OASL knockdown inhibits the progression of stomach adenocarcinoma by regulating the mTORC1 signaling pathway

Abstract

The present study investigated the effects of 2′‐5′ oligoadenylate synthetase‐like (OASL) on the biological functions of stomach adenocarcinoma (STAD) cells and tumor formation in nude mice. The differential expression levels of OASL in the different cancer types from TCGA dataset were analyzed using gene expression profiling interactive analysis. Overall survival and the receiver operating characteristic were analyzed using the KM plotter and R, respectively. Furthermore, OASL expression and its effects on the biological functions of STAD cells were detected. The possible upstream transcription factors of OASL were predicted using JASPAR. The downstream signaling pathways of OASL were analyzed using GSEA. Tumor formation experiments were performed to evaluate the effect of OASL on tumor formation in nude mice. The results showed that OASL was highly expressed in STAD tissues and cell lines. OASL knockdown markedly inhibited cell viability, proliferation, migration, and invasion and accelerated STAD cell apoptosis. Conversely, OASL overexpression had the opposite effect on STAD cells. JASPAR analysis revealed that STAT1 is an upstream transcription factor of OASL. Furthermore, GSEA showed that OASL activated the mTORC1 signaling pathway in STAD. The protein expression levels of p‐mTOR and p‐RPS6KB1 were suppressed by OASL knockdown and promoted by OASL overexpression. The mTOR inhibitor, rapamycin, markedly reversed the effect of OASL overexpression on STAD cells. Additionally, OASL promoted tumor formation and increased tumor weight and volume in vivo. In conclusion, OASL knockdown suppressed the proliferation, migration, invasion, and tumor formation of STAD cells by inhibiting the mTOR signaling pathway.

Resolving candidate genes of duck ovarian tissue transplantation via RNA-Seq and expression network analyses

“…These enzymes influence the detection and response to viral infections ( Guo et al, 2012 ). It also regulates cell growth, proliferation, and apoptosis ( Zhao et al, 2023 ).…”

Peptidase inhibitor 16 promotes proliferation of pancreatic ductal adenocarcinoma cells through OASL signaling

“…As reported, OASL is closely related to viral infection response and autoimmune diseases 13 . In addition, OASL plays a role in a variety of tumors, such as breast cancer, lung cancer, bladder cancer, and gastric cancer 14–17 . It has been reported that OASL is overexpressed in PDAC and is associated with poor outcomes in patients 18 .…”

“…13 In addition, OASL plays a role in a variety of tumors, such as breast cancer, lung cancer, bladder cancer, and gastric cancer. [14][15][16][17] It has been reported that OASL is overexpressed in PDAC and is associated with poor outcomes in patients. 18 Furthermore, we found that Pi16 can promote PDAC cell proliferation by regulating OASL, suggesting that the Pi16/OASL axis may be a promising new target for PDAC diagnosis and treatment.…”

Protumorigenic Interferon-Stimulated Genes in Cancer: A Comprehensive Review

“…Recurrence and tumour metastasis [34] Gastric cancer GES-1 and STAD cell lines Regulating mTORC signaling pathway Tumour progression [35] Oral cancer HEp-2…”