CoChat
Sign Up
Cited by 35

The DOI matches its Crossref record.

Pseudolaric acid B induces mitotic arrest and apoptosis in both 5-fluorouracil-sensitive and -resistant colorectal cancer cells

Wen, Chuangyu, Chen, Junxiong, Zhang, Di, Wang, Huihui, Che, Jia, Qin, Qiyuan, He, Lu, Cai, Zerong, Lin, Mengmeng, Lou, Qiong, Huang, Lanlan, Chen, Daici, Iwamoto, Aikichi, Ren, Donglin, Wang, Lei, Lan, Ping, Wang, Jianping, Liu, Huanliang, Yang, Xiangling·2016·Cancer Letters
DOI 10.1016/j.canlet.2016.09.007
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.canlet.2016.09.007

Cites

Statistics

Figures

Image 1
CC-BY-NC-ND · From the PDF
Fig. 1 PAB inhibits proliferation and induces mitotic arrest in RKO and HCT-15 cells. (A) The proliferation of RKO and HCT-15 cells was measured by real-time cell analysis. Mean ± SD (n ¼ 3). ** P < 0.01, *** P < 0.001, versus control group. (B) The colony formation of RKO and HCT-15 cells was counted after cells were treated with indicated concentrations of PAB for 9 days and then were washed, fi xed, and stained with crystal violet. Mean ± SD (n ¼ 3). * P < 0.05, *** P < 0.001. (C) RKO and HCT-15 cells were stained with PI for DNA contents, followed by fl ow cytometric analysis. Mean ± SD (n ¼ 3). *** P < 0.001. (D) Expression levels of cyclin B1 and p-histone h3 in RKO and HCT-15 were detected by western blot analysis. (For interpretation of the references to color in this fi gure legend, the reader is referred to the web version of this article.)
Fig. 1 PAB inhibits proliferation and induces mitotic arrest in RKO and HCT-15 cells. (A) The proliferation of RKO and HCT-15 cells was measured by real-time cell analysis. Mean ± SD (n ¼ 3). ** P < 0.01, *** P < 0.001, versus control group. (B) The colony formation of RKO and HCT-15 cells was counted after cells were treated with indicated concentrations of PAB for 9 days and then were washed, fi xed, and stained with crystal violet. Mean ± SD (n ¼ 3). * P < 0.05, *** P < 0.001. (C) RKO and HCT-15 cells were stained with PI for DNA contents, followed by fl ow cytometric analysis. Mean ± SD (n ¼ 3). *** P < 0.001. (D) Expression levels of cyclin B1 and p-histone h3 in RKO and HCT-15 were detected by western blot analysis. (For interpretation of the references to color in this fi gure legend, the reader is referred to the web version of this article.)CC-BY-NC-ND · From the PDF
Image 3
CC-BY-NC-ND · From the PDF
Fig. 3 Caspase activation is required for the apoptosis but has no effect in mitotic arrest induced by PAB in CRC cells. (A) RKO and HCT-15 cells were treated with PAB for 48 h and 72 h, respectively, in the absence and presence of 50 m Mpan-caspase inhibitor z-VAD-fmk and then apoptotic cell populations were analyzed by fl ow cytometry. Mean ± SD (n ¼ 3). *** P < 0.001. (B) RKO and HCT-15 cells were treated with PAB for 24 h in the absence and presence of 50 m Mpan-caspase inhibitor z-VAD-fmk and stained with PI for DNA contents, followed by fl ow cytometric analysis.
Fig. 3 Caspase activation is required for the apoptosis but has no effect in mitotic arrest induced by PAB in CRC cells. (A) RKO and HCT-15 cells were treated with PAB for 48 h and 72 h, respectively, in the absence and presence of 50 m Mpan-caspase inhibitor z-VAD-fmk and then apoptotic cell populations were analyzed by fl ow cytometry. Mean ± SD (n ¼ 3). *** P < 0.001. (B) RKO and HCT-15 cells were treated with PAB for 24 h in the absence and presence of 50 m Mpan-caspase inhibitor z-VAD-fmk and stained with PI for DNA contents, followed by fl ow cytometric analysis.CC-BY-NC-ND · From the PDF
Image 5
CC-BY-NC-ND · From the PDF
Fig. 5 CDK1 is involved in the effect of PAB to CRC cells. After 12 h PAB treatment, cells were treated with PAB in the absence and presence of RO-3306 or purvalanol A for 12 h and 36 h. (A) Expressions of p-histone h3 and (B) Expressions of cleaved-PARP and caspase3 were detected by western blot.
Fig. 5 CDK1 is involved in the effect of PAB to CRC cells. After 12 h PAB treatment, cells were treated with PAB in the absence and presence of RO-3306 or purvalanol A for 12 h and 36 h. (A) Expressions of p-histone h3 and (B) Expressions of cleaved-PARP and caspase3 were detected by western blot.CC-BY-NC-ND · From the PDF
Fig. 6 PAB induces proliferation inhibition and mitotic arrest in RKO/5FU-R and HCT-15/5FU-R cells. (A) The viability of RKO/5FU-R and HCT-15/5FU-R cells was measured by MTS assay. (B) The colony formation of cells was counted after PAB-treated RKO/5FU-R and HCT-15/5FU-R cells were washed, fi xed and stained with crystal violet. Mean ± SD (n ¼ 3). *** P < 0.001. (C) RKO/5FU-R and HCT-15/5FU-R cells were stained with PI for DNA contents, followed by fl ow cytometric analysis. Mean ± SD (n ¼ 3). * P < 0.05, ** P < 0.01, *** P < 0.001. (D) Expression levels of cyclin B1 and p-histone h3 in RKO/5FU-R and HCT-15/5FU-R cells were detected by western blot analysis. (For interpretation of the references to color in this fi gure legend, the reader is referred to the web version of this article.)
Fig. 6 PAB induces proliferation inhibition and mitotic arrest in RKO/5FU-R and HCT-15/5FU-R cells. (A) The viability of RKO/5FU-R and HCT-15/5FU-R cells was measured by MTS assay. (B) The colony formation of cells was counted after PAB-treated RKO/5FU-R and HCT-15/5FU-R cells were washed, fi xed and stained with crystal violet. Mean ± SD (n ¼ 3). *** P < 0.001. (C) RKO/5FU-R and HCT-15/5FU-R cells were stained with PI for DNA contents, followed by fl ow cytometric analysis. Mean ± SD (n ¼ 3). * P < 0.05, ** P < 0.01, *** P < 0.001. (D) Expression levels of cyclin B1 and p-histone h3 in RKO/5FU-R and HCT-15/5FU-R cells were detected by western blot analysis. (For interpretation of the references to color in this fi gure legend, the reader is referred to the web version of this article.)CC-BY-NC-ND · From the PDF
Image 8
CC-BY-NC-ND · From the PDF
Image 9
CC-BY-NC-ND · From the PDF
Fig. 9 The schematic diagram of possible molecular mechanism of PAB-induced cytotoxicity in CRC cells.
Fig. 9 The schematic diagram of possible molecular mechanism of PAB-induced cytotoxicity in CRC cells.CC-BY-NC-ND · From the PDF

