Analysis of immune status and prognostic model incorporating lactic acid metabolism-associated genes.

Background: Cancer development is intricately linked with metabolic dysregulation, including lactic acid metabolism, which plays a pivotal role in tumor progression and immune evasion. However, its specific implications in gastric adenocarcinoma (STAD) remain unclear. This study introduces a novel methodology to evaluate lactic acid metabolism comprehensively in STAD, aiming to elucidate its prognostic significance and impact on immunotherapy efficacy.

Chromosomal copy number amplification-driven Linc01711 contributes to gastric cancer progression through histone modification-mediated reprogramming of cholesterol metabolism.

Background: Chromosome gains or localized amplifications are frequently observed in human gastric cancer (GC) and are major causes of aberrant oncogene activation. However, the significance of long non-coding RNAs (LncRNAs) in the above process is largely unknown.

Methods: The copy number aberrations (CNAs) data of GC samples were downloaded and analyzed from the TCGA database.

Immune-Related lncRNAs Pairs to Construct a Novel Signature for Predicting Prognosis in Gastric Cancer.

Background: Immune-related long non-coding RNAs (irlncRNAs) appear valuable in predicting prognosis in patients with cancer. In this study, we used a fresh modeling algorithm to construct irlncRNAs signature and then assessed its predictive value for prognosis, tumor immune infiltration, and chemotherapy efficacy in gastric cancer (GC) patients.

Materials And Methods: The raw transcriptome data were extracted from the Cancer Genome Atlas (TCGA).

Essential role of ALKBH5-mediated RNA demethylation modification in bile acid-induced gastric intestinal metaplasia.

Bile acid reflux and subsequent caudal-related homeobox 2 (CDX2) activation contribute to gastric intestinal metaplasia (IM), a precursor of gastric cancer; however, the mechanism underlying this phenomenon is unclear. Here, we demonstrate that alkylation repair homolog protein 5 (ALKBH5), a major RNA N-adenosine demethylase, is required for bile acid-induced gastric IM. Mechanistically, we revealed the N-methyladenosine (mA) modification profile in gastric IM for the first time and identified ZNF333 as a novel mA target of ALKBH5.