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Non-Cell-Autonomous Tumor Suppression by p53
Open accessAbstract
The p53 tumor suppressor can restrict malignant transformation by triggering cell-autonomous programs of cell-cycle arrest or apoptosis. p53 also promotes cellular senescence, a tumor-suppressive program that involves stable cell-cycle arrest and secretion of factors that modify the tissue microenvironment. In the presence of chronic liver damage, we show that ablation of a p53-dependent senescence program in hepatic stellate cells increases liver fibrosis and cirrhosis associated with reduced survival and enhances the transformation of adjacent epithelial cells into hepatocellular carcinoma. p53-expressing senescent stellate cells release factors that skew macrophage polarization toward a tumor-inhibiting M1-state capable of attacking senescent cells in culture, whereas proliferating p53-deficient stellate cells secrete factors that stimulate polarization of macrophages into a tumor-promoting M2-state and enhance the proliferation of premalignant cells. Hence, p53 can act non-cell autonomously to suppress tumorigenesis by promoting an antitumor microenvironment, in part, through secreted factors that modulate macrophage function.
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“This response is mediated by SASP components and by the direct interaction between immune cells and senescent cells153,156–158.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [153]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Senescent fibroblasts contribute to wound healing (Demaria et al. 2014), and the SASP of senescent hepatic stellate cells (HSCs) participates in fibrotic scar degradation and restores tissue homeostasis in liver fibrosis (Lujambio et al. 2013).”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Lujambio et al. 2013
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This senescence-associated phenotype identified with secretion of pro-tumorigenic cytokines and chemokines can be restrained or qualitatively modified by p53 in several cell types in mouse [39, 41].”
From Ligand dependent restoration of human TLR3 signaling and death in p53 mutant cells (2016) · cites this paper as [41]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Senescent cells are indeed subjected to immunosurveillance by multiple components of innate and adaptive immunity, including NK cells, T cells and macrophages145,151,153–156.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [153]
The cited source says what the claim attributes to it.
In the citing paper
“Moreover, in a fibrosis-associated liver cancer model, the SASP can contribute to an anti-tumor microenvironment by skewing macrophage polarization to a tumor-inhibiting M1 state (Lujambio et al. 2013).”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Lujambio et al. 2013
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In the citing paper
“p53 cooperates with the NF- κB pathway to regulate SASP factors that can activate macrophages to form a tumour- suppressive microenvironment 147,148 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [148]
In the citing paper
“these secreted factors can stimulate the immune system to both suppress tumorigenesis and promote optimal repair of damaged tissues when senescent cells are removed after their beneficial actions (15–17).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [16]
In the citing paper
“Upon Dox withdrawal, senescence is induced by re-expression of p53 and mHSCs showed an increase in a number of markers of senescence (Figure S6A), concomitant with the accumulation of Itgb3”
From Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway (2017) · cites this paper as Lujambio et al., 2013
In the citing paper
“The SASP also attracts innate immune cells that in turn eliminate the senescent HSCs and facilitate the resolution of fibrosis 94,120”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [94]
In the citing paper
“activated HSCs become senescent, exhibiting a typical SASP, including the expression of extracellular matrix degrading enzymes and proinflammatory cytokines.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [94]
In the citing paper
“Conversely, cells that could not become senescent due to p53 deletion were not targeted by macrophages [266].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [266]
In the citing paper
“In mouse models, inactivating the senescence machinery results in the acceleration of tumor development, while restoration of senescence in growing tumors causes their regression consistent with the role of senescence in suppressing cancer [266,358].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [266]
In the citing paper
“In mouse models, inactivating the senescence machinery results in the acceleration of tumor development, while restoration of senescence in growing tumors causes their regression consistent with the role of senescence in suppressing cancer [266,358].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [266]
In the citing paper
“and can recruit immune cells to contribute to cancer cell removal, reinforcing the tumor suppressive role of senescent tumor cells [263,266].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [266]
In the citing paper
“Additional immunostimulatory effects linked to pharmacological p53 reactivation in cancer cells include (but are not limited to) (1) downregulation of immunomodulatory cytokines linked to tumor progression, such as IL6 (Sahin et al., 2020); (2) upregulation of NKALs (Textor et al., 2011); and (3) establishment of cellular senescence linked to an immunostimulatory SASP that favors the recruitment”
From Immunomodulation by targeted anticancer agents (2021) · cites this paper as Lujambio et al., 2013
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Citations
Cites
Macrophage Diversity Enhances Tumor Progression and Metastasis
Qian, B., & Pollard, J. W. (2010) · Cell · doi:10.1016/j.cell.2010.03.014 · Cited by 5,338 · cited 2×
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BackgroundBataller, R., & Brenner, D. A. (2005) · Journal of Clinical Investigation · doi:10.1172/jci24282 · Cited by 4,958
Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
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“Indeed, the senescent state triggered by p53 caused a significant increase in the secretion of factors known to promote M1 polarization, which is characterized by Il1b expression and an increased propensity for cell killing and phagocytosis (Biswas and Mantovani, 2010).”
BackgroundBlinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163 · cited 2×
“…and Prives, 2009). p53 binds DNA in a sequence-specific manner and controls the expression of target genes that mediate its diverse effects (Vousden and Prives, 2009). p53 can limit the propagation of premalignant cells by promoting cell-cycle exit or apoptosis, though p53 has other…”
BackgroundSenescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
Self-citationOncogene-Induced Senescence Relayed by an Interleukin-Dependent Inflammatory Network
Kuilman, T., Michaloglou, C., Vredeveld, L. C. W., Douma, S., van Doorn, R., Desmet, C. J., Aarden, L. A., Mooi, W. J., & Peeper, D. S. (2008) · Cell · doi:10.1016/j.cell.2008.03.039 · Cited by 2,086
Senescence of Activated Stellate Cells Limits Liver Fibrosis
Krizhanovsky, V., Yon, M., Dickins, R. A., Hearn, S., Simon, J., Miething, C., Yee, H., Zender, L., & Lowe, S. W. (2008) · Cell · doi:10.1016/j.cell.2008.09.015 · Cited by 2,027 · cited 16×
“In the context of certain wound-healing responses, SASP limits the extent of tissue damage and facilitates wound resolution (Kong et al., 2012; Krizhanovsky et al., 2008).”
BackgroundMethodResultInfluentialSelf-citationGender Disparity in Liver Cancer Due to Sex Differences in MyD88-Dependent IL-6 Production
Naugler, W. E., Sakurai, T., Kim, S., Maeda, S., Kim, K., Elsharkawy, A. M., & Karin, M. (2007) · Science · doi:10.1126/science.1140485 · Cited by 1,955
RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia
Zuber, J., Shi, J., Wang, E., Rappaport, A. R., Herrmann, H., Sison, E. A., Magoon, D., Qi, J., Blatt, K., Wunderlich, M., et al. (2011) · Nature · doi:10.1038/nature10334 · Cited by 1,870
Self-citationChemokine signaling via the CXCR2 receptor reinforces senescence
Acosta, J. C., O'Loghlen, A., Banito, A., Guijarro, M. V., Augert, A., Raguz, S., Fumagalli, M., Da Costa, M., Brown, C., Popov, N., et al. (2008) · Cell · doi:10.1016/j.cell.2008.03.038 · Cited by 1,801 · cited 3×
“We and others have identified a crucial role for NF-kB in the control of SASP and have shown that p53 cooperates with NF-kB to trigger senescence (Acosta et al., 2008; Chien et al., 2011; Jing et al., 2011).”
BackgroundKrtolica, A., Parrinello, S., Lockett, S., Desprez, P.-Y., & Campisi, J. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.211053698 · Cited by 1,730 · cited 2×
“However, the impact of SASP on malignant initiation or progression is poorly understood, with studies suggesting that the program can be either pro- or antitumorigenic (Coppé et al., 2008; Kang et al., 2011; Krtolica et al., 2001; Xue et al., 2007).”
