Fusobacterium nucleatum Promotes Bladder Cancer Development Through lncRNA IDH1-AS1-Mediated Autophagy

Bladder cancer is a prevalent malignancy with a high recurrence rate, necessitating the identification of novel molecular targets for diagnosis and therapy. Recent studies have highlighted the role of long noncoding RNAs (lncRNAs) in cancer progression. This study aims to investigate the role of the lncRNA IDH1-AS1 in bladder cancer, focusing on its effects on tumor growth, cell proliferation, and autophagy-related protein expression. We utilized both in vivo and in vitro models to assess the impact of IDH1-AS1 overexpression and knockdown. Tumor growth was evaluated in nude mice model of bladder cancer, while cell proliferation was measured using the EDU assay. Protein expression levels of Beclin1, P62, and LC3 were determined by Western Blot analysis. Gene expression of IDH1-AS1 was quantified using quantitative polymerase chain reaction (qPCR). Overexpression of IDH1-AS1 in nude mice model of bladder cancer led to a significant increase in tumor volume and weight, whereas knockdown of IDH1-AS1 resulted in a substantial decrease in tumor size. In vitro, IDH1-AS1 overexpression significantly enhanced cell proliferation, while its knockdown reduced proliferation. Western Blot analysis revealed that IDH1-AS1 overexpression increased the levels of autophagy-related proteins Beclin1 and LC3, and decreased P62 protein levels, with contrary effects observed upon IDH1-AS1 knockdown. qPCR confirmed successful modulation of IDH1-AS1 expression in experimental groups. Our findings indicate that IDH1-AS1 promotes tumor growth and cell proliferation in bladder cancer, potentially through the regulation of autophagy-related proteins. These results suggest that IDH1-AS1 could serve as a novel biomarker and therapeutic target for bladder cancer.