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Long intergenic non-protein coding RNA 1106 (LINC01106) is a long non-coding RNA (lncRNA) that does not encode a protein but regulates gene expression at transcriptional and post-transcriptional levels[7]. LINC01106 is overexpressed in several human cancers, notably colorectal cancer and lung adenocarcinoma, where it promotes cell proliferation, migration, invasion, maintenance of stem cell-like properties, and autophagy[1][4][6][8]. Mechanistically, in colorectal cancer, LINC01106 acts as a competing endogenous RNA (ceRNA) by sponging miR-449b-5p, thereby upregulating GLI family oncogenes, and in the nucleus, recruits RNA-binding proteins such as FUS to activate transcription of oncogenic factors (Gli1, Gli2)[1][2][4]. In lung adenocarcinoma, LINC01106 recruits TAF15 to stabilize TEAD4 mRNA and facilitate autophagy by upregulating autophagy-related genes[6]. High LINC01106 expression is correlated with poor prognosis and aggressive tumor features, making it a potential biomarker and investigational target for cancer therapy, though it is not a conventional receptor or enzyme drug target[1][4][6][8].
Not applicable for small molecules/biologics as no specific drugs are reported to interact with LINC01106.
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