BackgroundSelective depletion of macrophages reveals distinct, opposing roles during liver injury and repair
Duffield, J. S., Forbes, S. J., Constandinou, C. M., Clay, S., Partolina, M., Vuthoori, S., Wu, S., Lang, R., & Iredale, J. P. (2005) · Journal of Clinical Investigation · doi:10.1172/jci200522675 · Cited by 1,649 · cited 1×
“Among the many factors that contribute to this effect, macrophages have long been considered to be crucial for the formation of the fibrotic scar and, paradoxically, for the resolution of fibrosis (Duffield et al., 2005; Ramachandran et al., 2012).”
BackgroundSenescence surveillance of pre-malignant hepatocytes limits liver cancer development
Kang, T.-W., Yevsa, T., Woller, N., Hoenicke, L., Wuestefeld, T., Dauch, D., Hohmeyer, A., Gereke, M., Rudalska, R., Potapova, A., et al. (2011) · Nature · doi:10.1038/nature10599 · Cited by 1,621
Bataller, R. A. (2005) · Journal of Clinical Investigation · doi:10.1172/jci200524282c1 · Cited by 1,480 · cited 2×
“…an ongoing cycle of cell death, HSC proliferation, inflammation, and fibrosis eventually leads to organ failure through cirrhosis, which is the strongest risk factor for the emergence of hepatocellular carcinoma (HCC)—the third leading cause of cancer deaths worldwide (Bataller and Brenner, 2005).”
Control of Angiogenesis in Fibroblasts by p53 Regulation of Thrombospondin-1
Dameron, K. M., Volpert, O. V., Tainsky, M. A., & Bouck, N. (1994) · Science · doi:10.1126/science.7521539 · Cited by 1,437 · cited 2×
“surveillance and can limit the production of new blood vessels through the induction of antiangiogenic molecules (Dameron et al., 1994; Kang et al., 2011; Krizhanovsky et al., 2008).”
BackgroundPromotion of Hepatocellular Carcinoma by the Intestinal Microbiota and TLR4
Dapito, D. H., Mencin, A., Gwak, G.-Y., Pradere, J.-P., Jang, M.-K., Mederacke, I., Caviglia, J. M., Khiabanian, H., Adeyemi, A., Bataller, R., et al. (2012) · Cancer Cell · doi:10.1016/j.ccr.2012.02.007 · Cited by 1,346
Movahedi, K., Laoui, D., Gysemans, C. A., Baeten, M., Stangé, G. M., den Bossche, J. V., Mack, M., PIPELEERS, D. G., Veld, P. I. '., BAETSELIER, P. D., et al. (2010) · Cancer Research · doi:10.1158/0008-5472.can-09-4672 · Cited by 1,268 · cited 2×
“…by the differential expression of gene markers: M1 macrophages express higher levels of inflammatory and antiangiogenic cytokines such as Il1b, whereas M2 macrophages express arginase-1 (Arg1), mannose receptor-1 (Mrc1), and macrophage scavenger receptor 1 (Msr1) (Movahedi et al., 2010).”
BackgroundSenescence in tumours: evidence from mice and humans
Collado, M., & Serrano, M. (2010) · Nature Reviews Cancer · doi:10.1038/nrc2772 · Cited by 1,124 · cited 1×
“Cellular senescence is another p53-dependent program that limits tumorigenesis (Collado and Serrano, 2010).”
BackgroundIdentification and validation of oncogenes in liver cancer using an integrative oncogenomic approach
Zender, L., Spector, M. S., Xue, W., Flemming, P., Cordon-Cardo, C., Silke, J., Fan, S.-T., Luk, J. M., Wigler, M., Hannon, G. J., et al. (2006) · Cell · doi:10.1016/j.cell.2006.05.030 · Cited by 1,065
Self-citationChien, Y., Scuoppo, C., Wang, X., Fang, X., Balgley, B., Bolden, J. E., Premsrirut, P., Luo, W., Chicas, A., Lee, C. S., et al. (2011) · Genes & Development · doi:10.1101/gad.17276711 · Cited by 1,046 · cited 11×
“These results support the antitumorigenic role of NF-kB in senescent cells (Chien et al., 2011; Jing et al., 2011) and highlight the cooperation between NF-kB and p53 in executing the senescence program.”
