LINC00667 (Long Intergenic Non-Protein Coding RNA 667)

Furthermore, both individual and combined modulation of MSI2 knockdown, LINC00667 knockdown and IRF6 over-expression enhanced BTB permeability to doxorubicin (Dox), thereby increasing the apoptosis rate of GB cells. Collectively, the MSI2/LINC00667/IRF6 pathway plays an important role in modulating BTB permeability, offering potential targets for new molecular therapies in GB.

Up-regulated LINC00667 may serve as a biomarker for PTC. Knockdown of LINC00667 may inhibit the progression of PTC by regulating miR-34c-5p.

This study provides a blueprint for identifying mRNA-lncRNA networks in any cancer, facilitating the use of lncRNAs as prognostic biomarkers and aiding in the identification of therapeutic targets. Future research may focus on validating this research biologically to further substantiate the role of lncRNAs as prognostic biomarkers in breast cancer.

Cycloheximide (CHX) chase experiments revealed that LINC00667 overexpression accelerated POTEE degradation, while treatment with the proteasome inhibitor MG132 stabilized POTEE levels...Collectively, our findings demonstrate that LINC00667 inhibits breast cancer progression by promoting TRIM33-mediated ubiquitination and subsequent degradation of POTEE, thereby regulating mitochondrial OXPHOS activity. These results highlight the critical role of LINC00667 in the posttranslational regulation of protein stability and mitochondrial function in BC, and suggest that targeting the LINC00667-POTEE axis may represent a potential therapeutic strategy for this disease.

LINC00667 is up-regulated in ccRCC and enhances the ZEB1 expression by targeting miR-143-3p, which in turn accelerates ccRCC progression and induces chemoresistance.

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, functional experiments showed that knockdown of MIR181A2HG obviously inhibited the proliferation and migration of papillary thyroid cancer (PTC) cells in vitro, whereas LYPLAL1-DT overexpression promoted PTC cell proliferation and migration. Eleven of the m6A-associated lncRNAs were identified as a risk model to predict clinical outcomes and provide a novel and efficient immunotherapeutic strategy for THCA patients.Key messagesm6A-associated lncRNAs can be used to predict the clinical outcomes of thyroid cancer patients.An m6A-associated lncRNAs risk model, which can accurately evaluate the immune status and risk stratification in individual thyroid cancer patients, was established.Knockdown/overexpression of representative lncRNAs in the risk model significantly affected the proliferation and migration of papillary thyroid cancer cells.

Moreover, LINC00667 positively regulated the KIAA1429 via sponging miR-556-5p, forming a KIAA1429/mA/LINC00667/miR-556-5p feedback loop. Collectively, the central findings of our study suggest that KIAA1429-induced LINC00667 exerted its functions as an oncogene in BC progression through mA-dependent feedback loop.