Exogenous H2S promotes cancer progression by activating JAK2/STAT3 signaling pathway in esophageal EC109 cells

Hydrogen sulfide (H 2 S) plays an important role in diverse physiological and pathophysiological processes in cancer cells both in vitro and in vivo . We have previously shown that exogenous H 2 S exerts its biological effects on hepatoma, glioma, and esophageal cancer cells through the activation o...

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Published in:International journal of clinical and experimental pathology 2018-01, Vol.11 (7), p.3247-3256
Main Authors: Lei, Yi-Yan, Feng, Yan-Fen, Zeng, Bo, Zhang, Wei, Xu, Qing, Cheng, Fei, Lan, Jun, Luo, Hong-He, Zou, Jian-Yong, Chen, Zhen-Guang, Su, Chun-Hua, Zhen, Yu-Lan, Chen, Jing-Fu
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Language:English
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Summary:Hydrogen sulfide (H 2 S) plays an important role in diverse physiological and pathophysiological processes in cancer cells both in vitro and in vivo . We have previously shown that exogenous H 2 S exerts its biological effects on hepatoma, glioma, and esophageal cancer cells through the activation of NF-κB, p38-MAPK/ERK1/2-COX-2, and HSP90 pathways. However, the role of H 2 S and the underlying mechanism in esophageal squamous cell carcinoma remain unclear. Here we investigated whether exogenous H 2 S contributes to the biological behavior of esophageal squamous cancer cell line EC109, through the activation of JAK2/STAT3 signaling pathway. EC109 cells were treated with NaHS (a donor of H 2 S) and AG490 (a specific inhibitor of JAK2/STAT3 signaling pathway). The expression levels of p-JAK2, p-STAT3, caspase-3/9/12, Bax, Bcl-2, MMP-2/9, and VEGFR were measured by western blot analysis. Cell viability was detected by CCK-8 and quantified by direct counting of cells under a microscope. Cell migration was analyzed by the scratch-wound assay, while the level of VEGF was measured by ELISA. Cells treated with NaHS for 24 h showed significant upregulation of p-JAK2, and p-STAT3 expression, as well as increased cell viability when compared to the control cells. The expression levels of caspase-3/9/12 and Bax decreased, while those of Bcl-2, MMP-2/9, VEGFR, and VEGF increased. NaHS induced the migration of EC109 cells. However, co-treatment with NaHS and AG490 significantly inhibited these effects. Thus, JAK2/STAT3 signaling pathway may contribute to H 2 S-induced cell proliferation, anti-apoptosis, migration, and angiogenesis in EC109 cells.
ISSN:1936-2625