MAZ-mediated LAMA5 transcription activation promotes gastric cancer progression through the STAT3 signaling.

Laminin subunit alpha-5 (LAMA5) has been identified as an oncogene in many cancers, while its role and mechanism in gastric cancer (GC) remain to be explored. Here, the influences of LAMA5 knockdown on GC were investigated in vitro and in vivo. LAMA5 expression was silenced in GC cells alone or in combination with the signal transducer and activator of transcription 3 (STAT3) activator Colivelin, followed by CCK-8, colony formation, EdU, flow cytometry, wound healing assay, and Transwell assay.

Application of Bioinformatics in Predicting the Efficacy of Digestive Tumour Immunotherapy Target TIM-3 and its Inhibitors.

Our main objective is to apply bioinformatics in predicting the efficacy of digestive tumour immunotherapy target TIM-3 and its inhibitors. Our study used the gene expression omnibus (GEO) database to identify datasets associated with digestive tumours and the action of TIM-3. The GSE427729 dataset based on the GPL10192 platform.

Long non-coding RNA LINC00511 regulates the expression of microRNA-625-5p and activates signal transducers and activators of transcription 3 (STAT3) to accelerate the progression of gastric cancer.

This study aimed to investigate the expression, biological function, and downstream mechanism of LINC00511 in gastric cancer (GC). In paired GC samples, LINC00511, miR-625-5p and STAT3 mRNA expression levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR); STAT3 protein expression was detected by immunohistochemical (IHC). The gain-of-function and loss-of-function models were established, and the proliferative and migrative ability of GC cells were measured by CCK-8 and transwell assays, respectively.