miR-937 regulates the proliferation and apoptosis via targeting APAF1 in breast cancer.

Onco Targets Ther

Department of Breast Disease, Chongqing University Cancer Hospital, Chongqing City, 400000, People's Republic of China.

Published: July 2019

Previous research had shown that an imbalance in cell proliferation and apoptosis is a vital mechanism for tumorigenesis and cancer progression that may directly influence biological behaviors of cancer. microRNAs are associated with the occurrence and development of tumors. This study aimed to explore the influence of miR-937 on breast cancer regulation of APAF1 expression. Cancer Genome Altas microarray analysis (fold change > 2, p<0.05) was used to verify differentially expressed microRNAs and RT-qPCR was used to detect miR-937 mRNA level in breast cancer. Cell viability and proliferation were measured using CCK8 and colony formation assays, respectively, after the miR-937 mimics/inhibitors and their negative control were transfected into MCF7 cells. The variations in cell cycle and apoptosis were examined using flow cytometry. DAVID database was used to perform GO enrichment analysis. We use dual luciferase report system to detect the effect of miR-937 on the transcriptional activity of APAF1. APAF1 protein level was determined by Western blot assay. miR-937 was up-regulated in breast cancer cell lines and high miR-937 expression is associated with a poorer survival rate in cancer patients. miR-937 overexpression promoted the viability, down-regulated the G1 phase ratios and increased the ability of colony formation in breast cancer cells. miR-937 inhibition inhibited the viability and the ability of colony formation, promoted the apoptosis and up-regulated the G1 phase ratios. Our results showed that miR-937 targeted bind to the APAF1-3'UTR. APAF1 overexpression inhibited the viability and the ability of colony formation, promoted the apoptosis and up-regulated the G1 phase ratios. After cells were co-transfection miR-937 mimics and APAF1, cell apoptosis level was increased. APAF1 up-regulation or APAF1 down-regulation in breast cancer may regulate cell proliferation and apoptosis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6645689PMC
http://dx.doi.org/10.2147/OTT.S207091DOI Listing

Publication Analysis

Top Keywords

proliferation apoptosis
8
breast cancer
8
cancer
5
mir-937 regulates
4
regulates proliferation
4
apoptosis targeting
4
targeting apaf1
4
apaf1 breast
4
cancer previous
4
previous imbalance
4

Similar Publications

Background: Oral squamous cell carcinoma (OSCC) ranks as the sixth most common malignancy globally. Cisplatin is the standard chemotherapy for OSCC, but resistance often reduces its efficacy, necessitating new treatments with fewer side effects. Rumex dentatus L.

View Article and Find Full Text PDF

Background: Rex rabbit is famous for its silky and soft fur coat, a characteristic predominantly attributed to its hair follicles. Numerous studies have confirmed the crucial roles of mRNAs and non-coding RNAs (ncRNAs) in regulating key cellular processes such as cell proliferation, differentiation, apoptosis and immunity. However, their involvement in the regulation of the hair cycle in Rex rabbits remains unknown.

View Article and Find Full Text PDF

Tongue squamous cell carcinoma (TSCC) is a common malignant oral cancer characterized by substantial invasion, a high rate of lymph node and distant metastasis, and a high recurrence rate. This study aims to provide new ideas for the diagnosis and treatment of TSCC patients by exploring the related mechanisms that affect the migration and invasion of TSCC and inhibit the migration and spread of cancer cells. The results indicated the rate of high expression of IL-17 in cancer tissues was greater than that in tongue tissues, and the expression of IL-17 was related to the TNM stage.

View Article and Find Full Text PDF

The role of Box A of HMGB1 in producing γH2AX associated DNA breaks in lung cancer.

Sci Rep

January 2025

Center of Excellence in Molecular Genetics of Cancer and Human Diseases, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.

An ideal chemotherapeutic agent damages DNA, specifically in cancer cells, without harming normal cells. Recently, we used Box A of HMGB1 plasmid as molecular scissors to produce DNA gaps in normal cells. The DNA gap relieves DNA tension and increases DNA strength, preventing DNA double-strand breaks (DSBs).

View Article and Find Full Text PDF

Identification of a novel TOP2B::AFF2 fusion gene in B-cell acute lymphoblastic leukemia.

Sci Rep

January 2025

Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Diseases, Children's Hospital of Chongqing Medical University, No 136 Zhongshan 2 road, YuZhong district, Chongqing, 400014, China.

Genetic alterations play a pivotal role in leukemic clonal transformation, significantly influencing disease pathogenesis and clinical outcomes. Here, we report a novel fusion gene and investigate its pathogenic role in acute lymphoblastic leukemia (ALL). We engineer a transposon transfection system expressing the TOP2B::AFF2 transcript and introduce it into Ba/F3 cells.

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!