Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aberrant expression of long non-coding RNA DSCAM-AS1 (Down Syndrome Cell Adhesion Molecule antisense) has been observed in several cancers. However, the expression status, biological function and underling mechanism of DSCAM-AS1 in hepatocellular carcinoma (HCC) remain unclear. The expression of DSCAM-AS1 was detected in HCC tissues and serum from both HCC patients and healthy controls. MTS, wound healing and transwell invasion assays were used to examine the effects of DSCAM-AS1 on cell proliferation, migration, and invasion in HCC cells, respectively. MicroRNAs (miRNAs) targeted DSCAM-AS1 was predicated by Starbase2.0 and identified using luciferase reporter and RNA immunoprecipitation assays. The xenograft mice were established to examine the effect DSCAM-AS1 on tumor growth in vivo. We found that DSCAM-AS1 was up-regulated in HCC tissues relative to adjacent non-tumor tissues. Serum levels of DSCAM-AS1 were higher in HCC patients than that in healthy controls. Increased DSCAM-AS1 was associated with poor prognosis. Knockdown of DSCAM-AS1 significantly inhibited HCC cell proliferation, migration and invasion. Moreover, miR-338-3p was confirmed as a direct target of DSCAM-AS1 in HCC cells. The miR-338-3p inhibitor could partially reverse the inhibitory effect of DSCAM-AS1 depletion in HCC cells. DSCAM-AS1 positively regulated CyclinD1 and smoothened (SMO) expression (two targets of miR-338-3p) in HCC cells. Moreover, tumor growth was tremendously retarded in nude mice received injection of SMCC-7721 cells transfected with sh-DSCAM-AS1. Taken together, the present work suggested that DSCAM-AS1 functioned as an oncogenic lncRNA that promoted HCC progression by sponging miR-338-3p.
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PMID:Long non-coding RNA DSCAM-AS1 accelerates the progression of hepatocellular carcinoma via sponging miR-338-3p. 3139 35

Down Syndrome Cell Adhesion Molecule antisense1 (DSCAM-AS1), a novel long non-coding RNA (lncRNA), reportedly contributes to the development and progression of several cancers. There is a lack of information on its biological role and regulatory mechanism with respect to colorectal cancer (CRC). Here, we discovered that the expression of DSCAM-AS1 exhibited a significant upregulation in CRC tissues and cell lines in comparison with the corresponding control. Increased DSCAM-AS1 expression was associated with poor prognosis for those diagnosed with CRC. Loss-of function assay illustrated that knockdown of DSCAM-AS1 resulted in significant inhibition of cell proliferation, invasion and migration in vitro, and impaired tumor growth in vivo. MicroRNA-384(miR-384) was directly targeted by DSCAM-AS1 in CRC cells, and repression of DSCAM-AS1 inhibited the expression of AKT3, a known target of miR-384 in CRC. In addition, repression of miR-384 or overexpression of AKT3 could partially rescue the inhibitory effect of DSCAM-AS1 knockdown on CRC progression. In summary, DSCAM-AS1 exerted an oncogenic role in CRC by functioning as a competing endogenous RNA of miR-384 to bring about regulation of AKT3 expression. These results implied that DSCAM-AS1 might be a novel therapeutic target for patients suffering from CRC.
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PMID:LncRNA DSCAM-AS1 promotes colorectal cancer progression by acting as a molecular sponge of miR-384 to modulate AKT3 expression. 3245 6