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MicroRNA 301b (miR-301b) is a small, non-coding RNA molecule (part of the microRNA family) that post-transcriptionally regulates gene expression by binding to mRNA targets and repressing their translation or promoting mRNA degradation. It is involved in crucial cellular processes such as cell proliferation, apoptosis resistance, and migration. miR-301b has been found to be upregulated in several cancers, including breast (especially triple-negative breast cancer), pancreatic, prostate, lung, colorectal, gastric, liver, and bladder cancers. In cancer, miR-301b typically acts as an oncogene by inhibiting tumor suppressors such as CYLD and TGFBR2, leading to enhanced cell proliferation, migration, invasion, and resistance to apoptosis, partially via activation of the NF-κB pathway. Elevated levels of miR-301b can serve as a biomarker for disease progression and poor prognosis in certain cancers. There are ongoing experimental efforts to block miR-301b as a potential anticancer strategy, but therapeutic targeting faces challenges due to its pleiotropic effects and the risk of adverse impacts on normal physiological gene regulation[1][2][3][4].
Targeting the 3′-UTR of specific tumor suppressor mRNAs (e.g., CYLD, TP63, TGFBR2) to suppress their translation, thereby promoting oncogenic signaling[2][3]; Indirect activation of the NF-κB pathway through suppression of CYLD[2]; Promoting cell proliferation and survival through downregulation of pro-apoptotic or tumor suppressor genes[2][3]
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