BackgroundMethodResultInfluentialSelf-citationRamachandran, P., Pellicoro, A., Vernon, M. A., Boulter, L., Aucott, R. L., Ali, A., Hartland, S. N., Snowdon, V. K., Cappon, A., Gordon-Walker, T. T., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1119964109 · Cited by 1,001 · cited 2×
“populations could be identified using these markers, suggesting that yet other macrophage subclasses might be present in damaged livers (Ramachandran et al., 2012).”
BackgroundMarino, S., Vooijs, M., van der Gulden, H., Jonkers, J., & Berns, A. (2000) · Genes & Development · doi:10.1101/gad.14.8.994 · Cited by 920 · cited 4×
“Although the GFAP promoter is primarily expressed in the adult astroglia, GFAP-Cre; p53 conditional knockout mice show no increased evidence of brain tumors or any other disease (Marino et al., 2000), thus allowing us dissect the role of p53 in HSCs without other confounding phenotypes.”
BackgroundInfluentialTumor Suppression in the Absence of p53-Mediated Cell-Cycle Arrest, Apoptosis, and Senescence
Li, T., Kon, N., Jiang, L., Tan, M., Ludwig, T., Zhao, Y., Baer, R., & Gu, W. (2012) · Cell · doi:10.1016/j.cell.2012.04.026 · Cited by 912 · cited 2×
“…of target genes that mediate its diverse effects (Vousden and Prives, 2009). p53 can limit the propagation of premalignant cells by promoting cell-cycle exit or apoptosis, though p53 has other functions that contribute to its tumor-suppressive action depending on context (Li et al., 2012).”
BackgroundRole of NF-κB in p53-mediated programmed cell death
Ryan, K. M., Ernst, M. K., Rice, N. R., & Vousden, K. H. (2000) · Nature · doi:10.1038/35009130 · Cited by 735 · cited 1×
“As has been observed in other contexts (Ryan et al., 2000), p53 triggered NF-kB activation as assessed by the nuclear accumulation of the NF-kB subunit p65 (Figures 6B and S6A).”
BackgroundMacrophages and cathepsin proteases blunt chemotherapeutic response in breast cancer
Shree, T., Olson, O. C., Elie, B. T., Kester, J. C., Garfall, A. L., Simpson, K., Bell-McGuinn, K. M., Zabor, E. C., Brogi, E., & Joyce, J. A. (2011) · Genes & Development · doi:10.1101/gad.180331.111 · Cited by 541
Self-citationPten in stromal fibroblasts suppresses mammary epithelial tumours
Trimboli, A. J., Cantemir-Stone, C. Z., Li, F., Wallace, J. A., Merchant, A. S., Creasap, N., Thompson, J. C., Caserta, E., Wang, H., Chong, J.-L., et al. (2009) · Nature · doi:10.1038/nature08486 · Cited by 507 · cited 4×
“…and Prives, 2009). p53 binds DNA in a sequence-specific manner and controls the expression of target genes that mediate its diverse effects (Vousden and Prives, 2009). p53 can limit the propagation of premalignant cells by promoting cell-cycle exit or apoptosis, though p53 has other…”
BackgroundInfluentialLee, J.-S., Chu, I.-S., Mikaelyan, A., Calvisi, D., Heo, J., Reddy, J., & Thorgeirsson, S. (2004) · Nature Genetics · doi:10.1038/ng1481 · Cited by 472 · cited 1×
“This carcinogen generates tumors in mice resembling aggressive HCC as assessed histopathologically and by gene expression profiling (Lee et al., 2004).”
