Long noncoding RNA PSMA3-AS1 functions as a competing endogenous RNA to promote gastric cancer progression by regulating the miR-329-3p/ALDOA axis

• Published in: Biology direct Vol. 18; no. 1; p. 36
• Main Authors: Kan, Liang, Yang, Meiqi, Zhang, Huijing
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 04-07-2023; BioMed Central; BMC
• Subjects: 3' Untranslated regions; ALDOA; Aldolase; Animals; Apoptosis; Cancer; cancer progression; Cancer therapies; Cell cycle; Cell growth; Cell Line, Tumor; Cell migration; Cell Movement - genetics; Cell Proliferation - genetics; Chemotherapy; Colorectal carcinoma; Development and progression; Esophagus; Flow cytometry; Fructose-Bisphosphate Aldolase - genetics; Fructose-Bisphosphate Aldolase - metabolism; Fructosediphosphate aldolase; Gastric cancer; Gene expression; Gene Expression Regulation, Neoplastic; Genetic aspects; Health aspects; Humans; lncRNA PSMA3-AS1; Lung cancer; Matrix metalloproteinase; Matrix metalloproteinases; Metalloproteinase; Mice; Mice, Nude; MicroRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; miR-329-3p; Oncology, Experimental; Ovarian cancer; Oxidative stress; Proteasome Endopeptidase Complex - genetics; Proteasome Endopeptidase Complex - metabolism; RNA; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Stomach cancer; Stomach Neoplasms - genetics; Thermal cycling; Tumors; Wound healing; China; United States > US; lncRNA PSMA3-AS1; cancer progression; ALDOA; Gastric cancer; miR-329-3p
• ISSN: 1745-6150; 1745-6150
• DOI: 10.1186/s13062-023-00392-8

LncRNA PSMA3-AS1 functions as an oncogene in several cancers, including ovarian cancer, lung cancer, and colorectal cancer. However, its role in gastric cancer (GC) progression remains unclear. In this study, the levels of PSMA3-AS1, miR-329-3p, and aldolase A (ALDOA) in 20 paired human GC tissues and adjacent nontumorous tissues were measured by real-time PCR. GC cells were transfected with recombinant plasmid carrying full-length PSMA3-AS1 or shRNA targeting PSMA3-AS1. The stable transfectants were selected by G418. Then, the effects of PSMA3-AS1 knockdown or overexpression on GC progression in vitro and in vivo were evaluated. The results showed that PSMA3-AS1 was highly expressed in human GC tissues. Stable knockdown of PSMA3-AS1 significantly restrained proliferation/migration/invasion, enhanced cell apoptosis, and induced oxidative stress in vitro. Tumor growth and matrix metalloproteinase expression in tumor tissues were markedly inhibited, while oxidative stress was enhanced in nude mice after stable PSMA3-AS1 knockdown. Additionally, PSMA3-AS1 negatively regulated miR-329-3p while positively regulated ALDOA expression. MiR-329-3p directly targeted ALDOA-3'UTR. Interestingly, miR-329-3p knockdown or ALDOA overexpression partially attenuated the tumor-suppressive effects of PSMA3-AS1 knockdown. Conversely, PSMA3-AS1 overexpression exhibited the opposite effects. PSMA3-AS1 promoted GC progression by regulating the miR-329-3p/ALDOA axis. PSMA3-AS1 might serve as a promising and effective target for GC treatment.