The present study aimed to explore the biological functions and molecular mechanisms of the long non-coding rna ViM antisense rna 1 (ViM-aS1) in gastric cancer (Gc). The expression of ViM-aS1 was analyzed in tissues from patients with Gc and Gc cell lines by reverse transcription-quantitative (rT-q)Pcr. The relationship between ViM-aS1 expression and overall survival time of patients with Gc was also assessed. To determine the biological functions of ViM-aS1, cell counting Kit-8 assay, colony formation assay, flow cytometry, wound healing assay and Transwell assay were employed. The targeting relationship among ViM-aS1, microRNA (miR)-8052 and frizzled 1 (FZD1) was verified by the dual luciferase reporter gene assay. The underlying molecular mechanism of ViM-aS1 on Gc was determined by rT-qPcr and western blotting. in addition, tumor formation was detected in nude mice. The results of the present study demonstrated that ViM-aS1 was highly expressed in Gc tissues and cells. in addition, ViM-aS1 expression was demonstrated to be closely related to the prognosis of patients with Gc. notably, silencing ViM-aS1 inhibited the proliferation, migration and invasion, and enhanced apoptosis of aGS and HGC-27 cells. Silencing VIM-AS1 significantly increased the protein expression levels of cleaved caspase-3, Bax and e-cadherin, but decreased the protein expression levels of Bcl-2, n-cadherin, vimentin, matrix metalloproteinase (MMP)-2, MMP-9, β-catenin, cyclin d1, c-myc and FZd1. additionally, silencing ViM-aS1 inhibited tumor growth in nude mice. cumulatively, the present study demonstrated that ViM-aS1 may promote cell proliferation, migration, invasion and epithelial-mesenchymal transition by regulating FdZ1 and activating the Wnt/β-catenin pathway in Gc.

Cancer-associated fibroblasts (CAFs) are a major component of the tumor microenvironment (TME). In hepatocellular carcinoma (HCC), quiescent hepatic stellate cells (HSCs) could be activated to become CAFs, which play a critical role in tumor progression and drug resistance. Therefore, recent efforts have been focused on combining anti-HSC and pro-apoptotic activities to improve anti-tumor efficacy of drugs. In this study, glycyrrhetinic acid and hyaluronic acid–modified liposomes (GA-HA-Lip) were prepared for co-delivery of curcumin (CUR) and berberine (BBR) for the treatment of HCC. Furthermore, we established the LX-2+BEL-7402 co-cultured cell model and implanted the m-HSCs+H22 cells into a mouse to evaluate the anti-tumor effect of CUR&BBR/GA-HA-Lip both in vitro and in vivo. The results showed that CUR&BBR/GA-HA-Lip could accumulate in tumor tissues and be taken up by HSCs and BEL-7402 cells simultaneously. Compared with free CUR, the combination therapy based on GA-HA-Lip exhibits stronger pro-apoptotic and anti-proliferation effect both in vitro and in vivo. The anti-tumor mechanistic study revealed that CUR&BBR/GA-HA-Lip could inhibit the activation of HSCs and restrain drug resistance of tumor cells. In summary, CUR&BBR/GA-HA-Lip could be a promising nano-sized formulation for anti-tumor therapy.

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