ArticleOncogene2021
B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Ru3: a novel ruthenium-based compound overcomes cisplatin resistance in non-small cell lung cancer via the E2F2-IGFBP3-GPX4 pathway.Apoptosis : an international journal on programmed cell death · 2026Article
- A DLEU2/E2F1 regulatory axis promotes migration and invasion phenotypes in cervical squamous cell carcinoma.Scientific reports · 2026Article
- Article
- Hypoxic HPV-Positive Cancer Cells Are Particularly Sensitive to the Pro-Senescent Effects of B-MYB Repression Due to the Lack of Compensatory A-MYB Induction.Journal of medical virology · 2025Article
- MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells.Scientific reports · 2025Article
- Construction of a Prognostic Model for Cervical Cancer Related to lncRNA Based on Differential Co-expression Network and Functional Study of Key Gene EGFR-AS1.Journal of Cancer · 2025Article
- ETV4 interacts with LOXL2 to induce epigenetic activation of NID1 during colorectal cancer progression.International journal of biological sciences · 2025Article
- EMC2 promotes breast cancer progression and enhances sensitivity to PDK1/AKT inhibition by deubiquitinating ENO1.International journal of biological sciences · 2025Article
- B-Myb deficiency boosts bortezomib-induced immunogenic cell death in colorectal cancer.Scientific reports · 2024Article
- Genome-wide binding analysis unveils critical implication of B-Myb-mediated transactivation in cancers.International journal of biological sciences · 2024Article
- Integrated machine learning identifies a cellular senescence-related prognostic model to improve outcomes in uterine corpus endometrial carcinoma.Frontiers in immunology · 2024Article
- The role of E2F2 in cancer progression and its value as a therapeutic target.Frontiers in immunology · 2024Review
- The MYBL2-CCL2 axis promotes tumor progression and resistance to anti-PD-1 therapy in ovarian cancer by inducing immunosuppressive macrophages.Cancer cell international · 2023Article
- ESRRB Inhibits the TGFβ Signaling Pathway to Drive Cell Proliferation in Cervical Cancer.Cancer research · 2023Article
- Clinical evidence for a role of E2F1-induced replication stress in modulating tumor mutational burden and immune microenvironment.DNA repair · 2023Article
- Cancer Vaccines: From the State of the Art to the Most Promising Frontiers in the Treatment of Colorectal Cancer.Pharmaceutics · 2023Review
- RNA-seq reveals novel mechanistic targets of Livin in bladder cancer.BMC urology · 2023Article
- PFDN2 promotes cell cycle progression via the hnRNPD-MYBL2 axis in gastric cancer.Frontiers in oncology · 2023Article
- SKA2-mediated transcriptional downregulation of the key enzyme of CoQJournal of Cancer · 2023Article
- Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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