Journal
ONCOLOGY LETTERS
Volume 15, Issue 1, Pages 1350-1356Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2017.7391
Keywords
uterine cervical cancer; interleukin-8; interleukin-8 receptor; extracellular-signal-regulated kinase; endocytic adaptor protein
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Funding
- National Nature Science Foundation of China [81272854]
- Nature Science Foundation of Heilongjiang Province [D201129]
- Science and Innovation Team Foundation of Education Department of Heilongjiang Province [cxtd-2016-03]
- President Innovation and Entrepreneurship Foundation of Jiamusi University [xzyf2014-12]
- Innovation and Entrepreneurship Training Program for College Students of Heilongjiang Province [201410222036]
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Interleukin-8 (IL-8) serves an important function in chronic inflammation and cancer development; however, the underlying molecular mechanism(s) of IL-8 in uterine cervical cancer remains unclear. The present study investigated whether IL-8 and its receptors [IL-8 receptor (IL-8R)A and IL-8RB] contributed to the proliferative and migratory abilities of HeLa cervical cancer cells, and also investigated the potential underlying molecular mechanisms. Results demonstrated that IL-8 and its receptors were detected in HeLa cells, and levels of IL-8RA were significantly increased compared with those of IL-8RB. Furthermore, the level of IL-8 in cervical cancer tissues was significantly increased compared with that in normal uterine cervical tissues, and migratory and proliferative efficiencies of HeLa cells treated with exogenous IL-8 were increased, compared with untreated HeLa cells. In addition, exogenous IL-8 was able to downregulate endocytic adaptor protein (NUMB), and upregulate IL-8RA, IL-8RB and extracellular signal-regulated protein kinases (ERKs) expression levels in HeLa cells. Results suggest that IL-8 and its receptors were associated with the tumorigenesis of uterine cervical cancer, and exogenous IL-8 promotes the carcinogenic potential of HeLa cells by increasing the expression levels of IL-8RA, IL-8RB and ERK, and decreasing the expression level of NUMB.
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