Reynolds JE, 1994, Cancer Res., 54, 6348
- Packham G, 1995, Curr. Topics Microbiol. Immunol., 194, 283
- Packham G, 1994, Mol. Cell. Biol., 14, 41
- 10.1016/0968-0004(96)20008-8 · DOI
- 10.1182/blood.V83.5.1179.1179 · DOI
- 10.1210/me.10.3.306 · DOI
- Singh N, 1995, Oncol. Res., 7, 353
- Freemerman AJ, 1996, Mol. Pharmacol., 49, 788
- Bortner DM, 1995, Cell Growth Differ., 6, 1579
- Adams PD, 1996, Curr. Top. Microbiol. Immunol., 208, 79
- Lebowitz PF, 1997, Cancer Res., 57, 708
- Esteve P, 1995, Oncogene, 11, 2657
- Jimenez B, 1995, Oncogene, 10, 811
- Fukasawa K, 1995, Oncogene, 10, 1
- Jansen B, 1997, Cancer Res., 57, 362
- Fernandes RS, 1996, Anticancer Res., 16, 1691
Cited by
Sorted by citations
Items 101–200 of 334
Baena, E., Ortiz, M., Martínez‐A, C., & de Alborán, I. M. (2007) · Experimental Hematology · doi:10.1016/j.exphem.2007.05.015 · Cited by 51
Apoptosis and liver diseases: Recent concepts of mechanism and significance1
Ockner, R. K. (2001) · Journal of Gastroenterology and Hepatology · doi:10.1046/j.1440-1746.2001.02426.x · Cited by 47
Hussin, F., Eshkoor, S. A., Rahmat, A. B., Othman, F., & Akim, A. M. (2014) · BMC Complementary and Alternative Medicine · doi:10.1186/1472-6882-14-32 · Cited by 48
Druwe, I. L., Freudenrich, T. M., Wallace, K., Shafer, T. J., & Mundy, W. R. (2015) · Toxicology · doi:10.1016/j.tox.2015.03.011 · Cited by 46
Deshmukh, A. P., Kumar, S., Arfuso, F., Newsholme, P., & Dharmarajan, A. (2017) · Scientific Reports · doi:10.1038/s41598-017-02256-4 · Cited by 48
Wu, M., Bellas, R. E., Shen, J., Yang, W. E., & Sonenshein, G. E. (1999) · The Journal of Immunology · doi:10.4049/jimmunol.163.12.6530 · Cited by 46
bu, X., & Wang, L. (2024) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2024.5480 · Cited by 54
“Other regulatory factors include oncogenes such as c‑MYC, which directly binds to a conserved E box in intron 1 of TFRC (19), and HIF‑1, which activates TFRC expression under specific conditions, such as iron‑deficient conditions, by binding to an upstream hypoxia response element (20).”
ANP32A regulates histone H3 acetylation and promotes leukemogenesis
Yang, X., Lu, B., Sun, X., Han, C., Fu, C., Xu, K., Wang, M., Li, D., Chen, Z., Opal, P., et al. (2018) · Leukemia · doi:10.1038/s41375-018-0010-7 · Cited by 44
Gao, G., & Dou, Q. P. (2000) · Molecular Pharmacology · doi:10.1016/s0026-895x(24)12472-8 · Cited by 43
Qian, X., Zhu, L., Xu, M., Liu, H., Yu, X., Shao, Q., & Qin, J. (2023) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2023.110588 · Cited by 41
Ceballos, E., Muñoz-Alonso, M. J., Berwanger, B., Acosta, J. C., Hernández, R., Krause, M., Hartmann, O., Eilers, M., & León, J. (2005) · Oncogene · doi:10.1038/sj.onc.1208652 · Cited by 43
What retroviruses teach us about the involvement of c-Myc in leukemias and lymphomas
Dudley, J., Mertz, J., Rajan, L., Lozano, M. M., & Broussard, D. R. (2002) · Leukemia · doi:10.1038/sj.leu.2402451 · Cited by 40
Mechanisms of T-cell Apoptosis Induced by Glucocorticoids
Thompson, E. B. (1999) · Trends in Endocrinology and Metabolism · doi:10.1016/s1043-2760(99)00187-3 · Cited by 41
Self-citationMedh, R. D., Wang, A., Zhou, F. L., & Thompson, E. B. (2001) · Oncogene · doi:10.1038/sj.onc.1204680 · Cited by 41
“Depending on the cell type and conditions being studied, either deregulated overexpression or suppression of c-Myc can lead to apoptosis (Shi et al., 1992; Thompson, 1998).”
