Overexpression of long non coding RNA CA3-AS1 suppresses proliferation, invasion and promotes apoptosis via miRNA-93/PTEN axis in colorectal cancer.

07:00 EST 8th November 2018 | BioPortfolio

Summary of "Overexpression of long non coding RNA CA3-AS1 suppresses proliferation, invasion and promotes apoptosis via miRNA-93/PTEN axis in colorectal cancer."

In previous studies, dysregulated lncRNAs in colorectal cancer were screened using RNA-sequencing by Atsushi Yamada. In these dysregulated lncRNAs, a long non coding RNA named CA3-AS1 attracted our attention due to its high conservation and fold change, which was downregulated in colorectal cancer. In this study, we aimed to investigate the function and mechanism of lncRNA CA3-AS1 in colorectal cancer.


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This article was published in the following journal.

Name: Gene
ISSN: 1879-0038


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Medical and Biotech [MESH] Definitions

The B-cell leukemia/lymphoma-2 genes, responsible for blocking apoptosis in normal cells, and associated with follicular lymphoma when overexpressed. Overexpression results from the t(14;18) translocation. The human c-bcl-2 gene is located at 18q24 on the long arm of chromosome 18.

A proteolytically-cleaved membrane glycoprotein and member of the TNF superfamily that is highly expressed in a variety of tissues including heart, pancreas, brain, and peripheral blood lymphocytes. The secreted extracellular form is a weak inducer of APOPTOSIS for some cell types and a ligand for the FN14 RECEPTOR. It mediates activation of NF-KAPPA-B and promotes ANGIOGENESIS and proliferation of ENDOTHELIAL CELLS, as well as expression of cytokines involved in INFLAMMATION.

A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the mitochondria. In mammalian cells AIF is released in response to pro-apoptotic protein members of the bcl-2 protein family. It translocates to the CELL NUCLEUS and binds DNA to stimulate CASPASE-independent CHROMATIN condensation.

A serine peptidase that contains a C-terminal PDZ domain. It localizes to the mitochondrial membrane and intermembrane space, translocating to the cytoplasm following APOPTOSIS stimuli, such as UV irradiation; it promotes cell death by binding to and inhibiting INHIBITOR OF APOPTOSIS PROTEINS, resulting in an increase in activity of CASPASES. Mutations in the HTRA2 gene are associated with Type 13 PARKINSON DISEASE.

Securin is involved in the control of the metaphase-anaphase transition during MITOSIS. It promotes the onset of anaphase by blocking SEPARASE function and preventing proteolysis of cohesin and separation of sister CHROMATIDS. Overexpression of securin is associated with NEOPLASTIC CELL TRANSFORMATION and tumor formation.

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