LINC00473 (Long Intergenic Non-Protein Coding RNA 473)

Furthermore, silencing LINC00473 synergistically enhanced CDDP efficacy, particularly in A2780 cells exhibiting heightened sensitivity. These findings suggest that targeting LINC00473 may represent a novel therapeutic strategy for ovarian cancer; however further exploration of its molecular network and in vivo validation are warranted in the future.

High linc00473 expression has been detected across diverse tumor tissues, high linc00473 expression implies poor cancer prognosis, linc00473 potentially functions as a prospective therapeutic target and prognostic indicator. More high-quality documents were wished to implement to support the results of this study.

Conversely, in glioblastoma (GBM), PDE10A acts as a tumor suppressor, and its knockdown promotes tumor progression via activation of the PI3K/AKT pathway. These findings showed the ability of PDE10A to be considered as a promising biomarker and therapeutic target in oncology; however, it is suggested to examine the tissue-specific expression of PDE10A, baseline cyclic nucleotide levels, cross-talk with other pathways, differences in the degree and duration of PDE10A suppression, and the interplay between PDE10A-mediated cyclic nucleotide signaling and compensatory oncogenic pathways for an effective therapy as observed in other PDEs family reviewed in this manuscript.

LINC00473 can enhance the specificity of SEPT9 methylation-specific detection of precancerous lesions. The combined detection of SEPT9 and LINC00473 offers a simple and accurate screening tool for polyp detection, showing promise for the early non-invasive detection of CRC and associated precancerous lesions.

Furthermore, PDE10A loss and decreased protein expression corresponded with an epithelial-to-mesenchymal transition (EMT) phenotype in both cohorts, consistent with the known PN-MES shift observed in glioblastoma. In summary, PDE10A loss in colon adenocarcinoma is associated with decreased OS and PFS, more frequent lymphatic invasion, higher pathologic nodal stage, metastatic disease, and an EMT phenotype.

RNA ISH for CRTC1/3::MAML2 rearrangements and LINC00473 represent reasonable timely and cost-effective alternatives to FISH and NGS. Such markers may provide the means for accurate diagnosis to ensure appropriate therapy of MEC and HA-neoplasms that can arise in multiple anatomic sites and be encountered by a wide range of pathologists.

We have optimized the HEK-DP-Luc cells for HTS, and here we present our pipeline for primary screening and counter-screening to identify compounds that inhibit DP's downstream transcriptional activity. This HTS platform provides a novel approach for therapeutic drug discovery in FLC.

Mouse glioblastoma modeling using the RCAS/tv-a system confirmed that Pde10a suppression induced an aggressive glioma phenotype in vivo and resistance to temozolomide and radiation therapy in vitro...Single-nucleus RNA sequencing from our mouse gliomas in vivo, in combination with cell culture validation, further showed that Pde10a suppression was associated with a proneural-to-mesenchymal transition that exhibited increased cell adhesion and decreased cell migration. Our results indicate that glioblastoma patients harboring PDE10A loss have worse outcomes and potentially increased sensitivity to PI3K inhibition.

Overall, we propose that LINC00473 could be a viable target for this devastating disease. Schematic was created with BioRender.com.

Temozolomide (TMZ) offers substantial therapeutic benefits for glioblastoma (GB), yet its efficacy is hindered the development of chemoresistance...In conclusion, a novel CREB/LINC00473/CEBPα/MGMT pathway was revealed in the GB TMZ-resistance formation. In addition, an exosome-based mechanism of chemoresistance transmission was revealed, which suggested that LINC00473 could be used as a novel therapeutic target for GB.

RT-PCR showed that AKAP12 was downregulated in tumour tissues. The hub genes screened out in the present study may provide ideals for further treatment on BTCC.

Taken together, our study elucidates a novel role for PDE10A in cardiotoxicity induced by DOX and cancer growth. Given that PDE10A has been already proven to be a safe drug target, PDE10A inhibition may represent a novel therapeutic strategy in cancer therapy, with effects preventing DOX-induced cardiotoxicity and simultaneously antagonizing cancer growth.