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Article Publish Status: FREE
Abstract Title:

Melatonin Synergizes with Sorafenib to Suppress Pancreatic Cancer via Melatonin Receptor and PDGFR-β/STAT3 Pathway.

Abstract Source:

Cell Physiol Biochem. 2018 ;47(5):1751-1768. Epub 2018 Jun 28. PMID: 29953970

Abstract Author(s):

Zhenghuan Fang, Kyung Hee Jung, Hong Hua Yan, Soo-Jung Kim, Marufa Rumman, Jung Hee Park, Boreum Han, Ji Eun Lee, Yeo Wool Kang, Joo Han Lim, Soon Sun Hong

Article Affiliation:

Zhenghuan Fang

Abstract:

BACKGROUND/AIMS: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignant tumors with poor prognosis. Conventional chemotherapies including gemcitabine have failed owing to weak response and side effects. Hence novel treatment regimens are urgently needed to improve the therapeutic efficacy. In this study, we aimed to assess the anticancer activity of melatonin and sorafenib as a novel therapy against PDAC.

METHODS: We used various apoptosis assay and PDAC xenograft model to assess anticancer effect in vitro and in vivo. We applied phospho-receptor tyrosine kinase (RTK) array and phospho-tyrosine kinase array to explore the mechanism of the combined therapy. Western blotting, proximity ligation assay, and immunoprecipitation assay were also performed for validation.

RESULTS: Melatonin synergized with sorafenib to suppress the growth of PDAC both in vitro and in vivo. The effect was due to increased apoptosis rate of PDAC cells that was accompanied by mitochondria dysfunction. The enhanced anticancer efficacy by the co-treatment could be explained by blockade of PDGFR-β/STAT3 signaling pathway and melatonin receptor (MT)-mediated STAT3.

CONCLUSIONS: Melatonin reinforces the anticancer activity of sorafenib by downregulation of PDGFR-β/STAT3 signaling pathway and melatonin receptor (MT)-mediated STAT3. The combination of the two agents might be a potential therapeutic strategy for treating PDAC.

Study Type : In Vitro Study

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