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

No references could be resolved yet.

Research works printed but not linked: 50

  1. Ferlay, 2015, Cancer incidence and mortality worldwide: Sources, methods and major patterns in GLOBOCAN 2012, Int. J. Cancer, 136, 359, 10.1002/ijc.29210 · DOI · Paper page
  2. Colucci, 2005, Phase III randomized trial of FOLFIRI versus FOLFOX4 in the treatment of advanced colorectal cancer: a multicenter study of the Gruppo Oncologico Dell'Italia Meridionale, J. Clin. Oncol., 23, 4866, 10.1200/JCO.2005.07.113 · DOI
  3. Heinemann, 2014, FOLFIRI plus cetuximab versus FOLFIRI plus bevacizumab as first-line treatment for patients with metastatic colorectal cancer (FIRE-3): a randomised, open-label, phase 3 trial, Lancet Oncol., 15, 1065, 10.1016/S1470-2045(14)70330-4 · DOI · Paper page
  4. Longley, 2006, Drug resistance, predictive markers and pharmacogenomics in colorectal cancer, Biochim. Biophys. Acta, 1766, 184
  5. Newman, 2016, Natural products as Sources of new drugs from 1981 to 2014, J. Nat. Prod., 79, 629, 10.1021/acs.jnatprod.5b01055 · DOI · Paper page
  6. Breinbauer, 2002, From protein domains to drug candidates-natural products as guiding principles in the design and synthesis of compound libraries, Angew. Chem. Int. Ed. Engl., 41, 2879, 10.1002/1521-3773(20020816)41:16<2878::AID-ANIE2878>3.0.CO;2-B · DOI
  7. Zhou, 1991, Some progress on the chemistry of natural bioactive terpenoids from Chinese medicinal plants, Mem. Inst. Oswaldo Cruz., 86, 219, 10.1590/S0074-02761991000600049 · DOI
  8. Li, 1995, Antifungal evaluation of pseudolaric acid B, a major constituent of Pseudolarix kaempferi, J. Nat. Prod., 58, 57, 10.1021/np50115a007 · DOI
  9. Wong, 2005, Pseudolaric acid B, a novel microtubule-destabilizing agent that circumvents multidrug resistance phenotype and exhibits antitumor activity in vivo, Clin. Cancer Res., 11, 6002, 10.1158/1078-0432.CCR-05-0209 · DOI
  10. Ma, 2010, Selective inhibition of human leukemia cell growth and induction of cell cycle arrest and apoptosis by pseudolaric acid B, J. Cancer Res. Clin. Oncol., 136, 1333, 10.1007/s00432-010-0784-0 · DOI
  11. Yu, 2015, Pseudolaric acid B circumvents multidrug resistance phenotype in human gastric cancer SGC7901/ADR cells by downregulating Cox-2 and P-gp expression, Cell Biochem. Biophys., 71, 119, 10.1007/s12013-014-0170-7 · DOI
  12. Qi, 2013, MTOR inactivation by ROS-JNK-p53 pathway plays an essential role in psedolaric acid B induced autophagy-dependent senescence in murine fibrosarcoma L929 cells, Eur. J. Pharmacol., 715, 76, 10.1016/j.ejphar.2013.05.051 · DOI
  13. Tan, 2004, Pseudolarix acid B inhibits angiogenesis by antagonizing the vascular endothelial growth factor-mediated anti-apoptotic effect, Eur. J. Pharmacol., 499, 219, 10.1016/j.ejphar.2004.07.063 · DOI
  14. Li, 2015, Pseudolaric acid B inhibits T-cell mediated immune response in vivo via p38MAPK signal cascades and PPARgamma activation, Life Sci., 121, 88, 10.1016/j.lfs.2014.11.020 · DOI
  15. Gong, 2006, Involvement of JNK-initiated p53 accumulation and phosphorylation of p53 in pseudolaric acid B induced cell death, Exp. Mol. Med., 38, 428, 10.1038/emm.2006.50 · DOI
