GAS5‑mediated regulation of cell signaling (Review)

33Citations
Citations of this article
45Readers
Mendeley users who have this article in their library.

Abstract

in recent years, an increasing number of long non-coding rnas (lncrnas) have been discovered using microarrays and nucleic acid sequencing technology. lncrnas exert crucial biological functions by regulating signaling pathways. In particular, the lncRNA growth arrest‑specific transcript 5 (GaS5) has been documented to serve a crucial role in numerous signaling pathways. This article discusses the latest developments in the association between GaS5 and microrna (mirna), p53, mTor, glucocorticoid response element (Gre) and aKT in order to investigate the roles served by GaS5. mirnas can activate related signaling pathways and GaS5 can combine with mirna to regulate related signaling pathways. GaS5 may regulate p53 expression via derivation of snorna, but the underlying mechanism requires further investigation. GaS5 overxpresion reduces the expression level of mTor, which is induced by inhibiting mir-106a-5p expression. GaS5 is a sponge of Gr, and serves a role in controlling and maintaining glucocorticoid sensitivity and drug resistance via competitive combination with Gr. GaS5 can interact with mirnas, such as mir-21 and mir-532-5p, to regulate the expression of aKT signaling pathway, affecting cell survival and apoptosis. collectively, the data indicate that GaS5 serves a key role in the mirna, p53, mTor, Gre, and aKT signaling pathways. GaS5 regulates complex intracellular signaling pathways primarily through three modes of action, all of which are interrelated: Signal, decoy and guide. in the present article, latest developments in the association between GaS5 and a number of cellular signaling pathways are discussed to examine the tumor suppressive role of GaS5.

Cite

CITATION STYLE

APA

Zhou, Y., & Chen, B. (2020, October 1). GAS5‑mediated regulation of cell signaling (Review). Molecular Medicine Reports. Spandidos Publications. https://doi.org/10.3892/mmr.2020.11435

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free