4.6 Article

Downregulation of DPF3 promotes the proliferation and motility of breast cancer cells through activating JAK2/STAT3 signaling

期刊

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2019.04.170

关键词

DPF3; SWI/SNF complex; Migration; Invasion

资金

  1. Natural Science Foundation of China [81602701]
  2. Natural Science Foundation of Guangdong Province [2017A030313547, 2018A030313176]
  3. Science and Technology Projects Foundation of Guangdong Province [2015A070710006, 2016A020215053, 2016A040403049, 2017A010105029]
  4. Science and Technology Projects Foundation of Guangzhou City [201507020037, 201607010260]
  5. Scientific Research Projects of Guangdong Traditional Chinese Medicine Bureau [20171056]

向作者/读者索取更多资源

It is reported that the genetic variation of DPF3 is a risk factor of breast cancer through large-scale association research. However, the expression, function and mechanism in breast cancer is unknown. We applied OCR and western blotting to detect the levels of DPF3 in breast cancer tissues. MTT and Anchorage-independent growth ability assay were used to evaluate the effect of DPF3 on cell proliferation. Wound healing and transwell invasion assay were performed to detect the role of DPF3 on cell motility ability. Herein, we found that the mRNA and protein levels of DPF3 are both significantly downregulated in breast cancer tissues. And downregulation of DPF3 can promote the proliferation and motility of breast cancer cells. Further investigation illustrated that downregulation of DPF3 can activate the JAK2/STAT3 signaling. In conclusion, we found that the downregulation of DPF3 plays an indispensable function in the progression of breast cancer, and may be served as a novel therapeutic target to therapy breast cancer. (C) 2019 Elsevier Inc. All rights reserved.

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