  16. Zhao, 2012, Pseudolaric acid B induces apoptosis via proteasome-mediated Bcl-2 degradation in hormone-refractory prostate cancer DU145 cells, Toxicol. In Vitro, 26, 595, 10.1016/j.tiv.2012.02.004 · DOI
  17. Qi, 2012, Pseudolaric acid B induces mitotic catastrophe followed by apoptotic cell death in murine fibrosarcoma L929 cells, Eur. J. Pharmacol., 683, 16, 10.1016/j.ejphar.2012.02.035 · DOI
  18. Hou, 2012, Pseudolaric acid B inhibits inducible cyclooxygenase-2 expression via downregulation of the NF-kappaB pathway in HT-29 cells, J. Cancer Res. Clin. Oncol., 138, 885, 10.1007/s00432-011-1120-z · DOI
  19. Wen, 2015, Gambogic acid inhibits growth, induces apoptosis, and overcomes drug resistance in human colorectal cancer cells, Int. J. Oncol., 47, 1663, 10.3892/ijo.2015.3166 · DOI
  20. Mashima, 2005, P53-defective tumors with a functional apoptosome-mediated pathway: A new therapeutic target, J. Natl. Cancer Inst, 97, 765, 10.1093/jnci/dji133 · DOI
  21. Longley, 2006, C-FLIP inhibits chemotherapy-induced colorectal cancer cell death, Oncogene, 25, 838, 10.1038/sj.onc.1209122 · DOI
  22. Crosio, 2002, Mitotic phosphorylation of histone H3: Spatio-temporal regulation by mammalian Aurora kinases, Mol. Cell. Biol., 22, 874, 10.1128/MCB.22.3.874-885.2002 · DOI
  23. Brito, 2006, Mitotic checkpoint slippage in humans occurs via cyclin B destruction in the presence of an active checkpoint, Curr. Biol., 16, 1194, 10.1016/j.cub.2006.04.043 · DOI
  24. Hisatomi, 2012, The regulatory roles of apoptosis-inducing factor in the formation and regression processes of ocular neovascularization, Am. J. Pathol., 181, 53, 10.1016/j.ajpath.2012.03.022 · DOI
  25. Delbridge, 2016, Thirty years of BCL-2: translating cell death discoveries into novel cancer therapies, Nat. Rev. Cancer, 16, 99, 10.1038/nrc.2015.17 · DOI · Paper page
  26. Dynek, 2013, Antagonists of IAP proteins as cancer therapeutics, Cancer Lett., 332, 206, 10.1016/j.canlet.2010.06.013 · DOI
  27. Gascoigne, 2009, How do anti-mitotic drugs kill cancer cells?, J. Cell Sci., 122, 2579, 10.1242/jcs.039719 · DOI · Paper page
  28. Jordan, 2004, Microtubules as a target for anticancer drugs, Nat. Rev. Cancer, 4, 253, 10.1038/nrc1317 · DOI · Paper page
  29. Lara-Gonzalez, 2012, The spindle assembly checkpoint, Curr. Biol., 22, R966, 10.1016/j.cub.2012.10.006 · DOI
  30. Chu, 2012, Cdk1/cyclin B plays a key role in mitotic arrest-induced apoptosis by phosphorylation of Mcl-1, promoting its degradation and freeing Bak from sequestration, Biochem. Pharmacol., 83, 199, 10.1016/j.bcp.2011.10.008 · DOI
  31. Chang, 2016, Randomized controlled trial of intraportal chemotherapy combined with adjuvant chemotherapy (mFOLFOX6) for stage II and III colon cancer, Ann. Surg., 263, 434, 10.1097/SLA.0000000000001374 · DOI
  32. Allegra, 2011, Phase III trial assessing bevacizumab in stages II and III carcinoma of the colon: results of NSABP protocol C-08, J. Clin. Oncol., 29, 11, 10.1200/JCO.2010.30.0855 · DOI
  33. Ciardiello, 2016, Cetuximab continuation after first progression in metastatic colorectal cancer (CAPRI-GOIM): a randomized phase 2 trial of FOLFOX plus cetuximab versus FOLFOX, Ann. Oncol., 27, 1055, 10.1093/annonc/mdw136 · DOI