BackgroundSelf-citationNeuroblastoma: The impact of biology and cooperation leading to personalized treatments
Owens, C., & Irwin, M. S. (2012) · Critical Reviews in Clinical Laboratory Sciences · doi:10.3109/10408363.2012.683483 · Cited by 41
Deiana, M., Chand, K., Jamroškovič, J., Das, R. N., Obi, I. R., Chorell, E., & Sabouri, N. (2020) · Nanoscale · doi:10.1039/d0nr03404e · Cited by 39
Fassl, S., Leisser, C., Huettenbrenner, S., Maier, S., Rosenberger, G., Strasser, S., Grusch, M., Fuhrmann, G., Leuhuber, K., Polgar, D., et al. (2003) · Oncogene · doi:10.1038/sj.onc.1207047 · Cited by 38
“…enzymes (Wu et al., 1999), became limited and this may explain the dual role of c-Myc in the induction of cell proliferation and of apoptosis (Thompson, 1998; Fuhrmann et al., 1999), (c) Expression of H-ferritin protein after Myc:ER activation (by 4-OHT), or exposure to TNFa, FasL, and TRAIL.”
BackgroundThe role of Pim kinase in immunomodulation.
Liu, Z., Han, M., Ding, K., & Fu, R. (2020) · PubMed Central · Cited by 37
Cell death signaling in the cerebellum in Creutzfeldt-Jakob disease
Puig, B., & Ferrer, I. (2001) · Acta Neuropathologica · doi:10.1007/s004010100368 · Cited by 37
Semov, A., Marcotte, R., Semova, N., Ye, X., & Wang, E. (2002) · Analytical Biochemistry · doi:10.1006/abio.2001.5515 · Cited by 37
Alarcon-Vargas, D., Tansey, W. P., & Ronai, Z. A. (2002) · Oncogene · doi:10.1038/sj.onc.1205543 · Cited by 36
“Given that c-myc has also been implicated in promoting apoptosis (Askew et al., 1991; Evan et al., 1992; Thompson, 1998), the mechanisms that underlie the regulation of c-myc stability, as illustrated here for MEKK1 and its related kinases, is expected to play a pivotal role in Figure 4 DMEKK1…”
BackgroundBoth Gimap5 and the diabetogenic BBDP allele of Gimap5 induce apoptosis in T cells
Dalberg, U. N., Markholst, H., & Hornum, L. (2007) · International Immunology · doi:10.1093/intimm/dxm009 · Cited by 35
“Other examples of this are the proto-oncogenes c-Myc ( 27 ) and Ras (28) and cdk inhibitors such as p21 and p27 (29).”
BackgroundSurvival of Adult Generated Hippocampal Neurons Is Altered in Circadian Arrhythmic Mice
Rakai, B. D., Chrusch, M. J., Spanswick, S. C., Dyck, R. H., & Antle, M. C. (2014) · PLoS ONE · doi:10.1371/journal.pone.0099527 · Cited by 35
“Many genes involved in growth and apoptosis are regulated by the transcription factor Myc, which binds to E-boxes to regulate gene expression [36].”
BackgroundMa, J., Li, Y., Wu, M., & Li, X. (2017) · Chemosphere · doi:10.1016/j.chemosphere.2017.12.051 · Cited by 34
Cdc25A phosphatase suppresses apoptosis induced by serum deprivation
Fuhrmann, G., Leisser, C., Rosenberger, G., Grusch, M., Huettenbrenner, S., Halama, T., Mosberger, I., Sasgary, S., Cerni, C., & Krupitza, G. (2001) · Oncogene · doi:10.1038/sj.onc.1204499 · Cited by 34
“Therefore it is assumed that cell cycle regulation and apoptosis ought to be tightly connected and might share some early biochemical pathways and molecular mechanisms such as p53 dependence (King and Cidlowsky, 1998) or c-Myc transcriptional activity (Thompson, 1998).”
