Pulmonary Arterial Hypertension KnowledgeBase (bioinfom_tsdb)
bioinfom_tsdb
Pulmonary Arterial Hypertension KnowledgeBase
General information | Literature | Expression | Regulation | Mutation | Interaction

Basic Information

Gene ID

407018

Name

MIR27A

Synonymous

MIR27|MIRN27A;microRNA 27a;MIR27A;microRNA 27a

Definition

hsa-mir-27a

Position

19p13.13

Gene type

ncRNA

Title

Abstract

MiR-27a functions as a tumor suppressor in acute leukemia by regulating 14-3-3theta.

microRNAs (miRs) play major roles in normal hematopoietic differentiation and hematopoietic malignancies. In this work, we report that miR-27a, and its coordinately expressed cluster (miR-23a approximately miR-27a approximately miR-24-2), was down-regulated in acute leukemia cell lines and primary samples compared to hematopoietic stem-progenitor cells (HSPCs). Decreased miR-23a cluster expression in some acute leukemia cell lines was mediated by c-MYC. Replacement of miR-27a in acute leukemia cell lines inhibited cell growth due, at least in part, to increased cellular apoptosis. We identified a member of the anti-apoptotic 14-3-3 family of proteins, which support cell survival by interacting with and negatively regulating pro-apoptotic proteins such as Bax and Bad, as a target of miR-27a. Specifically, miR-27a regulated 14-3-3theta at both the mRNA and protein levels. These data indicate that miR-27a contributes a tumor suppressor-like activity in acute leukemia cells via regulation of apoptosis, and that miR-27a and 14-3-3theta may be potential therapeutic targets.

microRNA-27a functions as a tumor suppressor in esophageal squamous cell carcinoma by targeting KRAS.

microRNAs (miRNAs) have been suggested to play a vital role in regulating tumor progression and invasion. However, the expression of miR-27a in esophageal squamous cell carcinoma (ESCC) and its effect on the tumorigenesis of ESCC are unclear. In the present study, we found that miR-27a was downregulated in esophageal carcinoma cell lines and ESCC specimens with lymph node metastasis. Furthermore, we demonstrated that miR-27a binds to the 3-untranslated region (UTR) of KRAS and inhibits the expression of the KRAS protein. miR-27a levels were inversely correlated with levels of KRAS mRNA and protein in ESCC specimens. Both in vitro and in vivo assays revealed that miR-27a attenuated ESCC proliferation, invasion and tumor growth in nude mice. miR-27a exerts its tumor suppressor function through inhibition of the KRAS-related ERK pathways. Our findings suggest, for the first time, that miR-27a suppresses tumorigenesis of ESCC by targeting KRAS.

')