title: Overexpression of gelsolin reduces the proliferation and invasion of colon carcinoma cells.
abstract: The enhanced motility of cancer cells via the remodeling of the actin cytoskeleton is crucial in the process of cancer cell invasion and metastasis. It was previously demonstrated that gelsolin (GSN) may be involved as a tumor or a metastasis suppressor, depending on the cell lines and model systems used. In the present study, the effect of GSN on the growth and invasion of human colon carcinoma (CC) cells was investigated using reverse transcription quantitative polymerase chain reaction and western blotting. It was observed that upregulation of the expression of GSN in human CC cells significantly reduced the invasiveness of these cells. The expression levels of GSN were observed to be reduced in CC cells, and the reduced expression level of GSN was often associated with a poorer metastasis‑free survival rate in patients with CC (P=0.04). In addition, the overexpression of GSN inhibited the invasion of CC cells in vitro. Furthermore, GSN was observed to inhibit signal transducer and activator of transcription (STAT) 3 signaling in CC cells. Together, these results suggested that GSN is critical in regulating cytoskeletal events and inhibits the invasive and/or metastatic potential of CC cells. The results obtained in the present study may improve understanding of the functional and mechanistic links between GSN as a possible tumor suppressor and the STAT3 signaling pathway, with respect to the aggressive nature of CC. In addition, the present study demonstrated the importance of GSN in regulating the invasion and metastasis of CC cells at the molecular level, suggesting that GSN may be a potential predictor of prognosis and treatment success in CC.
authors: Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.
authors: Wen-Xiang
authors: WX
authors: Li
authors: Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.
authors: Meng-Xuan
authors: MX
authors: Yang
authors: Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.
authors: Xin-Qiang
authors: XQ
authors: Hong
authors: Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.
authors: Tian-Geng
authors: TG
authors: Dong
authors: Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.
authors: Tuo
authors: T
authors: Yi
authors: Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.
authors: Sheng-Li
authors: SL
authors: Lin
authors: Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.
authors: Xin-Yu
authors: XY
authors: Qin
authors: Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.
authors: Wei-Xin
authors: WX
authors: Niu
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D003106:Colon / Q000378:metabolism / Q000473:pathology*; D003110:Colonic Neoplasms / Q000235:genetics* / Q000473:pathology*; D005260:Female; D018260:Gelsolin / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000235:genetics; D008875:Middle Aged; D009361:Neoplasm Invasiveness / Q000235:genetics / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics; D050796:STAT3 Transcription Factor / Q000235:genetics; D016019:Survival Analysis; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D018260:Gelsolin; D019253:Proto-Oncogene Proteins c-bcl-2; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; C522361:MMP2 protein, human; D020778:Matrix Metalloproteinase 2