ArticleCommunications biology2023
The ATF2/miR-3913-5p/CREB5 axis is involved in the cell proliferation and metastasis of colorectal cancer.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- CREB5 regulates stem cell-like transcriptional programs to enhance tumor progression in prostate cancer.Oncotarget · 2026Article
- miR-3913-3p promoted the progression of lung adenocarcinoma by regulating STX3 expression.Hereditas · 2026Article
- Activating transcription factors: Orchestrators of macrophage biology in pathological settings (Review).International journal of molecular medicine · 2026Review
- CREB5 promotes nodal metastasis of cervical cancer by regulation of APLN-induced lymphangiogenesis.Cell death discovery · 2025Article
- DDHD2 provides a flux of saturated fatty acids for neuronal energy and function.Nature metabolism · 2025Article
- Regulatory role of ATF2 in trophoblast ferroptosis via the PI3K/Akt/Nrf2 pathway in gestational diabetes mellitus.Journal of diabetes investigation · 2025Article
- MicroRNAs in the Diagnosis of Digestive Diseases: A Comprehensive Review.Journal of clinical medicine · 2025Review
- Up-regulation of mBMC cancer · 2025Article
- Enhancing fibroblast-epithelial cell communications: Serpine2 as a key molecule inFrontiers in immunology · 2025Article
- Identification of key genes to predict response to chemoradiotherapy and prognosis in esophageal squamous cell carcinoma.Frontiers in molecular biosciences · 2024Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various miRNAs have been shown to participate in the tumor progression and development of colorectal cancer (CRC). However, the role of miR-3913-5p in CRC are yet to be clearly defined. In the present study, we determine that miR-3913-5p is downregulated in CRC cell lines and CRC tissues. Exogenous miR-3913-5p expression weakens the CRC cells growth, migration and invasion. Mechanistically, miR-3913-5p directly targets the 3'UTR of CREB5. Overexpression of CREB5 reverses the suppression of CRC cells proliferation, migration and invasion induced by miR-3913-5p. Furthermore, ATF2 negatively regulates the transcription of miR-3913-5p by binding to its promoter. CREB5 can cooperate with ATF2. CREB5 is required for ATF2 in regulating miR-3913-5p. Finally, inverse correlations can be found between the expressions of miR-3913-5p and CREB5 or ATF2 in CRC tissues. Thus, a plausible mechanism of ATF2/miR-3913-5p/CREB5 axis regulating CRC progression is elucidated. Our findings suggest that miR-3913-5p functions as a tumor suppressor in CRC. ATF2/miR-3913-5p/CREB5 axis might be a potential therapeutic target against CRC progression.
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