Knockdown of collagen α-1(III) inhibits glioma cell proliferation and migration and is regulated by miR128-3p.

Abstract

As a member of the collagen family, collagen α-1(III) (COL3A1) is an important protein in the development and progression of several tumors. However, the role of COL3A1 in glioma is not yet clear. The present study examined the expression and function of COL3A1 in glioma cell behavior and identified microRNA (miRNA) regulators. It was demonstrated that COL3A1 expression was upregulated in glioma and directly correlated with the tumor grade. Analysis of the GSE4290 and GSE7696 profiles acquired from the Gene Expression Omnibus database also revealed an increased COL3A1 expression in malignant gliomas compared with the lower grade gliomas and non-tumor brain tissue, which was directly correlated with glioma grade. To explore the functional role of COL3A1 in glioma cell growth, small interfering RNA interference was applied to inhibit COL3A1 expression in Hs683 and U251 cells. The relative COL3A1 mRNA and protein expression levels were significantly reduced in the knockdown cells as determined by western blot analysis. In addition, decreased COL3A1 expression in Hs683 and U251 glioma cells resulted in a delay in cell growth and colony disruption as determined by MTS and colony formation assays. Wound healing analysis indicated that cells with suppressed expression of COL3A1 had a reduced ability to migrate. COL3A1 mRNA levels were inversely correlated with the miR128-3p level in glioma, suggesting that miR128-3p expression is associated with COL3A1 inhibition as verified by reverse transcription-quantified polymerase chain reaction. These results suggest that COL3A1 may be a novel regulator of glioblastoma cell behavior and may represent a novel target for gene therapies against glioma.

• Authors: Yuan-Feng Gao, Tao Zhu, Juan Chen, Lin Liu, Rong Ouyang
• Journal: Oncology letters (Oncol Lett) Vol. 16 Issue 2 Pg. 1917-1923 (Aug 2018) ISSN: 1792-1074 [Print] Greece
• PMID: 30008884 (Publication Type: Journal Article)