ArticlePloS one2018
Single nucleotide polymorphisms in the MYLKP1 pseudogene are associated with increased colon cancer risk in African Americans.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- The noncoding RNAs regulating pyroptosis in colon adenocarcinoma were derived from the construction of a ceRNA network and used to develop a prognostic model.BMC medical genomics · 2022Article
- Whole genome sequencing of Malaysian colorectal cancer patients reveals specific druggable somatic mutations.Frontiers in molecular biosciences · 2022Article
- Review
- A novel tumor suppressor role of myosin light chain kinase splice variants through downregulation of the TEAD4/CD44 axis.Carcinogenesis · 2021Article
- Race, Income, and Survival in Stage III Colon Cancer: CALGB 89803 (Alliance).JNCI cancer spectrum · 2021Observational
- Pseudogenes as Biomarkers and Therapeutic Targets in Human Cancers.Methods in molecular biology (Clifton, N.J.) · 2021Review
- Impact of COL6A4P2 gene polymorphisms on the risk of lung cancer: A case-control study.PloS one · 2021Article
- Re-recognition of pseudogenes: From molecular to clinical applications.Theranostics · 2020Review
- Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
introductionPseudogenes are paralogues of functional genes historically viewed as defunct due to either the lack of regulatory elements or the presence of frameshift mutations. Recent evidence, however, suggests that pseudogenes may regulate gene expression, although the functional role of pseudogenes remains largely unknown. We previously reported that MYLKP1, the pseudogene of MYLK that encodes myosin light chain kinase (MLCK), is highly expressed in lung and colon cancer cell lines and tissues but not in normal lung or colon. The MYLKP1 promoter is minimally active in normal bronchial epithelial cells but highly active in lung adenocarcinoma cells. In this study, we further validate MYLKP1 as an oncogene via elucidation of the functional role of MYLKP1 genetic variants in colon cancer risk.
methodsProliferation and migration assays were performed in MYLKP1-transfected colon and lung cancer cell lines (H441, A549) and commercially-available normal lung and colon cells. Fourteen MYLKP1 SNPs (MAFs >0.01) residing within the 4 kb MYLKP1 promoter region, the core 1.4 kb of MYLKP1 gene, and a 4 kb enhancer region were selected and genotyped in a colorectal cancer cohort. MYLKP1 SNP influences on activity of MYLKP1 promoter (2kb) was assessed by dual luciferase reporter assay.
resultsCancer cell lines, H441 and A549, exhibited increased MYLKP1 expression, increased MYLKP1 luciferase promoter activity, increased proliferation and migration. Genotyping studies identified two MYLKP1 SNPs (rs12490683; rs12497343) that significantly increase risk of colon cancer in African Americans compared to African American controls. Rs12490683 and rs12497343 further increase MYLKP1 promoter activity compared to the wild type MYLKP1 promoter.
conclusionMYLKP1 is a cancer-promoting pseudogene whose genetic variants differentially enhance cancer risk in African American populations.
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