AI Article Synopsis
- Salivary adenoid cystic carcinoma (SACC) is a common but aggressive salivary gland cancer, and this study focuses on the role of a specific protein, WHSC1, in its progression.
- The researchers examined tissue samples and conducted experiments on SACC cells to see how reducing WHSC1 levels affected cell growth, survival, and tumor formation, revealing that lowering WHSC1 led to decreased proliferation and increased cell death.
- The findings suggest that targeting WHSC1 might be a viable therapeutic strategy for SACC, as its knockdown impacts key growth-related genes and the overall tumor development process.
Article Abstract
Background/aim: Salivary adenoid cystic carcinoma (SACC) is the most common malignancy of the salivary gland with a poor prognosis and survival. The present study aimed to investigate the role of histone methyltransferase WHSC1 in SACC.
Materials And Methods: Human SACC specimens were evaluated for WHSC1 expression by RT-PCR and immunohistochemistry. The effects of WHSC1 knockdown on SACC cells proliferation, cell cycle, clone and tumorsphere formation, and apoptosis as well as on the expression of related genes were examined. A xenograft mouse model of SACC was used to evaluate the in vivo effects of WHSC1 knockdown on SACC tumorigenesis.
Results: WHSC1 expression was up-regulated in human SACC tissues (p<0.01). WHSC1 knockdown in SACC cells significantly inhibited cell proliferation, clone and tumorsphere formation (p<0.05). Cell distribution at the S and G/M phases was significantly reduced by WHSC1 knockdown (p<0.05). WHSC1 knockdown significantly increased apoptosis of SACC cells (p<0.05). c-Myc, survivin, Bcl-2 and cyclin B1 genes were significantly down-regulated by WHSC1 knockdown cells (p<0.05). WHSC1 knockdown significantly reduced H3K36me2 modification of the MYC gene promoter in SACC cells and tumorigenesis of SACC cells in vivo (p<0.05).
Conclusion: Knockdown of WHSC1 inhibited cell proliferation, induced apoptosis and affected tumorigenesis in SACC.
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| http://dx.doi.org/10.21873/anticanres.13399 | DOI Listing |
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