BackgroundInterleukin-22 induces hepatic stellate cell senescence and restricts liver fibrosis in mice
Kong, X., Feng, D., Wang, H., Hong, F., Bertola, A., Wang, F.-S., & Gao, B. (2012) · Hepatology · doi:10.1002/hep.25744 · Cited by 448 · cited 1×
“In the context of certain wound-healing responses, SASP limits the extent of tissue damage and facilitates wound resolution (Kong et al., 2012; Krizhanovsky et al., 2008).”
BackgroundFibrosis-dependent mechanisms of hepatocarcinogenesis
Zhang, D. Y., & Friedman, S. L. (2012) · Hepatology · doi:10.1002/hep.25670 · Cited by 444 · cited 2×
“Following chemical injury to the liver, quiescent HSCs, which are of mesenchymal origin, enter the cell cycle, differentiate, and sustain a chronic inflammatory response accompanied by fibrosis (Zhang and Friedman, 2012).”
BackgroundAn Oncogenomics-Based In Vivo RNAi Screen Identifies Tumor Suppressors in Liver Cancer
Zender, L., Xue, W., Zuber, J. A., Semighini, C. P., Krasnitz, A., Ma, B., Zender, P., Kubicka, S., Luk, J. M., Schirmacher, P., et al. (2008) · Cell · doi:10.1016/j.cell.2008.09.061 · Cited by 428 · cited 1×
“Accordingly, liver damage in HSC-p53D/D mice was more pronounced, as indicated by decreased serum albumin and increased alanine transaminase levels measured after 13 weeks of treatment (Figure 2A).”
BackgroundSelf-citation黒瀬, 圭., Gilley, K., Matsumoto, S., Watson, P. H., Zhou, X.-P., & Eng, C. (2002) · Nature Genetics · doi:10.1038/ng1013 · Cited by 418 · cited 1×
“However, in other contexts, p53 mutations have been observed in stromal cells in bothmice and humans (Hill et al., 2005; Kurose et al., 2002), suggesting that such a possibility cannot be excluded.”
BackgroundCritical pathways in cellular senescence and immortalization revealed by gene expression profiling
Fridman, A. L., & Tainsky, M. A. (2008) · Oncogene · doi:10.1038/onc.2008.213 · Cited by 385 · cited 1×
“Gene set enrichment analysis (GSEA) revealed significant similarities between p53-arrested HSCs and the ‘‘KEGG_p53’’ pathway gene set, as well as a previously identified senescence signature (Figures S4C and S4D and Tables S1A and S1B) (Fridman and Tainsky, 2008).”
BackgroundSelective Evolution of Stromal Mesenchyme with p53 Loss in Response to Epithelial Tumorigenesis
Hill, R., Song, Y., Cardiff, R. D., & Van Dyke, T. (2005) · Cell · doi:10.1016/j.cell.2005.09.030 · Cited by 324 · cited 1×
“However, in other contexts, p53 mutations have been observed in stromal cells in bothmice and humans (Hill et al., 2005; Kurose et al., 2002), suggesting that such a possibility cannot be excluded.”
BackgroundA Rapid and Scalable System for Studying Gene Function in Mice Using Conditional RNA Interference
Premsrirut, P. K., Dow, L. E., Kim, S. Y., Camiolo, M., Malone, C. D., Miething, C., Scuoppo, C., Zuber, J., Dickins, R. A., Kogan, S. C., et al. (2011) · Cell · doi:10.1016/j.cell.2011.03.012 · Cited by 315
Self-citationCoppé, J.-P., Patil, C. K., Rodier, F., Sun, Y., Muñoz, D. P., Goldstein, J., Nelson, P. S., Desprez, P.-Y., & Campisi, J. (2008) · PLoS Biology · doi:10.1371/journal.pbio.0060301 · Cited by 302 · cited 8×
“Senescent HSCs preferentially secreted Il6, Icam1, and Ifng, whereas proliferating HSCs secreted Il3, Il4, and Il5, among other factors, in agreement with previously reported secretion profiles (Chien et al., 2011; Coppé et al., 2008; Crescenzi et al., 2011).”
