TAGLN2-mediated Actin Cytoskeleton Stabilization Promotes Proliferation and Metastasis of Ovarian Carcinoma.

Abstract

Transgelin-2 (TAGLN2) is an actin-binding protein associated with tumor progression, particularly in gastric and brain tumors. However, its role in ovarian cancer metastasis is still not fully understood. This study investigated the role of TAGLN2 and its potential mechanism in ovarian cancer metastasis. TAGLN2 expression in ovarian cancer and normal tissues was assessed using Oncomine, Human Protein Atlas (HPA), and immunocytochemistry (IHC). Skov3 cells with TAGLN2 knockdown (transient knockdown of TAGLN2 of homo TAGLN2 was performed using specific small interfering RNAs), and Skov3 cells transfected with scrambled siRNAs (negative control group) were subjected to colony formation and wound healing assays to assess cell proliferation and migration in vitro. RT-PCR and western blot were used to assess TAGLN2 mRNA and protein expression; immunofluorescence staining was used to investigate the TAGLN2 impact on the cytoskeletal organization. Elevated TAGLN2 levels were observed in ovarian cancer compared with normal tissues, which was confirmed by IHC of a tissue microarray containing 65 ovarian tumor samples. TAGLN2 knockdown reduced cell proliferation and migration in vitro. Also, TAGLN2 was found to co-localize with F-actin; the knockdown of TAGLN2 impaired cytoskeletal organization, emphasizing its influence on cellular structures. In summary, TAGLN2, highly expressed in ovarian cancer, promotes migration and proliferation through cytoskeletal reorganization; thus, it may be a new therapeutic target for ovarian cancer.