Abstract
Long noncoding RNAs (lncRNAs) are transcripts greater than 200 nucleotides that do not code for proteins but regulate gene expression. Recent studies indicate that lncRNAs are involved in the modulation of biological functions in human disease. KCNQ1 Opposite Strand/Antisense Transcript 1 (KCNQ1OT1) encodes a lncRNA from the opposite strand of KCNQ1 in the CDKN1C/KCNQ1OT1 cluster that is reported to play a vital role in the development and progression of cancer. KCNQ1OT1 regulates cancer cell proliferation, cell cycle, migration and invasion, metastasis, glucose metabolism, and immune evasion. The aberrant expression of KCNQ1OT1 in cancer patients is associated with poor prognosis and decreased survival. This review summarizes recent literature related to the biological functions and molecular mechanisms of KCNQ1OT1 in various human cancers, including colorectal, bladder, breast, oral, melanoma, osteosarcoma, lung, glioma, ovarian, liver, acute myeloid leukemia, prostate, and gastric. We also discuss the role of KCNQ1OT1 as a promising diagnostic biomarker and a novel therapeutic target in human cancers.
Highlights
Cancer remains a leading cause of death and a significant public health problem worldwide, with approximately 19.3 million new cancer cases and 10 million deaths occurring in 2020 [1]
We focus on LncRNA KCNQ1OT1 and cancer-associated immune responses [8,10,14,21]
A recent study by Qi et al reported that knockdown of KCNQ1OT1 decreased cell proliferation, migration, and invasion while promoting apoptosis and chemo-sensitivity of overall survival (OS) MG-63 cisplatin-resistant cells to cisplatin through the upregulation of KCNQ1 via DNA methyltransferase 1 (DNMT1) [20] (Table 1)
Summary
Cancer remains a leading cause of death and a significant public health problem worldwide, with approximately 19.3 million new cancer cases and 10 million deaths occurring in 2020 [1]. LncRNAs can interact with a variety of partners such as RNA/DNA-binding proteins, transcription factors, chromatin-modifying complexes, RNA transcripts, mature mRNA, microRNA (miRNA), DNA, and chromatin [17]. LncRNAs harboring microRNA recognition elements factors, function as competing complexes, RNA transcripts, mature mRNA, microRNA (miRNA), DNA, and chromatin endogenous RNAs (ceRNAs) that bind to and “sponge” miRNAs, downregulating and [17]. LncRNAs harboring microRNA recognition elements function as compreventing thempeting from endogenous binding to RNAs and regulating their target. Interaction two classes of RNA is mediated by RNA-induced complex (RISC)to and determines the level of post-transcriptional regulation of gene expresLncRNAs have been shown modulate multiple cancer hallmarks, including cell cycle sion [20].
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