ArticleCancer management and research2018
Trichostatin A promotes GLI1 degradation and P21 expression in multiple myeloma cells.
Article in Cancer management and research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Chromatin Accessibility in Cancer: Biological Functions, Mechanisms, Therapeutic Potential, and Future Directions.MedComm · 2026Review
- Pharmacological Properties of Trichostatin A, Focusing on the Anticancer Potential: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Advances in glioma-associated oncogene (GLI) inhibitors for cancer therapy.Investigational new drugs · 2022Review
- The role of protein acetylation in carcinogenesis and targeted drug discovery.Frontiers in endocrinology · 2022Review
- The roles of curcumin in regulating the tumor immunosuppressive microenvironment.Oncology letters · 2020Review
- HDAC6 inhibitor WT161 induces apoptosis in retinoblastoma cells and synergistically interacts with cisplatin.Translational cancer research · 2019Article
- The Role of the Cyclin Dependent Kinase Inhibitor p21Cancers · 2019Review
- Using Prognosis-Related Gene Expression Signature and Connectivity Map for Personalized Drug Repositioning in Multiple Myeloma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Non-canonical Hedgehog Signaling Pathway in Cancer: Activation of GLI Transcription Factors Beyond Smoothened.Frontiers in genetics · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHistone deacetylase inhibitors are promising drugs for the future application in cancer therapy. Trichostatin A (TSA), a histone deacetylase inhibitor, exhibits effective antitumor effects in various cancers. However, the effects and underlying mechanisms of TSA on multiple myeloma (MM) are not fully investigated.
methodsIn the present study, RPMI8226 and MM.1S cells treated with TSA were used for cell proliferation, cell cycle, and survival examinations, then the localization and post transcriptional modification of GLI1 protein as well as the target gene P21 were analyzed using immunofluorescence, immunoprecipitation, western blots and qPCR, respectively.
resultsTSA exerted a time and dose-dependent cytotoxicity on MM cell lines, and suppressed the proliferation of MM cells and induced an upregulation of p21 protein accompanied by a decreased expression of cyclin D1. TSA treatment led to a downregulation of GLI1, and the nuclear accumulation of GLI1 was also inhibited. As a result of hedgehog inhibition, the expression of
conclusionThese results indicated that TSA represses MM cell growth and induces cell apoptosis. The inhibition of hedgehog signaling is an important mechanism accounting for the cytotoxic effects of TSA.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.