{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent studies have revealed that miR‑1193 plays a critical role in T‑cell leukemia, where its expression is significantly downregulated compared to normal T cells. When restored in Jurkat cells, miR‑1193 markedly suppresses cellular proliferation and invasion by directly targeting and downregulating the pro‑oncogenic transmembrane protein TM9SF3, thereby impeding pathways that normally support malignant growth and dissemination."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of sporadic colorectal cancer, miR‑1193 has been implicated in modulating tumorigenesis through its interaction with the 3′‑untranslated region of the TGF‑β receptor II (TGFBR2) gene. A common single nucleotide polymorphism (rs11466537) in TGFBR2 alters miR‑1193 binding, with the T allele being more susceptible to miR‑1193–mediated repression. Functional assays demonstrated that enhanced miR‑1193 activity leads to significant suppression of TGFBR2 expression, ultimately promoting increased cell proliferation. Notably, the less frequent A allele, which disturbs miR‑1193 regulation, is underrepresented in patient samples, suggesting a contributory role of miR‑1193 dysregulation in colorectal 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": "\nMoreover, in glioblastoma multiforme—a highly aggressive brain tumor—miR‑1193 has emerged as a key factor in the context of DNA repair deficiencies. Inhibition of miR‑1193 in tumor cells lacking DNA‑PKcs function sensitizes them to DNA damage by directly targeting YY1AP1, which in turn affects the expression of critical repair protein FEN1. The subsequent accumulation of DNA double‑strand breaks triggers enhanced ATR checkpoint kinase activity and activation of the CHK1/p53/apoptosis axis, thereby rendering the glioblastoma cells more susceptible to cell death. This synthetic lethal relationship highlights the potential of targeting miR‑1193 for therapeutic benefit in glioblastomas with impaired DNA repair mechanisms."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Liyun Shen, Xingjun Du, Hongyan Ma, et al. "}, {"type": "b", "children": [{"type": "t", "text": "miR-1193 Suppresses the Proliferation and Invasion of Human T-Cell Leukemia Cells Through Directly Targeting the Transmembrane 9 Superfamily 3 (TM9SF3)."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Oncol Res (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.3727/096504017X14908284471361"}], "href": "https://doi.org/10.3727/096504017X14908284471361"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28390114"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28390114"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Hongjuan He, Lei Lei, Erfei Chen, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The screening of the functional microRNA binding site SNPs in sporadic colorectal cancer genes."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cancer Biol Ther (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1080/15384047.2017.1323584"}], "href": "https://doi.org/10.1080/15384047.2017.1323584"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28494187"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28494187"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Jing Zhang, Li Jing, Subee Tan, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Inhibition of miR-1193 leads to synthetic lethality in glioblastoma multiforme cells deficient of DNA-PKcs."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Death Dis (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41419-020-02812-3"}], "href": "https://doi.org/10.1038/s41419-020-02812-3"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32732911"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32732911"}]}]}]}