ArticleBMC cancer2024
HOXC11-mediated regulation of mitochondrial function modulates chemoresistance in colorectal cancer.
Article in BMC cancer, 2024. 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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Who cites it
3 citing papers in PubMed.
- Anticancer Potential of Streptomyces sp. Strain M12: Apoptosis Induction and Anti-Migratory Effects in Colorectal Cancer Cells.Applied biochemistry and biotechnology · 2026Article
- HOXC11 promotes head and neck squamous cell carcinomas (HNSCC) progression by regulating SPHK1 through the Wnt signaling pathway.Cancer gene therapy · 2026Article
- Identification and Validation of Prognostic Genes Related to Histone Lactylation Modification in Glioblastoma: An Integrated Analysis of Transcriptome and Single-cell RNA Sequencing.Journal of Cancer · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundChemoresistance remains a significant challenge in colorectal cancer (CRC) treatment, necessitating a deeper understanding of its underlying mechanisms. HOXC11 has emerged as a potential regulator in various cancers, but its role in CRC chemoresistance remains unclear.
methodsSulforhodamine B assay was employed to assess the cell viability of CRC cells following treatment with chemotherapeutic drugs. Immunofluorescence staining was performed to examine the subcellular localization of HOXC11 in normal and chemoresistant CRC cells. The Seahorse mito stress test was conducted to evaluate the mitochondrial respiratory function of CRC cells. Real-time PCR was utilized to measure the expression level and copy number of mitochondrial DNA (mtDNA).
resultsOur findings revealed that HOXC11 was overexpressed in CRC cells compared to normal colorectal cells and correlated with poorer prognosis in CRC patients. Knockout of HOXC11 reversed acquired chemoresistance in CRC cells. Furthermore, we observed a functional subset of HOXC11 localized to the mitochondria in chemoresistant CRC cells, which regulated mitochondrial function by modulating mtDNA transcription, thereby affecting chemoresistance.
conclusionsIn summary, our study reveals that HOXC11 regulates mitochondrial function through the modulation of mtDNA transcription, impacting chemoresistance in colorectal cancer cells. These findings underscore the significance of understanding the molecular mechanisms underlying chemoresistance and highlight the potential therapeutic implications of targeting mitochondrial function in CRC treatment.
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