Overexpression of gelsolin reduces the proliferation and invasion of colon carcinoma cells

التفاصيل البيبلوغرافية
العنوان: Overexpression of gelsolin reduces the proliferation and invasion of colon carcinoma cells
المؤلفون: Meng‑Xuan Yang, Tuo Yi, Wen‑Xiang Li, Tian‑Geng Dong, Xin‑Qiang Hong, Sheng‑Li Lin, Wei‑Xin Niu, Xin‑Yu Qin
المصدر: Molecular Medicine Reports
بيانات النشر: Spandidos Publications, 2016.
سنة النشر: 2016
مصطلحات موضوعية: Male, 0301 basic medicine, Cancer Research, gelsolin, Cell, colon carcinoma, Biochemistry, 0302 clinical medicine, Cell Movement, prognostic factor, Aged, 80 and over, Articles, Middle Aged, Cell cycle, Up-Regulation, Gene Expression Regulation, Neoplastic, medicine.anatomical_structure, Proto-Oncogene Proteins c-bcl-2, Oncology, 030220 oncology & carcinogenesis, Colonic Neoplasms, signal transducer and activator of transcription 3, Matrix Metalloproteinase 2, Molecular Medicine, Female, Adult, STAT3 Transcription Factor, Colon, Biology, Young Adult, 03 medical and health sciences, Cell Line, Tumor, Genetics, medicine, Humans, Neoplasm Invasiveness, Metastasis suppressor, Molecular Biology, Aged, Cell Proliferation, tumor metastasis, Oncogene, Cell growth, Actin cytoskeleton, Survival Analysis, 030104 developmental biology, Cancer cell, Cancer research, Gelsolin, overexpression
الوصف: 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.
تدمد: 1791-3004
1791-2997
DOI: 10.3892/mmr.2016.5652
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8b22ebde467bc7dc879e2bdd8dfae80e
https://doi.org/10.3892/mmr.2016.5652
Rights: OPEN
رقم الانضمام: edsair.doi.dedup.....8b22ebde467bc7dc879e2bdd8dfae80e
قاعدة البيانات: OpenAIRE
الوصف
تدمد:17913004
17912997
DOI:10.3892/mmr.2016.5652