{"title":"Exploring the role of miR-361-3p in gastric cancer therapeutics and tumor progression","authors":"Kulsum Akhtar , Gowhar Rashid , Tahseen Bilal Rather , Irfan Maqbool , Ishrat Parveiz , Gulzar Ahmad Bhat , Fazl Q. Parray , Syed Besina Yasin , Syed Mudassar","doi":"10.1016/j.abst.2024.11.002","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Gastric cancer (GC) remains a leading cause of cancer-related deaths globally. Even with advancements in treatment, it is not known precisely which molecular pathways cause GC to proceed. MicroRNAs, often referred to as small noncoding RNAs, have a crucial role in regulating gene expression, which impacts cancer growth, metastasis, and treatment resistance. Among these, miR-361–3p has drawn interest due to its possible role in the development of human cancer. While accumulating evidence highlights miR-361–3p involvement in various cancers, its precise biological function in gastric cancer remains largely unclear.</div></div><div><h3>Methodology</h3><div>The expression levels of miR-361–3p in gastric cancer tissues were compared with those of adjacent non-cancer tissues using real-time quantitative PCR (qRT-PCR). The investigation involved a thorough examination of the expression of miR-361–3p in GC samples in order to identify any possible correlations with clinicopathological characteristics.</div></div><div><h3>Results</h3><div>In 64.86 % of gastric cancer, expression levels of miR-361–3p mRNA were significantly reduced, which indicates that it may play a potential role in the pathophysiology of GC. However, no significant association has been found between miR-361–3p expression levels and clinical pathological features, such as tumor size, phase, or involvement of lymph nodes. This suggests that although miR-361–3p may contribute to GC progress, it is not related to traditional clinical markers.</div></div>","PeriodicalId":72080,"journal":{"name":"Advances in biomarker sciences and technology","volume":"6 ","pages":"Pages 260-264"},"PeriodicalIF":0.0000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in biomarker sciences and technology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2543106424000231","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background
Gastric cancer (GC) remains a leading cause of cancer-related deaths globally. Even with advancements in treatment, it is not known precisely which molecular pathways cause GC to proceed. MicroRNAs, often referred to as small noncoding RNAs, have a crucial role in regulating gene expression, which impacts cancer growth, metastasis, and treatment resistance. Among these, miR-361–3p has drawn interest due to its possible role in the development of human cancer. While accumulating evidence highlights miR-361–3p involvement in various cancers, its precise biological function in gastric cancer remains largely unclear.
Methodology
The expression levels of miR-361–3p in gastric cancer tissues were compared with those of adjacent non-cancer tissues using real-time quantitative PCR (qRT-PCR). The investigation involved a thorough examination of the expression of miR-361–3p in GC samples in order to identify any possible correlations with clinicopathological characteristics.
Results
In 64.86 % of gastric cancer, expression levels of miR-361–3p mRNA were significantly reduced, which indicates that it may play a potential role in the pathophysiology of GC. However, no significant association has been found between miR-361–3p expression levels and clinical pathological features, such as tumor size, phase, or involvement of lymph nodes. This suggests that although miR-361–3p may contribute to GC progress, it is not related to traditional clinical markers.