{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long intergenic non‐protein coding RNA 1232 (LINC01232) is emerging as an oncogenic long noncoding RNA that is upregulated in multiple cancer types and plays diverse roles in tumor progression. In pancreatic cancer, LINC01232 expression is elevated and its increased levels correlate with poor patient prognosis. Functionally, LINC01232 promotes cell migration and invasion by interacting with HNRNPA2B1, preventing its ubiquitin‐mediated degradation, modulating the alternative splicing of A‐Raf, and consequently activating the MAPK/ERK signaling pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In a related pancreatic adenocarcinoma study, LINC01232 upregulation was shown to support tumor progression by enhancing cell proliferation and migration via stabilization of TM9SF2 mRNA through recruitment of EIF4A3, a process that is driven by the transcription factor SP1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In non‐small cell lung carcinoma, the transcription factor FOXP3 activates LINC01232, which in turn recruits the RNA binding protein IGF2BP2 to stabilize TGFBR1 mRNA. This stabilization leads to activation of the TGF‐β signaling pathway, thereby promoting cancer cell stemness and influencing the tumor microenvironment through macrophage M2 polarization."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " Elevated LINC01232 expression is also observed in oral carcinoma, where its dysregulation is associated with poor overall and recurrence‐free survival, further supporting its role as a prognostic marker in malignancy."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In gastric cancer, LINC01232 is predominantly nuclear where it binds to EZH2 to epigenetically repress the tumor suppressor KLF2 through increased H3K27 trimethylation, thereby enhancing cancer cell proliferation and tumorigenicity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " In hepatocellular carcinoma (HCC), elevated LINC01232 not only correlates with worse overall survival but is also associated with HBV infection and liver cirrhosis. Mechanistic studies indicate that LINC01232 functions at least in part by sponging miR‑708‑5p, thus promoting HCC progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In bladder cancer, LINC01232 exerts its oncogenic effects by acting as a competing endogenous RNA, sequestering miR‑370‑5p and thereby upregulating the expression of the oncogene PIM3. This axis facilitates increased proliferation, migration, invasion, and reduced apoptosis in cancer cells."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Furthermore, in pancreatic adenocarcinoma, increased serum and tissue levels of LINC01232 have been linked with advanced TNM stage and unfavorable prognosis, with additional analyses suggesting that LINC01232 may sponge miR‑204‑5p, miR‑370‑5p, and miR‑654‑3p, highlighting its potential as both a diagnostic and prognostic biomarker."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these studies demonstrate that LINC01232 contributes to tumorigenesis by modulating key cellular processes—including mRNA stability, alternative splicing, and epigenetic regulation—and by interacting with various microRNAs and proteins. Such multifaceted roles underscore its promise as a potential target for novel diagnostic and therapeutic strategies across a range of cancers.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ling-Dong Meng, Guo-Dong Shi, Wan-Li Ge, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Linc01232 promotes the metastasis of pancreatic cancer by suppressing the ubiquitin-mediated degradation of HNRNPA2B1 and activating the A-Raf-induced MAPK/ERK signaling pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cancer Lett (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.canlet.2020.08.001"}], "href": "https://doi.org/10.1016/j.canlet.2020.08.001"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32814086"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32814086"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Qian Li, Chengbin Lei, Changliang Lu, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "FOXP3 activated-LINC01232 accelerates the stemness of non-small cell lung carcinoma by activating TGF-β signaling pathway and recruiting IGF2BP2 to stabilize TGFBR1."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Exp Cell Res (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.yexcr.2022.113024"}], "href": "https://doi.org/10.1016/j.yexcr.2022.113024"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "35026283"}], "href": "https://pubmed.ncbi.nlm.nih.gov/35026283"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Mingwei Chen, Xiaonan Xu, Haiqing Ma "}, {"type": "b", "children": [{"type": "t", "text": "Identification of oncogenic long noncoding RNAs CASC9 and LINC00152 in oral carcinoma through genome-wide comprehensive analysis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Anticancer Drugs (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1097/CAD.0000000000000725"}], "href": "https://doi.org/10.1097/CAD.0000000000000725"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30543527"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30543527"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Jing Liu, Zhen Li, Guohua Yu, et al. 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