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Title: Adrenaline promotes cell proliferation and increases chemoresistance in colon cancer HT29 cells through induction of miR-155

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [3];  [4];  [4];  [1]
  1. Department of General Surgery, Tangdu Hospital of the Fourth Military Medical University, Xi'an 710038 (China)
  2. Department of Cardiology, 323 Hospital of PLA, Xi'an 710054 (China)
  3. Department of Teaching and Medical Administration, Tangdu Hospital of the Fourth Military Medical University, Xi'an 710038 (China)
  4. Department of Nephrology, The 323 Hospital of PLA, Xi'an 710054 (China)

Highlights: Black-Right-Pointing-Pointer Adrenaline increases colon cancer cell proliferation and its resistance to cisplatin. Black-Right-Pointing-Pointer Adrenaline activates NF{kappa}B in a dose dependent manner. Black-Right-Pointing-Pointer NF{kappa}B-miR-155 pathway contributes to cell proliferation and resistance to cisplatin. -- Abstract: Recently, catecholamines have been described as being involved in the regulation of cancer genesis and progression. Here, we reported that adrenaline increased the cell proliferation and decreased the cisplatin induced apoptosis in HT29 cells. Further study found that adrenaline increased miR-155 expression in an NF{kappa}B dependent manner. HT29 cells overexpressing miR-155 had a higher cell growth rate and more resistance to cisplatin induced apoptosis. In contrast, HT29 cells overexpressing miR-155 inhibitor displayed decreased cell proliferation and sensitivity to cisplatin induced cell death. In summary, our study here revealed that adrenaline-NF{kappa}B-miR-155 pathway at least partially contributes to the psychological stress induced proliferation and chemoresistance in HT29 cells, shedding light on increasing the therapeutic strategies of cancer chemotherapy.

OSTI ID:
22210328
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 428, Issue 2; Other Information: Copyright (c) 2012 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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