ArticleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences2024
HDAC6-mediated deacetylation of FLOT2 maintains stability and tumorigenic function of FLOT2 in nasopharyngeal carcinoma.
Article in Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- The Role of HDAC6 in Glioblastoma Multiforme: A New Avenue to Therapeutic Interventions?Biomedicines · 2024Review
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4 authors.
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Abstract
objectivesFlotillin-2 (FLOT2) is a prototypical oncogenic and a potential target for cancer therapy. However, strategies for targeting FLOT2 remain undefined. Post-translational modifications are crucial for regulating protein stability, function, and localization. Understanding the mechanisms and roles of post-translational modifications is key to developing targeted therapies. This study aims to investigate the regulation and function of lysine acetylation of FLOT2 in nasopharyngeal carcinoma, providing new insights for targeting FLOT2 in cancer intervention.
methodsThe PhosphoSitePlus database was used to analyze the lysine acetylation sites of FLOT2, and a lysine acetylation site mutation of FLOT2 [FLOT2 (K211R)] was constructed. Nasopharyngeal carcinoma cells were treated with histone deacetylase (HDAC) inhibitor trichostatin A (TSA) and Sirt family deacetylase inhibitor nicotinamide (NAM). TSA-treated human embryonic kidney (HEK)-293T were transfected with FLOT2 mutant plasmids. Co-immunoprecipitation (Co-IP) was used to detect total acetylation levels of FLOT2 and the effects of specific lysine (K) site mutations on FLOT2 acetylation. Western blotting was used to detect FLOT2/FLAG-FLOT2 protein expression in TSA-treated nasopharyngeal carcinoma cells transfected with FLOT mutant plasmids, and real-time reverse transcription PCR (real-time RT-PCR) was used to detect
resultsThe PhosphoSitePlus database indicated that FLOT2 has an acetylation modification at the K211 site. Co-IP confirmed significant acetylation of FLOT2, with TSA significantly increasing overall FLOT2 acetylation levels, while NAM had no effect. Mutation at the K211 site significantly reduced overall FLOT2 acetylation, unaffected by TSA. TSA decreased FLOT2 protein expression in nasopharyngeal carcinoma cells without affecting
conclusionsThe K211 site of FLOT2 undergoes acetylation modification, and HDAC6 mediates deacetylation at this site, inhibiting proteasomal degradation of FLOT2 and maintaining its stability and tumor-promoting function in nasopharyngeal carcinoma.
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