BackgroundXu, W., Du, M., Zhao, Y., Wang, Q., Sun, W., & Chen, B. (2012) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2011.04.003 · Cited by 33
“The proto-oncogene c-myc encodes a transcription factor, c-Myc, which is of great importance in controlling cell growth and vitality [50].”
BackgroundSignificance of c-Myc and Bcl-2 Protein Expression in Nasopharyngeal Carcinoma
Yu, Y., Dong, W., Li, X., Yu, E., Zhou, X., & Li, S. (2003) · Archives of Otolaryngology - Head and Neck Surgery · doi:10.1001/archotol.129.12.1322 · Cited by 33
Apoptosis Induced by Oxysterol in CEM Cells Is Associated with Negative Regulation of c-Myc
Ayala‐Torres, S., Zhou, F. L., & Thompson, E. B. (1999) · Experimental Cell Research · doi:10.1006/excr.1998.4308 · Cited by 33
Self-citationDeng, Z., & Richardson, D. R. (2023) · Pharmacological Reviews · doi:10.1124/pharmrev.122.000795 · Cited by 32
“Moreover, Myc family members can amplify transcription by interacting with the promoter regions of downstream target genes (Lin et al., 2012; Nie et al., 2012, 2020).”
Backgroundc-Myc-deficient B lymphocytes are resistant to spontaneous and induced cell death
de Alborán, I. M., Baena, E., & Martínez‐A, C. (2003) · Cell Death and Differentiation · doi:10.1038/sj.cdd.4401319 · Cited by 32
“Overexpression of c-myc induces apoptosis in fibroblasts and myeloid cell lines in low serum conditions.(1,2,9) More recently, Hueber et al.”
BackgroundPorter, S. N., Howarth, G. S., & Butler, R. N. (2000) · European Journal of Pharmacology · doi:10.1016/s0014-2999(00)00237-5 · Cited by 32
Glucocorticoid mediated transcriptional repression of c-myc in apoptotic human leukemic CEM cells
Zhou, F. L., Medh, R. D., & Thompson, E. B. (2000) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/s0960-0760(00)00080-7 · Cited by 32
“The regulation of the c-myc gene and its products occurs by various mechanisms, including transcriptional, post-transcriptional, translational and combinations of these [1,10].”
BackgroundSelf-citationKorshunov, A., Savostikova, M. V., & Ozerov, S. S. (2002) · Journal of Neuro-Oncology · doi:10.1023/a:1016226319068 · Cited by 32
“Up-regulation of c-myc protein has also been implicated in triggering apoptosis pathways and various associations between both these processes have been established [36,37].”
BackgroundMyc-Induced Liver Tumors in Transgenic Zebrafish Can Regress in tp53 Null Mutation
Sun, L., Nguyễn, A. T., Spitsbergen, J. M., & Gong, Z. (2015) · PLoS ONE · doi:10.1371/journal.pone.0117249 · Cited by 31
Wang, S., Zhang, X., Wang, G., Cao, B., Yang, H., Jin, L., Cui, M., & Mao, Y. (2019) · BMC Cancer · doi:10.1186/s12885-019-6381-y · Cited by 31
RetractedCell Death in MMTV-c-myc Transgenic Mouse Mammary Tumors May Not Be Typical Apoptosis
Liao, D. J., & Dickson, R. B. (2003) · Laboratory Investigation · doi:10.1097/01.lab.0000090153.13977.ae · Cited by 32
c-Myc Oncoprotein: A Dual Pathogenic Role in Neoplasia and Cardiovascular Diseases?
Claudio Napoli, A., Lermant, L. O., de Nigris, F., & Sica, V. (2002) · Neoplasia · doi:10.1038/sj.neo.7900232 · Cited by 31
“interactions with other regulatory proteins [2-8,48].”
BackgroundOkada, M., Miller, T. C. R., Wen, L., & Shi, Y. (2017) · Cell Death and Disease · doi:10.1038/cddis.2017.198 · Cited by 30
Murakami, J., Asaumi, J., Kawai, N., Tsujigiwa, H., Yanagi, Y., Nagatsuka, H., Inoue, T., Kokeguchi, S., Kawasaki, S., Kuroda, M., et al. (2005) · Cancer Chemotherapy and Pharmacology · doi:10.1007/s00280-004-0976-x · Cited by 30
“Next, we sought to discover whether or not the effect of FR901228 on hTERT expression is related to a mechanism through one of the main hTERT transcription activators, c-myc, whose repression has been implicated in several apoptosis pathways [32].”
