title: Knockdown of biglycan expression by RNA interference inhibits the proliferation and invasion of, and induces apoptosis in, the HCT116 colon cancer cell line.
abstract: Biglycan is an important component of the extracellular matrix, and it is also a member of small leucine-rich proteoglycan family. Previous studies indicated that the expression of biglycan was increased in a variety of tumor tissues, including colon cancer. However, the mechanisms underlying its effects in colon cancer remain to be fully elucidated. In the present study, the effects of biglycan knockdown on colon cancer cell proliferation, migration, invasion and apoptosis were investigated. The mRNA expression levels of biglycan in the HCT116 colon cancer cell line were downregulated using RNA interference, and the stably transfected cell line was obtained through G418 screening for subsequent experiments. The results revealed that downregulation of the expression of biglycan suppressed cell proliferation and caused a cell cycle arrest at the G0/G1 phase. The results of the western blot analysis also revealed that the expression levels of cell cycle‑associated proteins, including cyclin A and cyclin D1, were markedly decreased following silencing of biglycan, whereas the expression levels of p21 and p27 were markedly increased compared with that of the short hairpin RNA control group. Furthermore, the decreased expression of biglycan inhibited colon cancer cell migration and invasion, and induced apoptosis. A complete inhibition of the p38 signaling pathway with SB203580 effectively reversed the increase in apoptotic cell numbers induced by biglycan downregulation. Taken together, the results of the present study indicated that biglycan exerts an important role in cell proliferation, migration, invasion and apoptosis in colon cancer, and that biglycan regulates the p38 MAPK signaling pathway by exerting an antiapoptotic effect. Therefore, biglycan may represent a putative target for colon cancer gene therapy.
authors.affiliation: Cancer Prevention and Treatment Office, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.
authors.forename: Xiaojing
authors.initials: X
authors.lastname: Xing
authors.affiliation: Department of Surgical Oncology, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.
authors.forename: Xiaohu
authors.initials: X
authors.lastname: Gu
authors.affiliation: Cancer Prevention and Treatment Office, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.
authors.forename: Tianfei
authors.initials: T
authors.lastname: Ma
mesh_terms: D017209:Apoptosis; D058578:Biglycan / Q000235:genetics* / Q000378:metabolism; D059447:Cell Cycle Checkpoints; D002465:Cell Movement; D049109:Cell Proliferation; D003110:Colonic Neoplasms / Q000378:metabolism* / Q000473:pathology; D055785:Gene Knockdown Techniques; D045325:HCT116 Cells; D006801:Humans; D020935:MAP Kinase Signaling System; D009361:Neoplasm Invasiveness; D034622:RNA Interference
chemical_list: C546884:BGN protein, human; D058578:Biglycan