MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells.

Oncotarget

The Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, The First Affiliated Hospital, Soochow University, Suzhou, China.

Published: September 2015

MicroRNAs (miRNAs) play a critical role in controlling tumor invasion and metastasis via regulating the expression of a variety of targets, which act as oncogenes or tumor suppressor genes. Abnormally expressed miR-625-3p has been observed in several types of human cancers. However, the molecular mechanisms of miR-625-3p-mediated tumorigenesis are largely elusive. Therefore, the aim of this study was to evaluate the biological function and molecular insight on miR-625-3p-induced oncogenesis in colorectal carcinoma (CRC). The effects of miR-625-3p in cell migration and invasion were analyzed by wound healing assay and transwell assay, respectively. In addition, the expression of miR-625-3p and its targets was detected in five human CRC cell lines. In the present study, we found that overexpression of miR-625-3p promoted migration and invasion in SW480 cells, whereas downregulation of miR-625-3p inhibited cell motility in SW620 cells. More importantly, we observed potential binding sites for miR-625-3p in the 3'-untranslated region of suppressor of cancer cell invasion (SCAI). Notably, we identified that overexpression of miR-625-3p inhibited the expression of SCAI, while depletion of miR-625-3p increased SCAI level, suggesting that SCAI could be a target of miR-625-3p. Additionally, we revealed that miR-625-3p exerts its oncogenic functions through regulation of SCAI/E-cadherin/MMP-9 pathways. Our findings indicate the pivotal role of miR-625-3p in invasion that warrants further exploration whether targeting miR-625-3p could be a promising approach for the treatment of CRC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4695027PMC
http://dx.doi.org/10.18632/oncotarget.4738DOI Listing

Publication Analysis

Top Keywords

mir-625-3p
13
migration invasion
12
cell migration
8
colorectal carcinoma
8
overexpression mir-625-3p
8
mir-625-3p inhibited
8
invasion
6
cell
5
scai
5
mir-625-3p promotes
4

Similar Publications

Development of Serum Cell-Free miRNA Panel for Identification of Central Precocious Puberty and Premature Thelarche in Girls.

Biochemistry (Mosc)

October 2024

Central laboratory, Suzhou Bay Clinical College, Xuzhou Medical University, Suzhou Ninth People's Hospital, Suzhou, Jiangsu, 215200, China.

Precocious puberty of children, especially girls, has attracted more and more public attention in recent years. In clinic practice, there is a lack of both convenient and effective way to identify central precocious puberty (CPP) and premature thelarche (PT). In this study, we enrolled total 88 girls [28 cases of CPP, 37 cases of PT, as well as 23 cases of normal control (NC)] as a training cohort, and another 270 subjects (92 cases of CPP, 122 cases of PT and 56 cases of NC) as a validation cohort.

View Article and Find Full Text PDF
Article Synopsis
  • The study focused on identifying marker genes and their molecular mechanisms involved in ultrasound (US)-guided microwave ablation (MWA) treatment for glioma in mice.
  • Researchers analyzed differentially expressed genes and long non-coding RNAs (lncRNAs) at different time points post-MWA, identifying key genes connected to immune functions and inflammatory responses.
  • The findings suggest that US-guided MWA could effectively modulate target gene functions, reduce inflammation, and boost immune responses in glioma treatment.
View Article and Find Full Text PDF

Background: Solasonine has been demonstrated to exert an inhibitory effect on bladder cancer (BC), but the potential mechanisms remain unclear. Therefore, the aim of this study is to explore the association between microRNAs (miRNAs)-mediated regulation and the anti-tumor activities of solasonine in BC.

Methods: MiRNA sequencing was performed to identify the differentially expressed microRNAs (DE-miRNAs) associated with solasonine in BC cells.

View Article and Find Full Text PDF

Reduced expression of miRNAs as potential biomarkers in axial spondyloarthritis.

Rev Assoc Med Bras (1992)

May 2024

Mersin University, Faculty of Medicine, Department of Medical Biochemistry - Mersin, Turkey.

Objective: This study aimed to investigate the value of miR-29a-3p, miR-27a, miR126-3p, miR-146a-5p, miR-625-3p, miR-130a, miR-32, miR-218, miR-131, and miR5196 in the diagnosis of axial spondyloarthritis and to determine whether there is a difference in miRNA expression levels between radiographic axial spondyloarthritis and non-radiographic axial spondyloarthritis, as well as the relationship between miRNA expression levels, disease activity, and uveitis history.

Methods: This study included 50 patients with axial spondyloarthritis (25 with radiographic axial spondyloarthritis and 25 with non-radiographic axial spondyloarthritis) and 25 healthy individuals. The fold change of miRNA expression for each miRNA was calculated using the 2-ΔΔCt method.

View Article and Find Full Text PDF

Keratinocyte-derived circulating microRNAs in extracellular vesicles: a novel biomarker of psoriasis severity and potential therapeutic target.

J Transl Med

March 2024

Department of Dermatology, Ajou University School of Medicine, Ajou University Hospital, 164, World Cup-Ro, Yeongtong-Gu, Suwon-Si, Gyeonggi-Do, 16499, South Korea.

Background: Psoriasis is a chronic inflammatory disorder characterized by pathogenic hyperproliferation of keratinocytes and immune dysregulation. Currently, objective evaluation tools reflecting the severity of psoriasis are insufficient. MicroRNAs in extracellular vesicles (EV miRNAs) have been shown to be potential biomarkers for various inflammatory diseases.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!