BackgroundPrognostic value of plasminogen activator inhibitor‐1 in head and neck squamous cell carcinoma
Speleman, L., Kerrebijn, J. D. F., Look, M. P., Meeuwis, C. A., Foekens, J. A., & Berns, E. M. J. J. (2006) · Head & Neck · doi:10.1002/hed.20527 · Cited by 30
Multiorgan mRNA misexpression in murine autosomal recessive polycystic kidney disease
Gattone, V. H., Ricker, J. L., Trambaugh, C. M., & Klein, R. M. (2002) · Kidney International · doi:10.1046/j.1523-1755.2002.00632.x · Cited by 30
“Elevated c-myc expression is associated with increased rates of apoptosis and proliferatio”
BackgroundThe Role of PKM2 in Multiple Signaling Pathways Related to Neurological Diseases
Zhang, X., Lei, Y., Zhou, H., Liu, H., & Xu, P. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03901-y · Cited by 30
“…by mediating the β-catenin/T-cell factor 4 (TCF4) signaling cascade under the conditions of ischemic injury. β-catenin and its induced TCF4 are combined with upregulating gene induction of Myc , CCND1 , and Sgk1 , thereby regulating cell proliferation and anti-apoptotic effects [30, 113–115] (Fig.”
Engür, S., & Dikmen, M. (2017) · Acta Clinica Belgica · doi:10.1080/17843286.2017.1302623 · Cited by 29
Sierra, À., Castellsagué, X., Escobedo, A., Moreno, A., Drudis, T., & Fabra, À. (1999) · Breast Cancer Research and Treatment · doi:10.1023/a:1006120006471 · Cited by 29
“suppressor of the apoptotic action of c-Myc, without affecting its ability to promote cell proliferation [5].”
BackgroundDovey, Z. S., Nair, S. S., Chakravarty, D., & Tewari, A. K. (2021) · Cancer Reports · doi:10.1002/cnr2.1340 · Cited by 29
Biological functions and research progress of eIF4E
Chen, X., An, Y., Tan, M., Xie, D., Liu, L., & Xu, B. (2023) · Frontiers in Oncology · doi:10.3389/fonc.2023.1076855 · Cited by 26
“c-Myc It promotes cell cycle progression, transforming cells in G1 phase into S phase, and regulates cell apoptosis (18).”
BackgroundNewman, E. A., Chukkapalli, S., Bashllari, D., Thomas, T. T., Noord, R. A. V., Lawlor, E. R., Hoenerhoff, M. J., Opipari, A. W., & Opipari, V. P. (2017) · Cell Death and Disease · doi:10.1038/s41419-017-0004-9 · Cited by 26
Novel approaches to the treatment of small-cell lung cancer
Zangemeister‐Wittke, U., & Stahel, R. A. (1999) · Cellular and Molecular Life Sciences · doi:10.1007/s000180050398 · Cited by 26
Oh, S., Yun, K., Nan, J., Sohn, D., & Lee, B. (2003) · Archives of Toxicology · doi:10.1007/s00204-002-0415-x · Cited by 26
“Therefore, the results of our present study and of others (Ryan et al. 1994; Thompson 1998 ) strongly suggest that Bcl-2 and c-Myc inhibit hepatocellular apoptosis at later stages of BDL by sequestering p53 in the cytoplasm.”
BackgroundResultLu, X., Shao, J., Li, H., & Yu, Y. (2009) · Genomics · doi:10.1016/j.ygeno.2008.12.007 · Cited by 25
“Deregulation of this gene was associated with cellular apoptosis [31].”
