VIM-AS1 (VIM Antisense RNA 1)

In the context of cancer biology, VIM-AS1 did not affect the antiproliferative actions of TGF-β, yet had an impact on the epithelial-mesenchymal transition gene program, and increased the invasion and motility of tumor cells, whereas its silencing sensitized cancer cells to chemotherapeutic agents. The molecular mechanism highlights how a lncRNA can modulate the nuclear pore's capacity to import SMAD complexes, by facilitating their capture by Nup358/RanBP2 and thereby enhancing nuclear accumulation of SMADs with distinct isoform composition, thus promoting selectively TGF-β signaling responses.

Paclitaxel, gemcitabine, and cisplatin (all p < 0.05) may be more useful in EC patients with high expression of targeted srlncRNAs in the GDSC database. The EC-18 PDO was more resistant to three drugs, which aligned with clinical observation. The srlncRNA signature (AL121906.2, AP002761.4, BX322234.1, LINC00662, LINC00908, VIM-AS1, and ZNF236-DT) could guide prognosis prediction and treatment choices for EC patients.

VIM-AS1 exhibited aberrant expression in breast cancer, playing a critical role in tumor development by targeting miR-29a-3p. Our findings highlight the potential of VIM-AS1 as a novel diagnostic and prognostic biomarker in breast cancer. However, further in vivo studies and exploration of miR-29a-3p downstream targets are needed to fully elucidate the mechanistic role of VIM-AS1 in breast cancer progression.

In vivo experiments further confirmed that the VIM-AS1‒EPHA3 axis controlled tumor growth and the tumor microenvironment in HCC. These findings suggest that the downregulation of VIM-AS1 due to hypermethylation at cg02746869 increased EPHA3 mRNA expression via a m6A-dependent mechanism to increase HCC aggressiveness.

Noncoding RNA analysis can provide specific biomarkers relevant to the prediction of normal tissue responses after radiation therapy, which opens perspectives of next-generation approaches for treatment, in the frame of the recent developments of RNA-based technologies.

Our study suggests that lncRNAs associated with anoikis may serve as potential diagnostic or therapeutic targets for NSCLC. The prognostic signatures we developed can independently predict patient outcomes and provide novel molecular biomarkers for NSCLC.

VIM-AS1 was significantly downregulated in LUAD tissues, and it can be a promising prognostic index for LUAD development. VIM-AS1 regulating apoptotic effects may play important roles in LUAD progression.

Rescue assays indicated that knockdown of HMGCS1 expression ameliorated the increase in proliferation and enzalutamide resistance of prostate cancer cells induced by VIM‑AS1 overexpression. Overall, the present study determined the roles and mechanism of the VIM‑AS1/IGF2BP2/HMGCS1 axis in regulating proliferation and enzalutamide sensitivity of prostate cancer cells and suggested that VIM‑AS1 may serve as a novel therapeutic target for the treatment of patients with CRPC.