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Review
. 2022 Aug 4:12:867670.
doi: 10.3389/fonc.2022.867670. eCollection 2022.

The emerging potentials of lncRNA DRAIC in human cancers

Affiliations
Review

The emerging potentials of lncRNA DRAIC in human cancers

Qinfan Yao et al. Front Oncol. .

Abstract

Long non-coding RNA (lncRNA) is a subtype of noncoding RNA that has more than 200 nucleotides. Numerous studies have confirmed that lncRNA is relevant during multiple biological processes through the regulation of various genes, thus affecting disease progression. The lncRNA DRAIC, a newly discovered lncRNA, has been found to be abnormally expressed in a variety of diseases, particularly cancer. Indeed, the dysregulation of DRAIC expression is closely related to clinicopathological features. It was also reported that DRAIC is key to biological functions such as cell proliferation, autophagy, migration, and invasion. Furthermore, DRAIC is of great clinical significance in human disease. In this review, we discuss the expression signature, clinical characteristics, biological functions, relevant mechanisms, and potential clinical applications of DRAIC in several human diseases.

Keywords: DRAIC; application; biological function; lncRNA; mechanism.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The role of lncRNA DRAIC in human cancers. It has been shown that lncRNA DRAIC acts as a tumor suppressor in prostate cancer, glioma, gastric cancer, and retinoblastoma. DRAIC also functioned as an oncogene in lung cancer, breast cancer, esophageal cancer and nasopharyngeal carcinoma.
Figure 2
Figure 2
In prostate cancer, lncRNA DRAIC played a tumor suppressive role through inhibiting cell migration and invasion. DRAIC was activated by FOXA1 and NKX3-1 and interacts with IKK to further decrease NF-κB expression in LNCaP cells.
Figure 3
Figure 3
Regulatory mechanisms of DRAIC on cell autophagy in cancers. In glioblastoma A172 and U87 cells, lncRNA DRAIC induced autophagy by downregulating the NF-κB target gene GLUT1, which activated AMPK, and blocked the expression of mTOR. In breast cancer MCF-7 cells, DRAIC enhanced ULK1 expression and inhibited cell autophagy. In esophageal cancer, lncRNA DRAIC suppressed cell autophagy through its interaction with miR-149-5p and up-regulation of NFIB.
Figure 4
Figure 4
The main mechanisms of DRAIC in cancers. DRAIC participated in the regulation of biological processes of cancers through interaction with diverse molecules.

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