ArticleDiscover oncology2023
WDR76 regulates 5-fluorouracil sensitivity in colon cancer via HRAS.
Article in Discover oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- Prognostic Significance and Immune Landscape of Neuroendocrine Differentiation-Related Genes in Non-Small Cell Lung Cancer.Biological procedures online · 2026Article
- An integrated structural model of the DNA damage-responsive H3K4me3 binding WDR76:SPIN1 complex with the nucleosome.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Integrated transcriptomic and immunogenomic analysis unravels the immunological functions and prognostic landscape of WD repeat domain 76.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWD repeat domain 76 (WDR76) has been reported in multiple tumors, while without relation to chemotherapy resistance. 5-fluorouracil (5-FU) is widely adopted in treating colon cancer. However, the resistance of WDR76 and 5-FU in colon cancer remains unclear.
methodsLimma package in R software was employed to analyze the differentially expressed genes. Western blot or quantitative real-time PCR (qRT-PCR) were run to assessed the gene expression. The cytotoxic effect was determined according to cell viability assay, colony formation assay in vitro. Cell apoptosis was assayed using flow cytometry. GSEA analysis was performed to identify pathways related to the target gene. Xenografted mice model was employed to evaluate the tumor growth.
resultsBioinformatic analysis revealed the higher expression of WDR76 in 5-FU sensitive colon cancer cells compared to resistant colon cancer cells, accompanied by the decreased mRNA expression of WDR76 in 5-FU resistant colon cancer cells. The overexpressed WDR76 resulted in the apoptosis and the downregulated colony numbers in 5-FU resistant colon cancer cells, leading to the elevated sensitivity of 5-FU. Meanwhile, knockdown of WDR76 enhances the resistance of 5-FU in colon cancer both in vitro and vivo, which was reversed by a specific inhibitor of HRAS, Kobe006. An important molecular mechanism of 5-FU resistance lies the degradation of HRAS induced by WDR76.
conclusionOur findings demonstrated a role of WDR76 as a promising target for reversing the resistance of colon cancer to 5-FU.
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