  34. Li, 2013, Gambogic acid is a tissue-specific proteasome inhibitor in vitro and in vivo, Cell Rep., 3, 211, 10.1016/j.celrep.2012.11.023 · DOI
  35. Shi, 2014, Gambogic acid induces apoptosis in imatinib-resistant chronic myeloid leukemia cells via inducing proteasome inhibition and caspase-dependent Bcr-Abl downregulation, Clin. Cancer Res., 20, 151, 10.1158/1078-0432.CCR-13-1063 · DOI
  36. Yu, 2016, Pseudolaric acid B activates autophagy in MCF-7 human breast cancer cells to prevent cell death, Oncol. Lett., 11, 1731, 10.3892/ol.2016.4103 · DOI
  37. Yu, 2015, Pseudolaric acid B inhibits proliferation in SW579 human thyroid squamous cell carcinoma, Mol. Med. Rep., 12, 7195, 10.3892/mmr.2015.4418 · DOI
  38. Yu, 2013, Pseudolaric acid B induced cell cycle arrest, autophagy and senescence in murine fibrosarcoma l929 cell, Int. J. Med. Sci., 10, 707, 10.7150/ijms.5726 · DOI
  39. Li, 2015, Pseudolaric acid B exerts antitumor activity via suppression of the Akt signaling pathway in HeLa cervical cancer cells, Mol. Med. Rep., 12, 2021, 10.3892/mmr.2015.3615 · DOI
  40. Khan, 2012, Pseudolaric Acid B induces caspase-dependent and caspase-independent apoptosis in u87 glioblastoma cells, Evid. Based Complement. Altern. Med., 2012, 957568, 10.1155/2012/957568 · DOI
  41. Wang, 2013, Pseudolaric acid B induces apoptosis in U937 human leukemia cells via caspase-9mediated activation of the mitochondrial death pathway, Mol. Med. Rep., 8, 787, 10.3892/mmr.2013.1571 · DOI
  42. Shi, 2008, Cell type variation in responses to antimitotic drugs that target microtubules and kinesin-5, Cancer Res., 68, 3269, 10.1158/0008-5472.CAN-07-6699 · DOI
  43. Gascoigne, 2008, Cancer cells display profound intra- and interline variation following prolonged exposure to antimitotic drugs, Cancer Cell, 14, 111, 10.1016/j.ccr.2008.07.002 · DOI · Paper page
  44. Li, 2016, Loss of p53-mediated cell-cycle arrest, senescence and apoptosis promotes genomic instability and premature aging, Oncotarget, 7, 11838, 10.18632/oncotarget.7864 · DOI
  45. Sarkar, 2012, Interaction of pseudolaric acid B with the colchicine site of tubulin, Biochem. Pharmacol., 84, 444, 10.1016/j.bcp.2012.05.014 · DOI
  46. Choi, 2015, Polo-like kinase 1 inhibitor BI2536 causes mitotic catastrophe following activation of the spindle assembly checkpoint in non-small cell lung cancer cells, Cancer Lett., 357, 591, 10.1016/j.canlet.2014.12.023 · DOI
  47. Galluzzi, 2012, Molecular definitions of cell death subroutines: recommendations of the nomenclature committee on cell death 2012, Cell Death Differ., 19, 107, 10.1038/cdd.2011.96 · DOI · Paper page
  48. Lanz, 2013, Mitotic catastrophe triggered in human cancer cells by the viral protein apoptin, Cell Death Dis., 4, e487, 10.1038/cddis.2013.2 · DOI
  49. Holt, 2009, Global analysis of Cdk1 substrate phosphorylation sites provides insights into evolution, Science, 325, 1682, 10.1126/science.1172867 · DOI
  50. Terrano, 2010, Cyclin-dependent kinase 1-mediated Bcl-xL/Bcl-2 phosphorylation acts as a functional link coupling mitotic arrest and apoptosis, Mol. Cell. Biol., 30, 640, 10.1128/MCB.00882-09 · DOI

