2. Academic Validation
  3. KIF17 maintains the epithelial phenotype of breast cancer cells and curbs tumour metastasis

KIF17 maintains the epithelial phenotype of breast cancer cells and curbs tumour metastasis

  • Cancer Lett. 2022 Nov 1;548:215904. doi: 10.1016/j.canlet.2022.215904.
Tianfu Li 1,  Duanyang Zhai 1,  Mengmeng Zhang 2,  Runyi Ye 2,  Xiaying Kuang 2,  Nan Shao 3,  Jiong Bi 4,  Ying Lin 5
Affiliations

Affiliations

  • 1 Breast Disease Center, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China; Laboratory of General Surgery, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China.
  • 2 Breast Disease Center, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China.
  • 3 Breast Disease Center, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China. Electronic address: shaon@mail.sysu.edu.cn.
  • 4 Laboratory of General Surgery, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China. Electronic address: bijiong@mail.sysu.edu.cn.
  • 5 Breast Disease Center, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China. Electronic address: linying3@mail.sysu.edu.cn.
PMID: 36089118 DOI: 10.1016/j.canlet.2022.215904
Abstract

Kinesin superfamily motor protein 17 (KIF17) was previously identified downregulated in breast Cancer and correlated with patient prognosis. However, its pathophysiological role in tumours remains unknown. Here, we confirmed that KIF17 was significantly under-expressed in breast Cancer tissues and low KIF17 expression correlated with poor outcomes in patients with breast Cancer. In vitro and in vivo experiments demonstrated that KIF17 overexpression in breast Cancer cell lines significantly inhibited breast Cancer invasion and metastasis. By establishing the lung metastatic MDA-MB-231 cell lines, we found a transient silence of KIF17 during the initiation of breast Cancer metastasis. Further experiments revealed that KIF17 might suppress metastasis by regulating the level of acetylated tubulin to maintain Cytoskeleton stability. Eventually, we found that the low expression of KIF17 in breast Cancer is regulated by DNMT1-mediated 5-mC DNA methylation and epigenetic silencing. Decitabine can effectively improve the expression level of KIF17 in breast Cancer cells. Our study demonstrates that KIF17 mediates microtubule acetylation to maintain the stability of microtubules, thereby inhibiting tumour invasion and metastasis.

Keywords

5-mC DNA methylation; Cytoskeleton stability; Decitabine; Kinesin superfamily; Tubulin acetylation.

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