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PTRF suppresses the progression of colorectal cancers.
Wang, Fengyun; Zheng, Yongqiu; Orange, Matthew; Yang, Chunlin; Yang, Bin; Liu, Jiong; Tan, Tao; Ma, Xiangxue; Chen, Tin; Yin, Xiaolan; Tang, Xudong; Zhu, Hua.
Afiliación
  • Wang F; Gastroenterology Department, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Zheng Y; Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Orange M; Department of Physical Education and Human Performance, Central Connecticut State University, New Britain, CT, USA.
  • Yang C; Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
  • Yang B; Gastroenterology Department, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Liu J; Gastroenterology Department, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Tan T; Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
  • Ma X; Gastroenterology Department, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Chen T; Gastroenterology Department, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Yin X; Gastroenterology Department, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Tang X; Gastroenterology Department, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Zhu H; Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Oncotarget ; 8(30): 48650-48659, 2017 Jul 25.
Article en En | MEDLINE | ID: mdl-27203393
As a key component of caveolae structure on the plasma membrane, accumulated evidence has suggested that Polymerase I and Transcript Release Factor (PTRF) plays a pivotal role in suppressing the progression of human malignances. However, the function of PTRF in the development of colorectal cancers is still unclear. Here we report that the expression of PTRF is significantly reduced in tumor tissues derived from human patients with colorectal cancers, and that the downregulation of PTRF correlates to the advanced stage of the disease. In addition, we found that the expression of PTRF negatively regulates the tumorigenic activities of colorectal cell lines (Colo320, HT29 and CaCo2). Furthermore, ectopic PTRF expression caused significant suppression of cellular proliferation, and anchorage-independent colony growth of Colo320 cells, which have the lowest expression level of PTRF in the three studied cell lines. Meanwhile, shRNA mediated knockdown of PTRF in CaCo2 cells significantly promoted cellular proliferation and anchorage-independent colony growth. In addition, in vivo assays further revealed that tumor growth was significantly inhibited in xenografts with ectopic PTRF expression as compared to untreated Colo320 cells, but was markedly enhanced in PTRF knockdown CaCo2 cells. Biochemical studies revealed that overexpression of PTRF led to the suppression of the AKT/mTOR pathway, as evidenced by reduced phosphorylation of AKT, mTOR, and downstream MMP-9. Thus, these findings, for the first time, demonstrated that PTRF inhibits the tumorigenesis of colorectal cancers and that it might serve as a potential therapeutic target for human colon cancer patients.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Proteínas de Unión al ARN Límite: Adult / Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Oncotarget Año: 2017 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Proteínas de Unión al ARN Límite: Adult / Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Oncotarget Año: 2017 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos