Effect of HDAC9 inhibition on epithelial-mesenchymal transition in CD133+ prostate cancer cell lines
| Autor: | Hong Moon Sohn, Wonbong Lim, Hoon Hyun, Bora Kim |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Male
Epithelial-Mesenchymal Transition Cell Survival Cell Histone Deacetylases Metastasis Prostate cancer DU145 Cell Movement Cancer stem cell Cell Line Tumor LNCaP medicine Humans Pharmacology (medical) AC133 Antigen Epithelial–mesenchymal transition Pharmacology Chemistry Prostatic Neoplasms medicine.disease Repressor Proteins Infectious Diseases medicine.anatomical_structure Oncology embryonic structures Cancer cell Neoplastic Stem Cells Cancer research Genes Neoplasm |
| Zdroj: | Journal of Chemotherapy. 34:45-54 |
| ISSN: | 1973-9478 1120-009X |
| DOI: | 10.1080/1120009x.2021.1963615 |
| Popis: | A small fraction of cancer cells known as cancer stem cells (CSCs) are considered to give rise to differentiated cancer cells and have been proposed to predict cancer recurrence and metastasis. There is further evidence that CSCs may act as metastatic precursors of epithelial-mesenchymal transition (EMT). In the present study, we investigated the key molecules involved in maintaining the stability of CSCs by inducing ectopic overexpression of CD133 to characterize EMT in human prostate cancer cell lines, including PC-3, DU145, and LnCaP cells. Additionally, we investigated whether a specific inhibitor of concomitantly expressed metastasis-related genes could alleviate EMT properties in CD133-overexpressing prostate cancer cells. Ectopic overexpression of CD133 in PC-3, DU145, and LnCaP cells led to an increase in the expression of HDAC9. Moreover, HDAC9 inhibition led to a decrease in EMT properties along with increased E-cadherin expression, a narrower wound gap distance, and enhanced cell invasiveness through the suppression of β-catenin activation and its translocation to the nucleus. Overall, these results suggest that HDAC9 inhibition plays a functional role in the modulation of EMT properties in CSC-like prostate cancer cells. Therefore, these findings could facilitate the development of therapeutic strategies for controlling prostate cancer metastasis. |
| Databáze: | OpenAIRE |
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