BackgroundChapman, N., Webster, G., Gillespie, P. J., Wilson, B. J., Crouch, D. H., & Perkins, N. D. (2002) · Biochemical Journal · doi:10.1042/bj20020444 · Cited by 24
Engür, S., Dikmen, M., & Öztürk, Y. (2015) · Immunopharmacology and Immunotoxicology · doi:10.3109/08923973.2015.1122616 · Cited by 24
PATHWAYS OF APOPTOSIS AND THE MODULATION OF CELL DEATH IN CANCER
Fisher, D. E. (2001) · Hematology/Oncology Clinics of North America · doi:10.1016/s0889-8588(05)70258-6 · Cited by 24
Pollard, H., Yang, Q., Dalgard, C. L., Eidelman, O., Jozwik, C., Pollard, B., & Srivastava, M. (2013) · Journal of Carcinogenesis · doi:10.4103/1477-3163.112268 · Cited by 24
“Both c‐MYC mRNA and c‐MYC protein have short half‐lives, of approximately 30 min, respectively.[20] Of the known transcriptional drivers for c‐MYC, one of the most critical appears to be nuclear factor of activated T‐cells (NFAT).”
BackgroundKaaya, E. E., Castaños‐Vélez, E., Heiden, T., Ekman, M., Catrina, A., Kitinya, J. N., Andersson, L. C., & Biberfeld, P. (2000) · Medical Oncology · doi:10.1007/bf02782199 · Cited by 24
Ding, H., Pei, Y., Li, Y., Xu, W., Mei, L., Hou, Z., Guang, Y., Cao, L., Li, P., Cao, H., et al. (2021) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2021.116512 · Cited by 23
Arunkumar, N., Liu, C., Hang, H., & Song, W. (2013) · Cellular and Molecular Immunology · doi:10.1038/cmi.2013.14 · Cited by 23
Mazur, L., Augustynek, A., Halicka, H. D., & Deptała, A. (2003) · Cell Biology and Toxicology · doi:10.1023/a:1022013630420 · Cited by 23
c-Myc degradation induced by DNA damage results in apoptosis of CHO cells
Jiang, M., Li, Y., Yang, Y., & Wu, J. (2003) · Oncogene · doi:10.1038/sj.onc.1206501 · Cited by 23
“Several studies found that lowered c-Myc content in different cell systems such as Jurkat cells or B-lymphoid cells led to apoptosis (Wood et al., 1994; Sonenshein, 1997; and reviewed by Thompson, 1998a).”
BackgroundRuggieri, A., Murdolo, M., Harada, T., Miyamura, T., & Rapicetta, M. (2003) · Archives of Virology · doi:10.1007/s00705-003-0202-x · Cited by 23
“In addition, c-myc oncogene has been reported to transform primary cells in cooperation with ras oncogene and when overexpressed c-myc may also induce apoptosis [2, 7, 37 ].”
BackgroundImportance of Sp1 consensus motifs in the MYCN promoter
Inge, T. H., Casson, L. K., Priebe, W., Trent, J. O., Georgeson, K. E., Miller, D. M., & Bates, P. J. (2002) · Surgery · doi:10.1067/msy.2002.125387 · Cited by 22
Analysis of the c‐myc, K‐ras and p53 Genes in Methylcholanthrene induced Mouse Sarcomas
Watanabe, H. K., Shimokado, K., Asahara, T., Dohi, K., & Niwa, O. (1999) · Japanese Journal of Cancer Research · doi:10.1111/j.1349-7006.1999.tb00663.x · Cited by 22
Piedra, M., Delgado, M. D., Ros, M. A., & León, J. (2002) · PubMed · Cited by 22
Yin, X.-Y., Grove, L. E., & Prochownik, E. V. (2001) · Oncogene · doi:10.1038/sj.onc.1204417 · Cited by 19
“The seemingly paradoxical ®nding that GCs down-regulate c-Myc, yet induce apoptosis in a cMyc-dependent manner in some systems (Thompson, 1998), might be explained by assuming that the overlap of c-myc- and GC-regulated genes includes some which play particularly important roles in apoptosis.”
BackgroundRegulation of p27Kip1 accumulation in murine B-lymphoma cells: role of c-Myc and calcium.
Donjerković, D., Zhang, L., & Scott, D. W. (1999) · PubMed · Cited by 21
Marculino, T. F. S., Pimenta, C. A. M., Neto, R. A., Castelo, P. M., Silva, M. D. S., Forones, N. M., & Oshima, C. T. F. (2020) · Asian Pacific Journal of Cancer Prevention · doi:10.31557/apjcp.2020.21.2.343 · Cited by 19
“…cells had frequently defects in the G1/S phase, leading to unregulated growth, development and progression of the tumor (White et al., 2012; Luo et al., 2017) The β-catenin protein acts on the Wnt signaling pathway and can induce the expression of the proteins cyclin-D1 and c-Myc (Thompson, 1998).”
BackgroundValla, S., Hassan, N., Vitale, D. L., Madanes, D., Spinelli, F. M., Teixeira, F. C. O. B., Greve, B., Espinoza‐Sánchez, N. A., Cristina, C., Alaniz, L. D., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115874 · Cited by 20
“Moreover, the combination of Sdc-1 depletion and HA treatment resulted in a synergistic upregulation of cMyc expression, which may have further contributed to the anti-apoptotic effect [57].”
BackgroundTanizaki, Y., Zhang, H., Shibata, Y., & Shi, Y. (2022) · Communications Biology · doi:10.1038/s42003-022-03061-0 · Cited by 20
Jasty, R., van Golen, C., Lin, H.-J., Solomon, G., Heidelberger, K. P., Polverini, P. J., Opipari, A. W., Feldman, E. L., & Castle, V. P. (2001) · Neoplasia · doi:10.1038/sj.neo.7900171 · Cited by 20
“Indeed the mechanism by which c-myc induces apoptosis appears to be closely associated with its effects on the cell cycle ( reviewed in Thompson [36] ).”
BackgroundBaisch, H., Bollmann, H., & Bornkessel, S. (1999) · Cell Proliferation · doi:10.1046/j.1365-2184.1999.3250303.x · Cited by 20
Prostate Specific Antigen. Current clinical application and future prospects
Duskova, K., & Veselý, Š. (2014) · Biomedical Papers · doi:10.5507/bp.2014.046 · Cited by 19
Rosenberger, G., Fuhrmann, G., Grusch, M., Fassl, S., Elford, H. L., Smid, K., Peters, G. J., Szekeres, T., & Krupitza, G. (2000) · Life Sciences · doi:10.1016/s0024-3205(00)00901-2 · Cited by 19
“1 cells and tightly links proliferation to apoptosis [35–37], because c-myc activation forces dormant cells to transit from growth arrest into cell cycle [35, 38].”
BackgroundSchmidt, M. E., Koller, R. P., Haviernik, P., Bies, J., Maciag, K., & Wolff, L. (2001) · Oncogene · doi:10.1038/sj.onc.1204821 · Cited by 19
“…promoting cell growth, c-Myb can counteract apoptosis by up-regulating the anti-apoptotic gene Bcl-2 (Frampton et al., 1996; Taylor et al., 1996; Schmidt et al., 2000), thus keeping cells with proliferative potential alive and counteracting apoptotic e ects of Myc over-expression (Thompson, 1998).”
BackgroundTIDD, D. M. (2000) · Nucleic Acids Research · doi:10.1093/nar/28.11.2242 · Cited by 19
Soriani, M., Williams, N., & Hirst, T. R. (2001) · Infection and Immunity · doi:10.1128/iai.69.8.4923-4930.2001 · Cited by 19
“It has recently become apparent that NF-kB can activate cell death pathways (13, 26) by transcriptional activation of one of its target genes, c-myc (9, 38, 43).”
BackgroundInfluentialThe role of programmed cell death in osteosarcoma: From pathogenesis to therapy
Liu, S., Liu, C., Wang, Y., Chen, J., He, Y., Hu, K., Li, T., Yang, J., Peng, J., & Hao, L. (2024) · Cancer Medicine · doi:10.1002/cam4.7303 · Cited by 20
“135,136 c-Myc has a dual role in apoptosis.”
BackgroundPregnancy and Cancer: Cellular Biology and Mechanisms Affecting the Placenta
Oliveira, M. D. M. S., Salgado, C. D. M., Viana, L. R., & Gomes‐Marcondes, M. C. C. (2021) · Cancers · doi:10.3390/cancers13071667 · Cited by 17
“Oestrogen is also responsible for the inhibition of the upregulation of antiapoptotic proteins Bcl-2 and Bcl-x [69,78].”
