AI Article Synopsis
- MicroRNAs (miRNAs) are natural regulators that inhibit protein production by binding to specific regions of target genes, influencing cancer development.
- miR-152, part of the miR-148/152 group, shows abnormal expression in various diseases, suggesting its involvement in cancer progression or suppression.
- The review focuses on the structure, functions, and tumor-suppressing abilities of miR-152, especially how it affects cell behaviors like proliferation and migration in cancer.
Article Abstract
MicroRNAs (miRNAs or miRs) are endogenous translation repressors of protein-coding genes that act by binding to the 3'-untranslated region of their target genes, and may contribute to tumorigenesis by functioning as oncogenes or tumor suppressor genes. miR-152, a member of the miR-148/152 family, is aberrantly expressed in various diseases, including various types of cancer. A growing body of evidence has demonstrated that miR-152 may act as a tumor suppressor gene by regulating its target genes, which are associated with cell proliferation, migration and invasion in human cancer. In the present review, the gene structure and functions of miR-152 are discussed, and in particular, its regulatory mechanism, experimentally validated targets and tumor suppressor role in cancer, are highlighted.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888271 | PMC |
| http://dx.doi.org/10.3892/ol.2016.4509 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
[Review of Multiple Endocrine Neoplasia Type 1 Based on a Clinical Case].
Rev Med Chil
June 2024
Departamento de endocrinología, Hospital Clínico San Borja Arriarán, Santiago, Chile.
Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominant disease with an estimated prevalence of 2 per 100,000. This disease is caused by a mutation in the tumor suppressor gene MEN1, which is located on chromosome 11 and codifies the menin protein. It is characterized by a predisposition of parathyroids, enteropancreatic, and anterior pituitary tumors, affecting the quality of life and lifespan of those who have the disease.
View Article and Find Full Text PDFDepletion of TP53 in Human Pluripotent Stem Cells Triggers Malignant-Like Behavior.
Adv Biol (Weinh)
January 2025
Anatomy and Physiology, Department Clinical Sciences, Faculty of Veterinary Medicine, Utrecht University, Utrecht, 3584 CL, The Netherlands.
Human pluripotent stem cells (hPSCs) tend to acquire genetic aberrations upon culture in vitro. Common aberrations are mutations in the tumor suppressor TP53, suspected to confer a growth-advantage to the mutant cells. However, their full impact in the development of malignant features and safety of hPSCs for downstream applications is yet to be elucidated.
View Article and Find Full Text PDFSeryl-tRNA synthetase inhibits Wnt signaling and breast cancer progression and metastasis.
FASEB J
January 2025
Department of Molecular Medicine, Scripps Research Institute, La Jolla, California, USA.
Tumors require ample protein synthesis to grow, and aminoacyl-tRNA synthetases, as critical translation factors, are expected to support cancer progression. Unexpectedly, overexpression of seryl-tRNA synthetase (SerRS) suppresses primary tumor growth of breast cancer. However, the effects of SerRS on metastasis have not been studied.
View Article and Find Full Text PDFInhibition of ASIC1a reduces ferroptosis in rheumatoid arthritis articular chondrocytes via the p53/NRF2/SLC7A11 pathway.
FASEB J
January 2025
School of Pharmacy, Anhui Medical University, Hefei, China.
The activation of acid-sensing ion channel 1a (ASIC1a) in response to extracellular acidification leads to an increase in extracellular calcium influx, thereby exacerbating the degeneration of articular chondrocytes in rheumatoid arthritis (RA). It has been suggested that the inhibition of extracellular calcium influx could potentially impede chondrocyte ferroptosis. The cystine transporter, solute carrier family 7 member 11 (SLC7A11), is recognized as a key regulator of ferroptosis.
View Article and Find Full Text PDFBioinformatics and assays identified miR-486-5p as a tumor suppressor miRNA in hepatocellular carcinoma.
Heliyon
December 2024
Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Background: This study aimed to explore key microRNAs (miRNAs) and their effects on hepatocellular carcinoma (HCC) progression.
Methods: Key deregulated miRNAs in HCC were screened from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The anti-cancer effects of miR-486-5p were validated using a cell counting kit-8 assay, flow cytometry, scratch assay, transwell assay, and an orthotopic transplantation tumor model.
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!