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- Title
The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells.
- Authors
MACHIKO KOJIMA; KENBUN SONE; KATSUTOSHI ODA; RYUJI HAMAMOTO; SYUZO KANEKO; SHINYA OKI; ASAKO KUKITA; AKIRA KAWATA; HARUNORI HONJOH; YOSHIKO KAWATA; TOMOKO KASHIYAMA; MASAKAZU SATO; AYUMI TAGUCHI; YUICHIRO MIYAMOTO; MICHIHIRO TANIKAWA; TETSUSHI TSURUGA; KAZUNORI NAGASAKA; OSAMU WADA-HIRAIKE; YUTAKA OSUGA; TOMOYUKI FUJII
- Abstract
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-G1 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.
- Subjects
SMALL interfering RNA; CELL cycle; APOPTOSIS inhibition; APOPTOSIS; HISTONE methylation; CELLS
- Publication
Oncology Letters, 2020, Vol 20, Issue 5, p1
- ISSN
1792-1074
- Publication type
Article
- DOI
10.3892/ol.2020.12014