2. Academic Validation
  3. Rab26 suppresses migration and invasion of breast cancer cells through mediating autophagic degradation of phosphorylated Src

Rab26 suppresses migration and invasion of breast cancer cells through mediating autophagic degradation of phosphorylated Src

  • Cell Death Dis. 2021 Mar 17;12(4):284. doi: 10.1038/s41419-021-03561-7.
Huiying Liu  # 1,  Yuxia Zhou  # 2,  Hantian Qiu 1,  Ruijuan Zhuang 1,  Yang Han 1,  Xiaoqing Liu 1,  Xi Qiu 1,  Ziyan Wang 1,  Liju Xu 1,  Ran Tan 1,  Wanjin Hong 1 3,  Tuanlao Wang 4
Affiliations

Affiliations

  • 1 School of Pharmaceutical Sciences, State Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, 361005, Fujian, China.
  • 2 School of Basic Medical Sciences, Guizhou Provincial Key Laboratory of Pathogenesis and Drug Research on Common Chronic Diseases, Guizhou Medical University, 550025, Guiyang, China.
  • 3 Institute of Molecular and Cell Biology, A STAR (Agency of ScienceTechnology and Research), 61 Biopolis Drive, Singapore, 138673, Singapore.
  • 4 School of Pharmaceutical Sciences, State Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, 361005, Fujian, China. [email protected].
  • # Contributed equally.
PMID: 33731709 DOI: 10.1038/s41419-021-03561-7
Abstract

Rab proteins play crucial roles in membrane trafficking. Some Rab proteins are implicated in Cancer development through regulating protein sorting or degradation. In this study, we found that the expression of Rab26 is suppressed in the aggressive breast Cancer cells as compared to the levels in non-invasive breast Cancer cells. Over-expression of Rab26 inhibits cell migration and invasion, while Rab26 knockdown significantly promotes the migration and invasion of breast Cancer cells. Rab26 reduces focal adhesion association of Src kinase and induces endosomal translocation of Src. Further experiments revealed that Rab26 mediates the autophagic degradation of phosphorylated Src through interacting with ATG16L1, consequently, resulting in the suppression of the migration and invasion ability of breast Cancer cells.

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