Backgroundİpek, S. L., Alkış, M. D. Ö., & Göktürk, D. (2023) · Applied Sciences · doi:10.3390/app13169382 · Cited by 18
Recovery of biological signals lost in single-cell batch integration with CellANOVA
Zhang, Z., Mathew, D., Lim, T., Mason, K., Martinez, C. M., Huang, S., Wherry, E. J., Suszták, K., Minn, A. J., Ma, Z., et al. (2024) · Nature Biotechnology · doi:10.1038/s41587-024-02463-1 · Cited by 30
Shimada, I., Matsui, K., Brinkmann, B., Hohoff, C., Hiraga, K., Tabuchi, Y., Takasaki, I., Kato, I., Kawaguchi, H., Takasawa, K., et al. (2008) · International Journal of Legal Medicine · doi:10.1007/s00414-008-0226-6 · Cited by 18
“It is generally accepted that Myc overexpression can induce the production of ROS in mitochondria, leading to DNA damage and genomic instability such as gene amplification and polyploidy [ 41 ].”
BackgroundInduction of the apoptosis of HL-60 promyelocytic leukemia cells by Eurya emarginata
Park, S. Y., Yang, H. C., Moon, J. Y., Lee, N. H., Kim, S. J., Kang, J., Lee, Y. K., Park, D. B., Yoo, E. S., & Kang, H. K. (2003) · Cancer Letters · doi:10.1016/j.canlet.2003.09.034 · Cited by 18
“c-Myc is widely known as a crucial regulator of cell proliferation in normal and neoplastic cells, but until recently, its apoptotic properties, which appear to be intrinsic, were not fully appreciated [27,28].”
BackgroundZeng, C., Wu, J., & Li, J.-M. (2024) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000001568 · Cited by 19
“78 Previous studies have shown that the b -catenin/TCF4 signaling pathway activates 35 and upregulates genes such as c-Myc, 79 cyclin D1, 80 and Sgk1, 81 which have anti-apoptotic effects on cardiomyocytes.”
BackgroundRyynänen, J., Seuter, S., Campbell, M. J., & Carlberg, C. (2013) · Cancers · doi:10.3390/cancers5041221 · Cited by 17
“Depending on the cellular model the Myc protein acts either as a pro- or an anti-survival factor [39].”
BackgroundKim, H., Jeong, S., Lee, J., Kim, B.-E., Kim, J. W., Jeong, S., & Kim, I. (2000) · Experimental & Molecular Medicine · doi:10.1038/emm.2000.32 · Cited by 16
“Reduction of c-myc expression and its inappropriate expression can be associated with cellular apoptosis (Thompson, 1998).”
BackgroundB-Myc: N-Terminal Recognition of Myc Binding Proteins
Burton, R. A., Mattila, S., Taparowsky, E. J., & Post, C. B. (2006) · Biochemistry · doi:10.1021/bi060379n · Cited by 16
Methamphetamine increases expression of the apoptotic c-myc and l-myc genes in the mouse brain
Thiriet, N., Jayanthi, S., McCoy, M. T., Ladenheim, B., & Cadet, J. L. (2001) · Molecular Brain Research · doi:10.1016/s0169-328x(01)00093-6 · Cited by 16
Bellas, R. E., & Sonenshein, G. E. (1999) · PubMed · Cited by 16
Funato, T., Kozawa, K., Kaku, M., & Sasaki, T. (2001) · Anti-Cancer Drugs · doi:10.1097/00001813-200111000-00006 · Cited by 16
“Thus the induction of apoptosis by cisplatin is related to cisplatin sensitivity and the expression of c-myc, because the c-myc gene is a well-known factor in the induction of apoptosis.(26) High c-myc levels are necessary for cisplatin-induced apoptosis in resistant 1 2 3 4”
BackgroundYang, J., Jiang, G., Ni, K., Fan, L., Tong, W., & Yang, J. (2022) · Phytotherapy Research · doi:10.1002/ptr.7680 · Cited by 15
“It not only mediates the occurrence and development of many cancers (Dang, 2012; McKeown & Bradner, 2014; Thompson, 1998), but also has been found an important role in fibrosis.”
BackgroundRole of Orai‐family channels in the activation and regulation of transcriptional activity
Nieto‐Felipe, J., Macias‐Díaz, A., Sánchez-Collado, J., Berna‐Erro, A., Jardín, I., Salido, G. M., López, J. J., & Rosado, J. A. (2023) · Journal of Cellular Physiology · doi:10.1002/jcp.30971 · Cited by 15
“5 | C‐MYC The transcription factor c‐myc, which is encoded by the proto‐oncogene c‐myc, is involved in vital processes for the cell such as cell growth, proliferation, and apoptosis as it is an important modulator of cell cycle progression through G1 phase (E. B. Thompson, 1998).”
