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Fan X, Wang Y, Jiang T, et al. B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2. Oncogene. 2021;40(37):5613-5625doi: 10.1038/s41388-021-01961-9.
Fan, X., Wang, Y., Jiang, T., Liu, T., Jin, Y., Du, K., Niu, Y., Zhang, C., Liu, Z., Lei, Y., & Bu, Y. (2021). B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2. Oncogene, 40(37), 5613-5625. https://doi.org/10.1038/s41388-021-01961-9
Fan, Xiaoyan, et al. "B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2." Oncogene vol. 40,37 (2021): 5613-5625. doi: https://doi.org/10.1038/s41388-021-01961-9
Fan X, Wang Y, Jiang T, Liu T, Jin Y, Du K, Niu Y, Zhang C, Liu Z, Lei Y, Bu Y. B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2. Oncogene. 2021 Sep;40(37):5613-5625. doi: 10.1038/s41388-021-01961-9. Epub 2021 Jul 27. PMID: 34316028; PMCID: PMC8445821.
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Oncogene. 2021 Sep;40(37):5613-5625. doi: 10.1038/s41388-021-01961-9. Epub 2021 Jul 27.

B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2.

Oncogene

Xiaoyan Fan, Yitao Wang, Tinghui Jiang, Tao Liu, Yuelei Jin, Kailong Du, Yulong Niu, Chunxue Zhang, Zhongyu Liu, Yunlong Lei, Youquan Bu

Affiliations

  1. Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, China.
  2. Dermopathic Research Institute, Taizhou University Hospital, Taizhou University, Taizhou, China.
  3. Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China.
  4. Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, China. [email protected].
  5. Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China. [email protected].
  6. Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, China. [email protected].
  7. Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China. [email protected].

PMID: 34316028 PMCID: PMC8445821 DOI: 10.1038/s41388-021-01961-9

Abstract

B-Myb is an important transcription factor that plays a critical role in gene expression regulation and tumorigenesis. However, its functional implication in colorectal cancer remains elusive. In this study, we found that B-Myb was significantly upregulated at both mRNA and protein levels in colorectal cancer samples compared to non-tumor counterparts. B-Myb overexpression accelerated cell proliferation, cell cycle progression and cell motility in colorectal cancer cells, and promoted tumor growth in orthotopic nude mouse models in vivo. In contrast, B-Myb depletion inhibited these malignant phenotypes. Mechanistic investigations revealed that E2F2 was a novel transcriptional target of B-Myb and is essential to B-Myb-induced malignant phenotypes. Notably, B-Myb and E2F2 exhibited positive expression correlation, and interacted with each other in colorectal cancer cells. In addition to their autoregulatory mechanisms, B-Myb and E2F2 can also directly transactivate each other, thus constituting consolidated reciprocal feed-forward transactivation loops. Moreover, both B-Myb and E2F2 are required for the activation of ERK and AKT signaling pathways in colorectal cancer cells. Taken together, our data clarified a critical role for B-Myb in colorectal cancer and unraveled an exquisite mutual collaboration and reciprocal cross regulation between B-Myb and E2F2 that contribute to the malignant progression of human colorectal cancer.

© 2021. The Author(s).

References

  1. Ann N Y Acad Sci. 2006 Dec;1091:270-81 - PubMed
  2. J Clin Oncol. 2010 Sep 1;28(25):3937-44 - PubMed
  3. Nature. 2001 Nov 22;414(6862):457-62 - PubMed
  4. J Gastrointest Oncol. 2013 Jun;4(2):144-57 - PubMed
  5. World J Gastroenterol. 2013 Jun 7;19(21):3189-98 - PubMed
  6. Dev Cell. 2005 Feb;8(2):153-66 - PubMed
  7. Hepatology. 2011 Apr;53(4):1226-36 - PubMed
  8. Dis Esophagus. 2005;18(2):109-13 - PubMed
  9. Genes Dev. 2005 Jul 1;19(13):1499-511 - PubMed
  10. Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10415-9 - PubMed
  11. Appl Immunohistochem Mol Morphol. 2014 Jul;22(6):471-7 - PubMed
  12. Oncotarget. 2017 Jun 29;8(38):63605-63619 - PubMed
  13. Am J Physiol Gastrointest Liver Physiol. 2011 Sep;301(3):G508-18 - PubMed
  14. Nucleic Acids Res. 1988 Dec 9;16(23):11075-89 - PubMed
  15. J Hepatol. 2011 Jul;55(1):111-9 - PubMed
  16. Cell Mol Life Sci. 2003 Nov;60(11):2389-401 - PubMed
  17. Biochim Biophys Acta Rev Cancer. 2020 Dec;1874(2):188407 - PubMed
  18. Int J Biochem Cell Biol. 2013 Mar;45(3):645-56 - PubMed
  19. Biochim Biophys Acta. 2015 Sep;1849(9):1133-44 - PubMed
  20. Oncogene. 2009 Feb 5;28(5):742-51 - PubMed
  21. Aging Cell. 2014 Oct;13(5):773-9 - PubMed
  22. Lung Cancer. 2006 Nov;54(2):155-62 - PubMed
  23. Mol Cell Biol. 2016 Nov 14;36(23):2945-2955 - PubMed
  24. Mol Cell Biol. 2007 Jan;27(1):65-78 - PubMed
  25. J Biol Chem. 2006 Nov 24;281(47):36124-31 - PubMed
  26. CA Cancer J Clin. 2019 Sep;69(5):363-385 - PubMed
  27. Int J Mol Sci. 2018 May 16;19(5): - PubMed
  28. Cell Death Dis. 2017 Jun 22;8(6):e2895 - PubMed
  29. Int J Mol Sci. 2017 May 27;18(6): - PubMed
  30. J Biol Chem. 2004 Mar 12;279(11):10476-83 - PubMed
  31. Clin Cancer Res. 2007 Dec 1;13(23):6938-46 - PubMed
  32. Nat Rev Cancer. 2009 Nov;9(11):785-97 - PubMed
  33. J Cancer Res Clin Oncol. 2021 Jan;147(1):129-138 - PubMed
  34. Nature. 1997 Apr 17;386(6626):713-7 - PubMed
  35. Lancet. 2014 Apr 26;383(9927):1490-1502 - PubMed
  36. CA Cancer J Clin. 2016 Jan-Feb;66(1):7-30 - PubMed
  37. Am J Cancer Res. 2015 Mar 15;5(4):1542-52 - PubMed
  38. Nat Rev Cancer. 2019 Jun;19(6):326-338 - PubMed
  39. Theranostics. 2019 Jul 28;9(19):5577-5594 - PubMed

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