AI Article Synopsis
- Evidence indicates that the long non-coding RNA (lncRNA) DSCAM-AS1 promotes tumor growth in various cancers, particularly in endometrial adenocarcinoma.
- Analyses show that higher levels of DSCAM-AS1 are linked to poor survival rates in endometrial cancer patients, associating it with key tumor-promoting genes and hormone receptor expression.
- Silencing DSCAM-AS1 in specific cancer cell lines led to reduced cell growth and activation of tumor-suppressing pathways, confirming its role as an oncogenic factor in endometrial cancer.
Article Abstract
Accumulating evidence suggests that lncRNA DSCAM-AS1 acts tumor-promoting in various cancer entities. In breast cancer, DSCAM-AS1 was shown to be the lncRNA being most responsive to induction by estrogen receptor α (ERα). In this study, we examined the function of DSCAM-AS1 in endometrial adenocarcinoma using in silico and different in vitro approaches. Initial analysis of open-source data revealed DSCAM-AS1 overexpression in endometrial cancer (EC) (p < 0.01) and a significant association with shorter overall survival of EC patients (HR = 1.78, p < 0.01). In EC, DSCAM-AS1 was associated with endometrial tumor promotor gene PRL and with expression of ERα and its target genes TFF1 and PGR. Silencing of this lncRNA by RNAi in two EC cell lines was more efficient in ERα-negative HEC-1B cells and reduced their growth and the expression of proliferation activators like NOTCH1, PTK2 and EGR1. DSCAM-AS1 knockdown triggered an anti-tumoral transcriptome response as revealed by Affymetrix microarray analysis, emerging from down-regulation of tumor-promoting genes and induction of tumor-suppressive networks. Finally, several genes regulated upon DSCAM-AS1 silencing in vitro were found to be inversely correlated with this lncRNA in EC tissues. This study clearly suggests an oncogenic function of DSCAM-AS1 in endometrial adenocarcinoma via activation of a tumor-promoting transcriptome profile.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9313190 | PMC |
| http://dx.doi.org/10.3390/biomedicines10071727 | DOI Listing |
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