miR-302b: A Comprehensive Review | Zenodo Skip to main Communities My dashboard Log in Sign up Published April 29, 2026 | Version v1 Preprint Open miR-302b: A Comprehensive Review Authors/Creators Bakaleinikova, Evgeniia Description MicroRNA-302b (miR-302b) is a small non-coding RNA belonging to the evolutionarily conserved miR-302/367 cluster located on chromosome 4q25. Originally identified as a hallmark of human embryonic stem cells (hESCs), miR-302b has since emerged as a critical regulator at the intersection of developmental biology, oncology, and regenerative medicine. This comprehensive review synthesizes findings from over 150 published studies to provide an integrated view of miR-302b's genomic organization, biogenesis, molecular targets, and functional roles across multiple biological contexts. In normal physiology, miR-302b maintains pluripotency and controls the G1/S cell cycle checkpoint by targeting key regulators including Cyclin D1, Cyclin D2, CDK2, and epigenetic modifiers such as DNMT1 and AOF1/2. Through modulation of the TGF-β/Nodal, BMP, and Wnt/β-catenin signaling pathways, miR-302b plays an indispensable role in early embryogenesis and somatic cell reprogramming to induced pluripotent stem cells (iPSCs). In cancer, miR-302b predominantly functions as a tumor suppressor, showing consistent downregulation across hepatocellular carcinoma (HCC), gastric cancer, esophageal squamous cell carcinoma (ESCC), breast cancer (particularly triple-negative breast cancer, TNBC), colorectal cancer, glioma, ovarian cancer, and lung cancer. Its anti-tumor activities encompass inhibition of cell proliferation, induction of apoptosis, suppression of epithelial-mesenchymal transition (EMT), attenuation of metastasis and invasion, and reversal of chemotherapy resistance. Key oncogenic targets include EGFR, EphA2, ErbB4, CDK2, Mcl-1, DPYD, and TGFBR2. Upstream regulation of miR-302b involves long non-coding RNAs (lncRNAs) such as MIAT and CASC11 acting as competing endogenous RNAs (ceRNAs). The therapeutic potential of miR-302b is underscored by preclinical evidence demonstrating that miR-302b mimics enhance cisplatin sensitivity in TNBC xenograft models and that miR-302b expression correlates with improved overall survival in cancer patients. This review discusses current delivery strategies, biological challenges, and future directions for translating miR-302b into clinical practice. Keywords: miR-302b; miR-302/367 cluster; tumor suppressor miRNA; cancer stem cells; pluripotency; epithelial-mesenchymal transition; EGFR; cisplatin sensitivity; iPSC reprogramming; ceRNA Files Files (30.5 kB) Name Size Download all miR302b_Comprehensive_Review_v2.docx md5:74fe03c8529eaaa219971f9af8cad86f 30.5 kB Download 128 Views 4 Downloads Show more details All versions This version Views Total views 128 128 Downloads Total downloads 4 4 Data volume Total data volume 122.0 kB 122.0 kB More info on how stats are collected.... Versions External resources Indexed in OpenAIRE Communities Details DOI DOI Badge DOI 10.5281/zenodo.19895363 Markdown [](https://doi.org/10.5281/zenodo.19895363) reStructuredText .. image:: https://zenodo.org/badge/DOI/10.5281/zenodo.19895363.svg :target: https://doi.org/10.5281/zenodo.19895363 HTML <a href="https://doi.org/10.5281/zenodo.19895363"><img src="https://zenodo.org/badge/DOI/10.5281/zenodo.19895363.svg" alt="DOI"></a> Image URL https://zenodo.org/badge/DOI/10.5281/zenodo.19895363.svg Target URL https://doi.org/10.5281/zenodo.19895363 Resource type Preprint Publisher Zenodo Rights License Creative Commons Attribution 4.0 International The Creative Commons Attribution license allows re-distribution and re-use of a licensed work on the condition that the creator is appropriately credited. Read more Citation Export Technical metadata Created April 29, 2026 Modified April 29, 2026 Jump up About About Policies Infrastructure Principles Projects Roadmap Contact Blog Blog Support Help FAQ Developers REST API OAI-PMH Contribute GitHub Donate Funded by Powered by CERN Data Centre & InvenioRDM Status Privacy policy Cookie policy Terms of Use This site uses cookies. Find out more on how we use cookies Accept all cookies Accept only essential cookies