한빛사논문
- 조회760
Kwangho Kim1,2,8, Tae Young Ryu1,8, Eunsun Jung1,8, Tae-Su Han1,3,4,8, Jinkwon Lee1,3, Seon-Kyu Kim 1, Yu Na Roh1,3,Moo-Seung Lee1, Cho-Rok Jung1,3, Jung Hwa Lim1, Ryuji Hamamoto5, Hye Won Lee6, Keun Hur 7, Mi-Young Son 1,3,4, Dae-Soo Kim 1,3 and Hyun-Soo Cho 1,3,4
1Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
2College of Pharmacy, Chungnam National University, Daejeon, Republic of Korea.
3Department of Functional Genomics, Korea University of Science and Technology, Daejeon, Republic of Korea.
4Department of Biological Science, Sungkyunkwan University, Suwon, Republic of Korea.
5Division of Molecular Modification and Cancer Biology, National Cancer Center, Tokyo, Japan.
6Department of Pathology, Keimyung University School of Medicine, Daegu, Republic of Korea.
7Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
8These authors contributed equally: Kwangho Kim, Tae Young Ryu, Eunsun Jung, Tae-Su Han.
Corresponding authors : Correspondence to Keun Hur, Mi-Young Son, Dae-Soo Kim or Hyun-Soo Cho.
Abstract
Epigenetic alterations, especially histone methylation, are key factors in cell migration and invasion in cancer metastasis. However, in lung cancer metastasis, the mechanism by which histone methylation regulates metastasis has not been fully elucidated. Here, we found that the histone methyltransferase SMYD2 is overexpressed in lung cancer and that knockdown of SMYD2 could reduce the rates of cell migration and invasion in lung cancer cell lines via direct downregulation of SMAD3 via SMYD2-mediated epigenetic regulation. Furthermore, using an in vitro epithelial-mesenchymal transition (EMT) system with a Transwell system, we generated highly invasive H1299 (In-H1299) cell lines and observed the suppression of metastatic features by SMYD2 knockdown. Finally, two types of in vivo studies revealed that the formation of metastatic tumors by shSMYD2 was significantly suppressed. Thus, we suggest that SMYD2 is a potential metastasis regulator and that the development of SMYD2-specific inhibitors may help to increase the efficacy of lung cancer treatment.
논문정보
- Research article
- 2023년 05월 (BRIC 등록일 2023-05-19)
- 국내(교신)+국외 연구진
- 생명과학 > 노화/암생물학
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