ArticleAging2022
KCNQ1OT1 polymorphism rs35622507 and methylation status of KCNQ1OT1 promoter influence the drug resistance to L-OHP.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 2 citations in OpenAlex.
- Long non-coding RNAs in the crosstalk between diabetes and colorectal cancer: molecular mechanisms and endocrine pathways.Frontiers in molecular biosciences · 2026Review
- Long non-coding RNAs as molecular links and circulating biomarkers between type 2 diabetes and colorectal cancer: focus on shared signaling pathways, epigenetic regulation, and ubiquitination mechanisms.Frontiers in molecular biosciences · 2026Review
- The functions and mechanisms of long non-coding RNA in colorectal cancer.Frontiers in oncology · 2024Review
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundLncRNA potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) has been reported to promote resistance to chemotherapy in colon cancer by inhibiting the expression of miR-34a. And the methylation of KCNQ1OT1 was also reported in the pathogenesis of various diseases. In this study, we aimed to study the combined effect of allele variation of KCNQ1OT1 polymorphism rs35622507 and methylation status of KCNQ1OT1 promoter in the treatment of colon cancer.
methodsThe expression levels of KCNQ1OT1, miR-34a, and ATG4B mRNA were assessed by qRT-PCR. ATG4B protein expression was analyzed by Western blot analysis. TUNEL and MTT assay were performed to examine the cell apoptosis and viability. Luciferase assays revealed the relationship between KCNQ1OT1, miR-34a and ATG4B.
resultsCarrier of allele 10 and methylated promoter in KCNQ1OT1 was associated with decreased KCNQ1OT1/ATG4B expression, increased miR-34a expression and enhanced apoptosis in colon cancer tissue samples. And subsequent luciferase assay showed that miR-34a could bind to KCNQ1OT1 and ATG4B at specific binding sites. The knockdown of KCNQ1OT1 significantly suppressed the KCNQ1OT1/ATG4B expression, improved the miR-34a expression and reduced the viability of HCT116 and SW480 cells. The over-expression of ATG4B notably restored the cell viability loss and apoptosis increase induced by the knockdown of KCNQ1OT1. Moreover, oxaliplatin (L-OHP) treatment elevated the apoptosis of HCT116 and SW480 cells.
conclusionsThe drug resistance in the treatment of colon cancer is most reduced in patients carrying allele 10 and methylated in KCNQ1OT1 promoter. This function is accomplished by the signaling pathway of KCNQ1OT1/miR-34a/ATG4B.
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