Identification of Pax protein inhibitors that suppress target gene expression and cancer cell proliferation

MicroRNAs (miRNAs) are endogenous non-coding small RNAs that downregulate target gene expression by imperfect base-pairing with the 3′ untranslated regions (3′UTRs) of target gene mRNAs. MiRNAs play important roles in regulating cancer cell proliferation, stemness maintenance, tumorigenesis, cancer metastasis, and cancer therapeutic resistance. While studies have shown that dysregulation of miRNA-205-5p (miR-205) expression is controversial in different types of human cancers, it is generally observed that miR-205-5p expression level is downregulated in breast cancer and that miR-205-5p exhibits a tumor suppressive function in breast cancer. This review focuses on the role of miR-205-5p dysregulation in different subtypes of breast cancer, with discussions on the effects of miR-205-5p on breast cancer cell proliferation, epithelial–mesenchymal transition (EMT), metastasis, stemness and therapy-resistance, as well as genetic and epigenetic mechanisms that regulate miR-205-5p expression in breast cancer. In addition, the potential diagnostic and therapeutic value of miR-205-5p in breast cancer is also discussed. A comprehensive list of validated miR-205-5p direct targets is presented. It is concluded that miR-205-5p is an important tumor suppressive miRNA capable of inhibiting the growth and metastasis of human breast cancer, especially triple negative breast cancer. MiR-205-5p might be both a potential diagnostic biomarker and a therapeutic target for metastatic breast cancer.

Download Full-text

Cell Cycle and Anti-Estrogen Effects Synergize to Regulate Cell Proliferation and ER Target Gene Expression

PLoS ONE ◽

10.1371/journal.pone.0011011 ◽

2010 ◽

Vol 5 (6) ◽

pp. e11011 ◽

Cited By ~ 31

Author(s):

Mathieu Dalvai ◽

Kerstin Bystricky

Keyword(s):

Gene Expression ◽

Cell Cycle ◽

Cell Proliferation ◽

Target Gene ◽

Target Gene Expression ◽

Estrogen Effects

Download Full-text

The lncRNA H19 Promotes Cell Proliferation by Competitively Binding to miR-200a and Derepressing β-Catenin Expression in Colorectal Cancer

BioMed Research International ◽

10.1155/2017/2767484 ◽

2017 ◽

Vol 2017 ◽

pp. 1-8 ◽

Cited By ~ 9

Author(s):

Weiwei Yang ◽

Ning Ning ◽

Xiaoming Jin

Keyword(s):

Colorectal Cancer ◽

Colon Cancer ◽

Cell Proliferation ◽

Cancer Cell ◽

Noncoding Rna ◽

Target Gene ◽

Colon Cancer Cell ◽

Cancer Cell Proliferation ◽

Cell Viability Assay ◽

Viability Assay

H19, a paternally imprinted noncoding RNA, has been found to be overexpressed in various cancers, including colorectal cancer (CRC), and may function as an oncogene. However, the mechanism by which H19 regulates CRC progression remains poorly understood. In this study, we aimed to assess H19 expression levels in CRC tissues, determine the effect of H19 on CRC proliferation, and explore the mechanism by which H19 regulates the proliferation of CRC. We measured H19 expression using qRT-PCR and analysed the effects of H19 on colon cancer cell proliferation via cell growth curve, cell viability assay, and colony formation assays. To elucidate the mechanism underlying these effects, we analysed the interactions between H19 and miRNAs and identified the target gene to which H19 and miRNA competitively bind using a series of molecular biological techniques. H19 expression was upregulated in CRC tissues compared with adjacent noncancerous tissues. H19 overexpression facilitated colon cancer cell proliferation, whereas H19 knockdown inhibited cell proliferation. miR-200a bound to H19 and inhibited its expression, thereby decreasing CRC cell proliferation. β-Catenin was identified as a target gene of miR-200a. H19 regulated β-catenin expression and activity by competitively binding to miR-200a. H19 promotes cell proliferation by competitively binding to miR-200a and derepressing β-catenin in CRC.

Download Full-text