ArticleWorld journal of gastroenterology2022
Lentivirus-mediated short hairpin RNA interference of CENPK inhibits growth of colorectal cancer cells with overexpression of Cullin 4A.
Article in World journal of gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
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- Integrative machine learning identifies lactylation-related gene signature prognostic for chemotherapeutic efficacy in colorectal carcinoma.Discover oncology · 2025Article
- Colon cancer versus colitis: a microRNA and gene expression analysis via system biology tools.Gastroenterology and hepatology from bed to bench · 2025Article
- Ribosome Biogenesis and Cancer: Insights into NOB1 and PNO1 Mechanisms.Current pharmaceutical design · 2024Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
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Abstract
backgroundColorectal cancer (CRC) is one of the most common malignant tumors worldwide. The identification of novel diagnostic and prognostic biomarkers for CRC is a key research imperative. Immunohistochemical analysis has revealed high expression of centromere protein K (CENPK) in CRC. However, the role of CENPK in the progression of CRC is not well characterized.
aimTo evaluate the effects of knockdown of CENPK and overexpression of Cullin 4A (CUL4A) in RKO and HCT116 cells.
methodsHuman colon cancer samples were collected and tested using a human gene expression chip. We identified CENPK as a potential oncogene for CRC based on bioinformatics analysis.
resultsWe demonstrated overexpression of CENPK in human colon cancer samples. CENPK was an independent risk factor in patients with CRC. The downstream genes FBX32, CUL4A, and Yes-associated protein isoform 1 were examined to evaluate the regulatory action of CENPK in RKO cells. Significantly delayed xenograft tumor emergence, slower growth rate, and lower final tumor weight and volume were observed in the CENPK short hairpin RNA virus infected group compared with the CENPK negative control group. The CENPK gene interference inhibited the proliferation of RKO cells
conclusionWe indicated a potential role of CENPK in promoting tumor proliferation, and it may be a novel diagnostic and prognostic biomarker for CRC.
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