Journal
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
Volume 32, Issue 3, Pages -Publisher
WILEY
DOI: 10.1002/jbt.22039
Keywords
chemoresistance; hypoxia-inducible factor-1; interleukin-6; MDA-MB-231 cells
Categories
Funding
- Foundation of Wuxi City Health and Family Planning [MS201501]
- First Grade Postdoctorate Foundation of China [2014M560437]
- Major Project of Wuxi Municipal Health Bureau [Z201508, ZS201401]
- Project of science and technology development fund of Nanjing Medical University [2013NJMU200]
- Foundation of Six Talent Peaks Project of Jiangsu Province [2014-WSW-059]
- Special Postdoctorate Foundation of China [2015T80570]
- Postdoctorate Foundation of Jiangsu Province [1401017A]
- Project of Wuxi Municipal Science and Technology Bureau [CSE31N1520, CSE31N1621]
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Chemoresistance is a critical challenge in the clinical treatment of triple-negative breast cancer (TNBC). It has been well documented that inflammatory mediators from tumor microenvironment are involved in the pathogenesis of TNBC and might be related to chemoresistance of cancer cells. In this study, the contribution of interleukin-6 (IL-6), one of the principal oncogenic molecules, in chemoresistance of a TNBC cell line MDA-MB-231 was first investigated. The results showed that IL-6 treatment could induce upregulation of HIF-1 via the activation of STAT3 in MDA-MB-231 cells, which consequently contributed to its effect against chemotherapeutic drug-induced cytotoxicity and cell apoptosis. However, knockdown of HIF-1 attenuated such effect via affecting the expressions of apoptosis-related molecules as Bax and Bcl-2 and drug transporters as P-gp and MRP1. This study indicated that targeting at IL-6/HIF-1 signaling pathway might be an effective strategy to overcome chemoresistance in TNBC therapy.
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