DLGAP1-AS2 (DLGAP1 Antisense RNA 2)

DLGAP1-AS2 is a potential biomarker for evaluating the severity of BLCA and for predicting clinical prognosis. DLGAP1-AS2 regulates the malignant progression of BLCA via miR-451a.

Moreover, our study demonstrated that the combination of DLGAP1-AS2 inhibition through siRNA-DLGAP1-AS2 transfection and carboplatin treatment had a tumor-suppressive function, inhibiting the progression and proliferation of A549 lung cancer cells. Therefore, it can be concluded that targeting DLGAP1-AS2 using specific siRNA in combination with carboplatin chemotherapy holds promise as a valuable therapeutic approach for lung cancer.

However, it reduced the stemness feature, the rate of cell viability, proliferation, and metastasis compared to the effect of each treatment alone; the results also showed the arrest of the cell cycle in the Sub G1 phase after the combined treatment and a further reduction in the number and size of the formed colonies. Suppressing the expression of lncRNA DLGAP1-AS2 by siRNA followed by treatment with oxaliplatin can be utilized as an effective and new therapeutic technique for gastric cancer therapy.

Rescue assays revealed that the DLGAP1-AS2/miR-451a/HK2 axis contributed to OS cell malignancy by promoting aerobic glucose metabolism. Overall, these findings revealed a new regulatory pathway where DLGAP1-AS2 upregulated HK2 expression by sponging miR-451a to accelerate OS development.

Using the STRING website, we assessed interactions between the target proteins and built networks. Our analysis revealed that the JAK-STAT and Hippo signaling pathways, cytokine pathways, the VEGFA-VEGFR2 pathway, mechanisms of cell cycle regulation, and neovascularization are the most relevant to the effect of lncRNA on NSCLC.

The RMM-I molecular subtype constituted the novel molecular characteristic subtype of LUAD, which complemented the existing pathological typing. More refined and accurate molecular subtypes provide help to reveal the mechanism of LUAD development. In addition, the RMM-I score offers a reliable tool for accurate prognosis of LUAD.

The ferroptosis-related lncRNAs risk model and genomic clinicopathological nomogram have the potential to accurately predict the prognosis of patients with ccRCC and could serve as potential therapeutic targets in the future.

Finally, distinct studies have reported down-regulation of circCDYL and up-regulation of circ0093740 and circSLC7A6 in this tumor. Dysregulation of these transcripts represents a new avenue for identification of the pathetiology of this pediatric tumor as well as design of targeted therapies.

Furthermore, this signature based on the 6 NRLs could provide a promising method to predict the prognosis and immune response of KIRC patients. To some extent, our findings helped give a reference for further research between NRLs and KIRC and find more effective therapeutic drugs for KIRC.

The discovery of DLGAP1-AS2, a promising prognostic biomarker, reveals a new dimension into the molecular pathogenesis of CRC and provides a prospective treatment target for this disease.

The second hairpin structure of DLGAP1-AS2 was critical for the interaction between DLGAP1-AS2 and CTCF in the nucleus. Taken together, our study reveals the oncogenic regulatory axis of DLGAP1-AS2/CTCF/Myc in CRC, implying a promising targeted therapy for clinical application.

We identified 24 potential molecularly targeted drugs with significant sensitivity differences between high- and low-risk UVM patients, of which 13 may be potential targeted drugs for high-risk patients. Our findings have important implications for early prediction and early clinical intervention in high-risk UVM patients.