فهرست نشریات علمی دسترسی آزاد ایران

   Background and Objectives: Gastric carcinoma (GC) remains a significant global health challenge with poor prognostic outcomes. Recent research has highlighted the critical role of long non-coding RNAs (lncRNAs) in modulating gene expression, cellular signaling, and chromatin remodeling during tumorigenesis. Among these, Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is frequently dysregulated. This review aims to synthesize existing knowledge on the relationship between MALAT1 expression, the molecular mechanisms of GC pathogenesis, and its potential as a clinical biomarker or therapeutic target.   Methods: This review article compiled and analyzed available literature concerning MALAT1’s biosynthesis, its structure—specifically its unique triple-helix configuration—and its diverse molecular functions. The analysis focused on in-vitro and in-vivo studies investigating MALAT1's role in transcriptional control, post-transcriptional regulation, and its specific pathways within gastric cancer.  Results: MALAT1 is significantly upregulated in GC tissues, serum, and cell lines. It functions as a molecular scaffold and a competing endogenous RNA (ceRNA), often acting as a "microRNA sponge" to regulate pathways such as PI3K/Akt, Wnt/β-catenin, and various miRNA axes (e.g., miR-122, miR-202). These interactions drive critical oncogenic processes, including cell proliferation, invasion, metastasis via epithelial-to-mesenchymal transition (EMT), and chemotherapy resistance.  Conclusion: MALAT1 plays a pivotal role in the progression and metastasis of gastric carcinoma. Its elevated expression serves as a potential biomarker for primary diagnosis and prognosis. Furthermore, targeting MALAT1 suppression represents a promising strategy for novel gastric cancer therapies.