MicroRNA‐4286 promotes cell proliferation, migration, and invasion via PTEN regulation of the PI3K/Akt pathway in non‐small cell lung cancer. (10th May 2019)

• Record Type: Journal Article
• Authors: Ling, Chunhua; Wang, Xueting; Zhu, Jianjie; Tang, Haicheng; Du, Wenwen; Zeng, Yuanyuan; Sun, Lin; Huang, Jian‐An; Liu, Zeyi
• Is Part Of: Cancer medicine. Volume 8:Number 7(2019:Jul.)
• Page Start: 3520
• Page End: 3531
• Publication Date: 2019-05-10
• Subjects: microRNA -- miR‐4286 -- non‐small cell lung cancer -- phosphatase and tensin homologue deleted on chromosome 10 -- PI3K/AKT signaling; 616.994005
• DOI: 10.1002/cam4.2220
• Languages: English
• ISSNs: 2045-7634

Abstract

Abstract: It is well‐known that phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor which negatively regulates PI3K/AKT signaling and is activated widely in non‐small cell lung cancers (NSCLC). However, genetic alterations in PTEN genes are rare, suggesting an undefined mechanism(s) for their suppression. Notably, growing evidence indicates that PTEN can be regulated by microRNAs involved in cancer progression. In this study, we discover that the miR‐4286 is overexpressed in NSCLC and negatively regulates the expression of PTEN. Furthermore, we found that miR‐4286 reduces PTEN expression by directly binding to PTEN 3′‐untranslated region (UTR), thereby inhibiting NSCLC cell proliferation and mobility. Moreover, mechanistic investigations revealed that miR‐4286 overexpression was a result of PTEN‐mediated activation of the PI3K/AKT pathway. Taken together, our findings elucidate that miR‐4286 promotes the tumorigenesis of NSCLC by interacting with PTEN. This miR‐4286‐mediated upregulation of PTEN might lead to new therapeutic strategies for NSCLC. Abstract : Genetic alterations in PTEN genes are rare, suggesting an undefined mechanism(s) for their suppression. In this study, we found that miR‐4286 expression is upregulated in non‐small cell lung cancers (NSCLC) and correlated with a decrease in PTEN expression. Mechanistic investigations revealed that miR‐4286 overexpression was a result of PTEN‐mediated activation of the PI3K/Akt pathway.