Cited by

Sorted by citations

See all 35

Metadata

Authors
Wen, C., Chen, J., Zhang, D., Wang, H., Che, J., Qin, Q., He, L., Cai, Z., Lin, M., Lou, Q., Huang, L., Chen, D., Iwamoto, A., Ren, D., Wang, L., Lan, P., Wang, J., Liu, H., & Yang, X.
Venue
Cancer Letters
Publisher
Elsevier BV
Published
2016-12
Volume
383
Issue
2
Pages
295-308
ISSN
0304-3835
DOI
10.1016/j.canlet.2016.09.007
Cited by
35
References
0
Language
en
Licence
Funders
  • Guangdong Innovative Research Team Program (2009010058)
  • Guangdong Provincial Department of Science and Technology (2012B050500004, 2014B020212016)
  • National Key Clinical Discipline
  • National Natural Science Foundation of China (81301978)
  • Overseas Excellent Professor Project, Ministry of Education, China
  • Japan Ministry of Education, Culture, Sports, Science and Technology

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

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Pseudolaric acid B induces mitotic arrest and apoptosis in both 5-fluorouracil-sensitive and -resistant colorectal cancer cells. https://app.cochat.ai/papers/10.1016/j.canlet.2016.09.007
The paper
Wen, C., Chen, J., Zhang, D., Wang, H., Che, J., Qin, Q., He, L., Cai, Z., Lin, M., Lou, Q., Huang, L., Chen, D., Iwamoto, A., Ren, D., Wang, L., Lan, P., Wang, J., Liu, H., & Yang, X. (2016). Pseudolaric acid B induces mitotic arrest and apoptosis in both 5-fluorouracil-sensitive and -resistant colorectal cancer cells. Cancer Letters. https://doi.org/10.1016/j.canlet.2016.09.007