期刊
ONCOLOGY LETTERS
卷 20, 期 5, 页码 -出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2020.12014
关键词
histone methyltransferase; SMYD2; ovarian clear cell carcinoma; epigenetic modification; SMYD2 selective inhibitor
类别
资金
- Ministry of Education, Culture, Sports, Science and Technology of Japan [18K09249, 15K10705, 17K11268, 15H06173]
- Project for Cancer Research and Therapeutic Evolution from The Japan Agency for Medical Research and Development [17K11268]
- Grants-in-Aid for Scientific Research [15K10705, 17K11268, 18K09249, 15H06173] Funding Source: KAKEN
Previous studies have suggested that histone methylation can modulate carcinogenesis and cancer progression. For instance, the histone methyltransferase SET and MYND domain containing 2 (SMYD2) is overexpressed in several types of cancer tissue. The aim of the present study was to determine whether SMYD2 could serve a therapeutic role in ovarian clear cell carcinoma (OCCC). Reverse transcription-quantitative PCR was used to examine SMYD2 expression in 23 clinical OCCC specimens. Moreover, OCCC cell proliferation and cell cycle progression were also examined following small interfering RNA-mediated SMYD2 silencing or treatment with a selective SMYD2 inhibitor. SMYD2 was significantly upregulated in clinical OCCC specimens, compared with normal ovarian tissue. In addition, SMYD2 knockdown decreased cell viability as determined via a Cell Counting Kit-8 assay. Moreover, the proportion of cells in the sub-G(1) phase increased following SMYD2 knockdown, suggesting increased apoptosis. Treatment with the SMYD2 inhibitor LLY-507 suppressed OCCC cell viability. These results suggested that SMYD2 could promote OCCC viability, and that SMYD2 inhibition induced apoptosis in these cells. Thus, SMYD2 inhibitors may represent a promising molecular targeted approach for OCCC treatment.
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