BackgroundInfluentialZimmermann, H. W., Seidler, S., Gaßler, N., Nattermann, J., Luedde, T., Trautwein, C., & Tacke, F. (2011) · PLoS ONE · doi:10.1371/journal.pone.0021381 · Cited by 277
ASC is a Bax adaptor and regulates the p53–Bax mitochondrial apoptosis pathway
Ohtsuka, T., Ryu, H., Minamishima, Y. A., Macip, S., Sagara, J., Nakayama, K. I., Aaronson, S. A., & Lee, S. W. (2004) · Nature Cell Biology · doi:10.1038/ncb1087 · Cited by 243 · cited 1×
“…we note that several genes upregulated in senescent HSCs (e.g., Eda2r or Pycard) are known NF-kB activators and either established p53 targets (Ohtsuka et al., 2004; Tanikawa et al., 2009) or (e.g., Tnf, Camk2a, Card11, and Ikbkb) harbored consensus p53-binding motifs (Figures S6B and S6C and…”
BackgroundTumor Stroma-Derived TGF-β Limits Myc-Driven Lymphomagenesis via Suv39h1-Dependent Senescence
Reimann, M., Lee, S., Loddenkemper, C., Dörr, J. R., Tabor, V., Aichele, P., Stein, H., Dörken, B., Jenuwein, T., & Schmitt, C. A. (2010) · Cancer Cell · doi:10.1016/j.ccr.2009.12.043 · Cited by 184 · cited 2×
“, 2008) and/or provoke immune surveillance of the senescent cells, leading to their elimination (Kang et al., 2011; Krizhanovsky et al., 2008; Reimann et al., 2010; Xue et al., 2007).”
BackgroundForni, P. E., Scuoppo, C., Imayoshi, I., Taulli, R., Dastrù, W., Sala, V., Betz, U. A. K., Muzzi, P., Martinuzzi, D., Vercelli, A., et al. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.2815-06.2006 · Cited by 167 · cited 1×
“Though the basis for the male bias remains unclear, we suspect that some form of Cre-mediated damage impacts the proliferation of HSCs as has been seen in some other settings (Forni et al., 2006).”
ResultSun, J. C.-Y., Beilke, J. N., Bezman, N., & Lanier, L. L. (2011) · The Journal of Experimental Medicine · doi:10.1084/jem.20100479 · Cited by 142
Evidence for Nonautonomous Effect of p53 Tumor Suppressor in Carcinogenesis
Kiaris, H., Chatzistamou, I., Trimis, G., Frangou-Plemmenou, M., Pafiti-Kondi, A., & Kalofoutis, A. (2005) · Cancer Research · doi:10.1158/0008-5472.can-04-3791 · Cited by 128 · cited 2×
“These results are consistent with the observation that MCF7 breast cancer cells produce more tumors when injected subcutaneously into p53 null mice compared to wild-type controls (Kiaris et al., 2005) and are reminiscent of studies supporting a non-cell-autonomous role for Pten in suppressing breast cancer development…”
BackgroundResultNuclear Factor-κB1 (p50) Limits the Inflammatory and Fibrogenic Responses to Chronic Injury
Oakley, F., Mann, J., Nailard, S., Smart, D. E., Mungalsingh, N., Constandinou, C., Ali, S., Wilson, S. J., Millward-Sadler, H., Iredale, J. P., et al. (2005) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)62291-2 · Cited by 123
Hesse, M., Cheever, A. W., Jankovic, D. L., & Wynn, T. A. (2000) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)64607-x · Cited by 117 · cited 2×
“Consistent with this view, M2 macrophages accumulate in patients with chronic liver disease (Zimmermann et al., 2011), whereas the accumulation of M1 macrophages has been linked to reduced fibrosis (Hesse et al., 2000).”
