{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent findings have demonstrated that miR-6734 can act as an endogenous regulator of cancer cell proliferation. In one study on colon cancer cells, miR-6734 was shown to bind the p21WAF1/CIP1 promoter and induce RNA activation, which up-regulated p21 expression at both the mRNA and protein levels. This activation led to cell cycle arrest and apoptosis, resulting in diminished cell growth. The mechanistic investigation further confirmed that the tumor‑suppressive effects of miR-6734 were mediated through inhibition of Rb phosphorylation and reduction in caspase‐3 and PARP cleavage, all of which could be reversed by p21 knockdown."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a separate study focusing on non‑small cell lung cancer (NSCLC), miR-6734-3p was found to be downregulated in clinical specimens, serum, and cancer cell lines. Restoration of miR‑6734-3p expression inhibited NSCLC progression both in vitro and in vivo by targeting the 3' untranslated region of zinc finger E‑box binding homeobox 2 (ZEB2) mRNA. Downregulation of ZEB2, a known promoter of epithelial-to-mesenchymal transition and chemoresistance, not only suppressed tumor growth but also enhanced cisplatin sensitivity in resistant NSCLC cells. Conversely, depletion of miR‑6734-3p promoted cancer development."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these studies underscore the multifaceted role of miR-6734 as a tumor suppressor in distinct cancer types. By modulating critical pathways—up‑regulating an essential cell cycle inhibitor in colon cancer and targeting key mediators of metastasis and drug resistance in NSCLC—miR‑6734 emerges as a promising biomarker and potential therapeutic target in oncology.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Moo Rim Kang, Ki Hwan Park, Jeong-Ook Yang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "miR-6734 Up-Regulates p21 Gene Expression and Induces Cell Cycle Arrest and Apoptosis in Colon Cancer Cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0160961"}], "href": "https://doi.org/10.1371/journal.pone.0160961"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "27509128"}], "href": "https://pubmed.ncbi.nlm.nih.gov/27509128"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Linying Wei, Jianyang Jiang "}, {"type": "b", "children": [{"type": "t", "text": "Targeting the miR-6734-3p/ZEB2 axis hampers development of non-small cell lung cancer (NSCLC) and increases susceptibility of cancer cells to cisplatin treatment."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Bioengineered (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1080/21655979.2021.1936891"}], "href": "https://doi.org/10.1080/21655979.2021.1936891"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "34107856"}], "href": "https://pubmed.ncbi.nlm.nih.gov/34107856"}]}]}]}