ArticleCancer chemotherapy and pharmacology2024
TMEM120A-mediated regulation of chemotherapy sensitivity in colorectal cancer cells.
Article in Cancer chemotherapy and pharmacology, 2024. 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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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Age-associated decline of Coenzyme A leads to intestinal stem cells dysfunction via disturbing iron homeostasis.PLoS genetics · 2025Article
- A quinoline-2-thione derivative as a novel chemotherapy drug candidate displays anti-tumor activity in vitro and in vivo.BMC cancer · 2024Article
- Phosphatidic acid is an endogenous negative regulator of PIEZO2 channels and mechanical sensitivity.Nature communications · 2024Article
- TMEM120B strengthens breast cancer cell stemness and accelerates chemotherapy resistance via β1-integrin/FAK-TAZ-mTOR signaling axis by binding to MYH9.Breast cancer research : BCR · 2024Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeEnhancing chemotherapy sensitivity in colorectal cancer (CRC) is critical for improving treatment outcomes. TMEM120A has been reported to interact with coenzyme A (CoA), but its biological significance in CRC is unknown. In this study, we aimed to investigate the functional implications of TMEM120A in CRC and its impact on chemotherapy sensitivity.
methodsStable knockout of TMEM120A in CRC cell lines was conducted using CRISPR/Cas9 technology. Overexpression of various derivatives of TMEM120A was achieved through lentiviral transduction. Cell fractionation was employed to isolate the nuclear and cytoplasmic fraction. Total histones were isolated by acid extraction and then subjected to determine histone acetylation levels using western blot analysis. Cell viability was evaluated using the MTS assay.
resultsWe demonstrate that TMEM120A's nuclear localization is crucial for its role in regulating CRC chemosensitivity. Mechanistically, the nuclear subpopulation of TMEM120A plays a key role in sustaining the nuclear CoA levels, which in turn influences the levels of nuclear acetyl-CoA and histone acetylation in CRC cells. Notably, direct inhibition of histone acetylation recapitulated the phenotypic effects observed upon TMEM120A depletion, leading to increased chemosensitivity in CRC cells.
conclusionOur study provides novel insights into the role of TMEM120A in modulating chemotherapy sensitivity in CRC. Nuclear TMEM120A regulates CoA levels, which in turn modulates nuclear acetyl-CoA levels and histone acetylation, thereby influencing the response of CRC cells to chemotherapy agents. Targeting TMEM120A-mediated pathways may represent a promising strategy for enhancing chemotherapy efficacy in CRC treatment.
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