BackgroundOpposing roles of NF-κB in anti-cancer treatment outcome unveiled by cross-species investigationsPreprint
Hua, J., Kase, J., Dörr, J. R., Milanovic, M., Lenze, D., Grau, M., Beuster, G., Ji, S., Reimann, M., Lenz, P., et al. (2011) · Genes & Development · doi:10.1101/gad.17620611 · Cited by 102 · cited 6×
“These results support the antitumorigenic role of NF-kB in senescent cells (Chien et al., 2011; Jing et al., 2011) and highlight the cooperation between NF-kB and p53 in executing the senescence program.”
BackgroundResultInfluentialCrescenzi, E., Pacifico, F., Lavorgna, A., Palma, R. D., D’Aiuto, E., Palumbo, G. A., Formisano, S., & Leonardi, A. (2011) · Oncogene · doi:10.1038/onc.2011.1 · Cited by 76 · cited 3×
“Senescent HSCs preferentially secreted Il6, Icam1, and Ifng, whereas proliferating HSCs secreted Il3, Il4, and Il5, among other factors, in agreement with previously reported secretion profiles (Chien et al., 2011; Coppé et al., 2008; Crescenzi et al., 2011).”
BackgroundFormation of Normal Desmin Intermediate Filaments in Mouse Hepatic Stellate Cells Requires Vimentin
Geerts, A. E., Eliasson, C., Niki, T., Wielant, A., Vaeyens, F., & Pekny, M. (2001) · Hepatology · doi:10.1053/jhep.2001.21045 · Cited by 75
XEDAR as a putative colorectal tumor suppressor that mediates p53-regulated anoikis pathway
Tanikawa, C., Furukawa, Y., Yoshida, N., Arakawa, H., Nakamura, Y., & Matsuda, K. (2009) · Oncogene · doi:10.1038/onc.2009.154 · Cited by 67 · cited 2×
“, Eda2r or Pycard) are known NF-kB activators and either established p53 targets (Ohtsuka et al., 2004; Tanikawa et al., 2009) or (e.”
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Binnewies, M., Roberts, E. W., Kersten, K., Chan, V., Fearon, D. F., Merad, M., Coussens, L. M., Gabrilovich, D. I., Ostrand-Rosenberg, S., Hedrick, C. C., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0014-x · Cited by 6,145
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Self-citation
Metadata
- Authors
- Lujambio, A., Akkari, L., Simon, J., Grace, D., Tschaharganeh, D. F., Bolden, J. E., Zhao, Z., Thapar, V., Joyce, J. A., Krizhanovsky, V., & Lowe, S. W.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Cold Spring Harbor Laboratory (US)
- Corresponding author
- Krizhanovsky, Valery
- Lowe, Scott W.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 153
- Issue
- 2
- Pages
- 449-460
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3702034
- OpenAlex
- W2104397341
- Cited by
- 766
- References
- 48
- Citations by year
- 2026: 35 · 2025: 67 · 2024: 61 · 2023: 52 · 2022: 66 · 2021: 74 · 2020: 70 · 2019: 51 · 2018: 62 · 2017: 57 · 2016: 49 · 2015: 47 · 2014: 46 · 2013: 28
- FWCI
- 39.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (submittedVersion)
- Swinburne figshare (Swinburne University of Technology) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Memorial Sloan-Kettering Cancer Center
- Cold Spring Harbor Laboratory
- Deutsche Forschungsgemeinschaft
- Weizmann Institute of Science
- Israel Science Foundation
- National Institute on Aging (R56AG016379, AG-16379, R01AG016379)
- National Cancer Institute (P01CA087497, U54CA148967, P01CA013106, P30CA008748)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- p53, cellular senescence, hepatic stellate cells, liver fibrosis, liver cirrhosis, hepatocellular carcinoma, macrophage polarization, M1/M2 macrophages, tumor microenvironment, chronic liver injury, premalignant cells, secreted factors
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Fibrosis, Humans, Inflammation, Kupffer Cells, Liver, Liver Neoplasms, Macrophages, Tumor Suppressor Protein p53, NF-kappa B, Cellular Senescence, Mice, Hepatic Stellate Cells, Cellular Microenvironment
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