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Suppressor of Variegation 3-9 Homolog 2, a Novel Binding Protein of Translationally Controlled Tumor Protein, Regulates Cancer Cell Proliferation.
Kim, A-Reum; Sung, Jee Young; Rho, Seung Bae; Kim, Yong-Nyun; Yoon, Kyungsil.
Afiliação
  • Kim AR; Division of Translational Science, Research Institute, National Cancer Center, Goyang 10408, Republic of Korea.
  • Sung JY; Division of Clinical Research, Research Institute, National Cancer Center, Goyang 10408, Republic of Korea.
  • Rho SB; Division of Translational Science, Research Institute, National Cancer Center, Goyang 10408, Republic of Korea.
  • Kim YN; Division of Translational Science, Research Institute, National Cancer Center, Goyang 10408, Republic of Korea.
  • Yoon K; Division of Translational Science, Research Institute, National Cancer Center, Goyang 10408, Republic of Korea.
Biomol Ther (Seoul) ; 27(2): 231-239, 2019 Mar 01.
Article em En | MEDLINE | ID: mdl-30763986
ABSTRACT
Suppressor of Variegation 3-9 Homolog 2 (SUV39H2) methylates the lysine 9 residue of histone H3 and induces heterochromatin formation, resulting in transcriptional repression or silencing of target genes. SUV39H1 and SUV39H2 have a role in embryonic development, and SUV39H1 was shown to suppress cell cycle progression associated with Rb. However, the function of human SUV39H2 has not been extensively studied. We observed that forced expression of SUV39H2 decreased cell proliferation by inducing G1 cell cycle arrest. In addition, SUV39H2 was degraded through the ubiquitin-proteasomal pathway. Using yeast two-hybrid screening to address the degradation mechanism and function of SUV39H2, we identified translationally controlled tumor protein (TCTP) as an SUV39H2-interacting molecule. Mapping of the interacting regions indicated that the N-terminal 60 amino acids (aa) of full-length SUV39H2 and the C-terminus of TCTP (120-172 aa) were critical for binding. The interaction of SUV39H2 and TCTP was further confirmed by co-immunoprecipitation and immunofluorescence staining for colocalization. Moreover, depletion of TCTP by RNAi led to up-regulation of SUV39H2 protein, while TCTP overexpression reduced SUV39H2 protein level. The half-life of SUV39H2 protein was significantly extended upon TCTP depletion. These results clearly indicate that TCTP negatively regulates the expression of SUV39H2 post-translationally. Furthermore, SUV39H2 induced apoptotic cell death in TCTP-knockdown cells. Taken together, we identified SUV39H2, as a novel target protein of TCTP and demonstrated that SUV39H2 regulates cell proliferation of lung cancer cells.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Biomol Ther (Seoul) Ano de publicação: 2019 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Biomol Ther (Seoul) Ano de publicação: 2019 Tipo de documento: Article