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hSulf‑1 inhibits cell proliferation and migration and promotes apoptosis by suppressing stat3 signaling in hepatocellular carcinoma

hSulf‑1 inhibits cell proliferation and migration and promotes apoptosis by suppressing stat3... Human sulfatase‑1 (hSulf‑1) has been shown to desulfate cellular heparin sulfate proteoglycans and modulate several growth factors and cytokines. However, hSulf‑1 has not been previously shown to mediate the signal transducer and activator of transcription 3 (stat3) signaling pathway, which is known to regulate cell proliferation, motility and apoptosis. The present study investigated the role of hSulf‑1 in stat3 signaling in hepatocellular cancer. hSulf‑1 expression vector and stat3 small interfering RNA (siRNA) were constructed to control the expression of hSulf‑1 and stat3 in HepG2 cells. hSulf‑1 was found to inhibit the phosphorylation of stat3 and downregulate its targeted protein. MTT and Transwell chamber assays, as well as Annexin V/propidium iodide double‑staining methods, were used to examine the effects of hSulf‑1 on stat3‑mediated motility, proliferation and apoptosis in HepG2 cells. Transfection with hSulf‑1 cDNA and/or stat3 siRNA inhibited cell proliferation and motility, concurrent with G0/G1 and G2/M phase cell cycle arrest and apoptosis. Overall, the results of the current study suggested that hSulf‑1 functions as a negative regulator of proliferation and migration and as a positive regulator of apoptosis in hepatocellular carcinoma, at least partly via the downregulation of stat3 signaling. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Oncology Letters Spandidos Publications

hSulf‑1 inhibits cell proliferation and migration and promotes apoptosis by suppressing stat3 signaling in hepatocellular carcinoma

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Publisher
Spandidos Publications
Copyright
Copyright © Spandidos Publications
ISSN
1792-1074
eISSN
1792-1082
DOI
10.3892/ol.2014.1848
Publisher site
See Article on Publisher Site

Abstract

Human sulfatase‑1 (hSulf‑1) has been shown to desulfate cellular heparin sulfate proteoglycans and modulate several growth factors and cytokines. However, hSulf‑1 has not been previously shown to mediate the signal transducer and activator of transcription 3 (stat3) signaling pathway, which is known to regulate cell proliferation, motility and apoptosis. The present study investigated the role of hSulf‑1 in stat3 signaling in hepatocellular cancer. hSulf‑1 expression vector and stat3 small interfering RNA (siRNA) were constructed to control the expression of hSulf‑1 and stat3 in HepG2 cells. hSulf‑1 was found to inhibit the phosphorylation of stat3 and downregulate its targeted protein. MTT and Transwell chamber assays, as well as Annexin V/propidium iodide double‑staining methods, were used to examine the effects of hSulf‑1 on stat3‑mediated motility, proliferation and apoptosis in HepG2 cells. Transfection with hSulf‑1 cDNA and/or stat3 siRNA inhibited cell proliferation and motility, concurrent with G0/G1 and G2/M phase cell cycle arrest and apoptosis. Overall, the results of the current study suggested that hSulf‑1 functions as a negative regulator of proliferation and migration and as a positive regulator of apoptosis in hepatocellular carcinoma, at least partly via the downregulation of stat3 signaling.

Journal

Oncology Letters – Spandidos Publications

Published: Apr 1, 2014

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