BackgroundAbaza, M. S. I., Al‐Attiyah, R., Al-Saffar, A. M., Al‐Sawan, S., & Moussa, N. M. (2003) · Tumor Biology · doi:10.1159/000076139 · Cited by 15
Induction of apoptosis dependent on caspase activities and growth arrest in HL-60 cells by PGA2
Kim, H., Rhim, H., Jeong, S., Kim, J. W., & Kim, I. (2002) · Prostaglandins & Other Lipid Mediators · doi:10.1016/s0090-6980(02)00064-3 · Cited by 15
Korhonen, P., Tapiola, T., Suuronen, T., & Salminen, A. (1998) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1998.9629 · Cited by 15
Fitzgerald, M. J., Arsura, M., Bellas, R. E., Yang, W. E., Wu, M., Chin, L., Mann, K. K., DePinho, R. A., & Sonenshein, G. E. (1999) · Oncogene · doi:10.1038/sj.onc.1202611 · Cited by 15
“These ®ndings indicate that the LZ is the major structural determinant governing dMax heterodimerization activity. dMax induces apoptosis in WEHI 231 cells WEHI 231 B cells are a commonly used paradigm for studying control of cell suicide (Thompson, 1998).”
BackgroundGardner, L. B., Lee, L. A., & Dang, C. V. (2002) · Elsevier eBooks · doi:10.1016/b0-12-227555-1/00055-1 · Cited by 15
Chun, J., Han, L., Xu, M. Y., Wang, B., Cheng, M. S., & Kim, Y. S. (2013) · Archives of Pharmacal Research · doi:10.1007/s12272-013-0279-z · Cited by 14
“Additionally, the ER-a-mediated reduction of c-Myc contributed to cellular apoptosis and a cell cycle arrest (Lukas et al. 1996; Thompson 1998).”
BackgroundPeng, Y. Y., Zhu, G., Ma, Y., Huang, K., Chen, G., Liu, C., & Tao, Y. (2022) · Frontiers in Medicine · doi:10.3389/fmed.2022.697644 · Cited by 14
pVHL-Mediated Transcriptional Repression of c-Myc by Recruitment of Histone Deacetylases
Hwang, I., Roe, J., Seol, J.-H., Kim, H.-R., Cho, E., & Youn, H. (2012) · Molecules and Cells · doi:10.1007/s10059-012-2268-3 · Cited by 14
“…between HIF1α and c-Myc is reported to induce metabolic switching (Dang et al., 2008). c-Myc, a proto-oncogene, regulates 15% of all protein expression of genes covering the cell cycle, apoptosis, development and signal transduction (Cho et al., 2010; Facchini and Penn, 1998; Thompson, 1998).”
BackgroundCell death during lymphocyte development and activation
DEALBORAN, I. (2003) · Seminars in Immunology · doi:10.1016/s1044-5323(03)00032-0 · Cited by 14
Rubio, N., & Torres, C. (1999) · Molecular Brain Research · doi:10.1016/s0169-328x(99)00177-1 · Cited by 14
Metadata
- Authors
- Thompson, E. B.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Thompson, E. Brad
- ORCID
- Thompson, E. Brad
- Venue
- Annual Review of Physiology
- Publisher
- Annual Reviews
- Published
- 1998-10
- Volume
- 60
- Issue
- 1
- Pages
- 575-600
- ISSN
- 0066-4278 (ISSN-L)
- 1545-1585
- OpenAlex
- W2104373533
- Cited by
- 328
- References
- 159
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 24 · 2023: 31 · 2022: 17 · 2021: 10 · 2020: 6 · 2019: 2 · 2018: 3 · 2017: 6 · 2015: 10 · 2014: 3 · 2013: 6 · 2012: 3
- FWCI
- 3.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- c-Myc, c-myc proto-oncogene, apoptosis, transcription factor regulation, gene expression regulation, gene repression, cell growth regulation, transcriptional regulation
- MeSH terms
- Proto-Oncogene Mas, Animals, Humans, Genes, myc, Proto-Oncogene Proteins c-myc, Apoptosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review