Your browser doesn't support javascript.
loading
SF3B4 promotes Twist1 expression and clear cell renal cell carcinoma progression by facilitating the export of KLF 16 mRNA from the nucleus to the cytoplasm.
Yang, Zhan; Wang, Ya-Xuan; Wen, Jin-Kun; Gao, Hai-Tao; Han, Zhen-Wei; Qi, Jin-Chun; Gu, Jun-Fei; Zhao, Chen-Ming; Zhang, Hong; Shi, Bei; Wang, Dan-Dan; Wang, Xiao-Lu; Qu, Chang-Bao.
Afiliação
  • Yang Z; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Wang YX; Molecular Biology Laboratory, Talent and Academic Exchange Center, The Second Hospital of Hebei Medical University, Shijiazhang, China.
  • Wen JK; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Gao HT; Department of Biochemistry and Molecular Biology, Ministry of Education of China, Hebei Medical University, No. 361 Zhongshan E Rd, Shijiazhuang, 050017, China.
  • Han ZW; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Qi JC; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Gu JF; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Zhao CM; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Zhang H; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Shi B; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Wang DD; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Wang XL; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
  • Qu CB; Department of Urology, The Second Hospital of Hebei Medical University, 215 Heping W Rd, Shijiazhuang, 050000, China.
Cell Death Dis ; 14(1): 26, 2023 01 13.
Article em En | MEDLINE | ID: mdl-36639679
ABSTRACT
Splicing factor 3B subunit 4 (SF3B4) plays important functional roles not only in pre-mRNA splicing, but also in the regulation of transcription, translation, and cell signaling, and its dysregulation contributes to various diseases including Nager syndrome and tumorigenesis. However, the role of SF3B4 and underlying mechanisms in clear cell renal cell carcinoma (ccRCC) remain obscure. In the present study, we found that the expression of SF3B4 was significantly elevated in ccRCC tissues and negatively correlated with the overall survival of ccRCC patients. Upregulation of SF3B4 promotes migration and invasion of ccRCC cells in vitro and in vivo. The promoting effect of SF3B4 on cell migration and invasion is mediated by Twist1, a key transcription factor to mediate EMT. Interestingly, SF3B4, a component of the pre-mRNA spliceosome, is able to promote KLF16 expression by facilitating the transport of KLF16 mRNA into the cytoplasm. Mechanistically, SF3B4 promotes the export of KLF16 mRNA from the nucleus to the cytoplasm and thus enhances KLF16 expression, and in turn elevated KLF16 directly binds to the Twist1 promoter to activate its transcription, leading to EMT and ccRCC progression. Our findings provide evidence that the SF3B4-KLF16-Twist1 axis plays important functional roles in the development and progression of ccRCC, and manipulating this pathway may be a novel therapeutic target for the treatment of ccRCC.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Carcinoma de Células Renais / Neoplasias Renais Limite: Humans Idioma: En Revista: Cell Death Dis Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Carcinoma de Células Renais / Neoplasias Renais Limite: Humans Idioma: En Revista: Cell Death Dis Ano de publicação: 2023 Tipo de documento: Article