Publication: Kaempferia parviflora extract inhibits STAT3 activation and interleukin-6 production in hela cervical cancer cells
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Issued Date
2019-09-01
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ISSN
14220067
16616596
16616596
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2-s2.0-85071763180
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Mahidol University
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SCOPUS
Bibliographic Citation
International Journal of Molecular Sciences. Vol.20, No.17 (2019)
Suggested Citation
Benjamart Suradej, Siriwoot Sookkhee, Jukreera Panyakaew, Pitchaya Mungkornasawakul, Nitwara Wikan, Duncan R. Smith, Saranyapin Potikanond, Wutigri Nimlamool Kaempferia parviflora extract inhibits STAT3 activation and interleukin-6 production in hela cervical cancer cells. International Journal of Molecular Sciences. Vol.20, No.17 (2019). doi:10.3390/ijms20174226 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/50089
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Title
Kaempferia parviflora extract inhibits STAT3 activation and interleukin-6 production in hela cervical cancer cells
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Abstract
© 2019 by the authors. Licensee MDPI, Basel, Switzerland. Kaempferia parviflora (KP) has been reported to have anti-cancer activities. We previously reported its effects against cervical cancer cells and continued to elucidate the effects of KP on inhibiting the production and secretion of interleukin (IL)-6, as well as its relevant signaling pathways involved in cervical tumorigenesis. We discovered that KP suppressed epidermal growth factor (EGF)-induced IL-6 secretion in HeLa cells, and it was associated with a reduced level of Glycoprotein 130 (GP130), phosphorylated signal transducers and activators of transcription 3 (STAT3), and Mcl-1. Our data clearly showed that KP has no effect on nuclear factor kappa B (NF-κB) localization status. However, we found that KP inhibited EGF-stimulated phosphorylation of tyrosine 1045 and tyrosine 1068 of EGF receptor (EGFR) without affecting its expression level. The inhibition of EGFR activation was verified by the observation that KP significantly suppressed a major downstream MAP kinase, ERK1/2. Consistently, KP reduced the expression of Ki-67 protein, which is a cellular marker for proliferation. Moreover, KP potently inhibited phosphorylation of STAT3, Akt, and the expression of Mcl-1 in response to exogenous IL-6 stimulation. These data suggest that KP suppresses EGF-induced production of IL-6 and inhibits its autocrine IL-6/STAT3 signaling critical for maintaining cancer cell progression. We believe that KP may be a potential alternative anti-cancer agent for suppressing cervical tumorigenesis.