MiR-23b PROMOTES HUMAN BREAST CANCER GROWTH AND METASTASIS BY DOWNREGULATING NISCHARIN EXPRESSION
Document Type
Presentation
Start Date
22-10-2010 10:45 AM
End Date
22-10-2010 12:00 PM
Description
MicroRNAs (miRs) are a new class of small (21-25 nucleotides) non-coding endogenous RNAs implicated in negative gene expression regulation by binding to the 3'UTR of a target mRNA molecule resulting in either degradation transcript or translational inhibition. We have profiled a highly invasive human breast cancer cell line MDA-MB-231 and a Nischarin-overexpressing MDA-MB-231 cell line by miRNA microarrays and found that the expression levels of miR-23b were significantly high in MDA-MB-231, while the levels are low in Nischarin-overexpressing cells. Computer algorithms predicted that the 3'UTR of Nischarin harbors a putative miR-23b binding site. The regulatory roles of miR-23b on endogenous Nischarin in human breast cancer cells were determined by introducing pre-miR-23b or anti-miR-23b in MCF-7, a human breast cancer cell line, and the expression of Nischarin was confirmed by Western blotting as well as RT-qPCR approaches. We also examined the expresssion levels of miR-23b and Nischarin in human breast cancer and normal tissues, and found significantly higher expression of miR-23b in 74 cancer tissues than in normal tissues, while Nischarin levels are high in normal tissues compared to cancerous tissues. Furthermore, we found that knocking-down of miR-23b/27b inhibited breast cancer growth and metastasis in vitro as well as in vivo. We are currently investigating the function of miR-23b/27b in breast tumorigenesis in vitro and in vivo through over-expression of miR-23b/27b. Our study is the first to demonstrate that miR-23b negatively regulates Nischarin through a specific regulatory element located in its 3'UTR region.
This work is supported by the NIH RO1-CA 115706 grant and funds from Louisiana Cancer Research Consortium to SKA.
Recommended Citation
Jin, Lianjin, "MiR-23b PROMOTES HUMAN BREAST CANCER GROWTH AND METASTASIS BY DOWNREGULATING NISCHARIN EXPRESSION" (2010). Dr. Joseph M. Moerschbaecher, III Graduate Research Day. 14.
https://digitalscholar.lsuhsc.edu/grad_rs/2010/poster1/14
MiR-23b PROMOTES HUMAN BREAST CANCER GROWTH AND METASTASIS BY DOWNREGULATING NISCHARIN EXPRESSION
MicroRNAs (miRs) are a new class of small (21-25 nucleotides) non-coding endogenous RNAs implicated in negative gene expression regulation by binding to the 3'UTR of a target mRNA molecule resulting in either degradation transcript or translational inhibition. We have profiled a highly invasive human breast cancer cell line MDA-MB-231 and a Nischarin-overexpressing MDA-MB-231 cell line by miRNA microarrays and found that the expression levels of miR-23b were significantly high in MDA-MB-231, while the levels are low in Nischarin-overexpressing cells. Computer algorithms predicted that the 3'UTR of Nischarin harbors a putative miR-23b binding site. The regulatory roles of miR-23b on endogenous Nischarin in human breast cancer cells were determined by introducing pre-miR-23b or anti-miR-23b in MCF-7, a human breast cancer cell line, and the expression of Nischarin was confirmed by Western blotting as well as RT-qPCR approaches. We also examined the expresssion levels of miR-23b and Nischarin in human breast cancer and normal tissues, and found significantly higher expression of miR-23b in 74 cancer tissues than in normal tissues, while Nischarin levels are high in normal tissues compared to cancerous tissues. Furthermore, we found that knocking-down of miR-23b/27b inhibited breast cancer growth and metastasis in vitro as well as in vivo. We are currently investigating the function of miR-23b/27b in breast tumorigenesis in vitro and in vivo through over-expression of miR-23b/27b. Our study is the first to demonstrate that miR-23b negatively regulates Nischarin through a specific regulatory element located in its 3'UTR region.
This work is supported by the NIH RO1-CA 115706 grant and funds from Louisiana Cancer Research Consortium to SKA.