CLIC6 (Chloride Intracellular Channel 6)

This study identified CLIC6 as a novel gene associated with radioresistance in ER+/HER2- breast cancer and showed that theaflavin functions as a natural radiosensitizer in a CLIC6-dependent manner, consistent with its high-affinity interaction with CLIC6. Targeting CLIC6 may provide a promising strategy to enhance radiotherapy efficacy in this common breast cancer subtype.

To summarize, this integrative model identified a novel methylation-based risk classifier/molecular subtype for BRCA, highlighting FABP7 and CLIC6 as a key prognostic biomarker with potential utility for risk stratification for strategic treatment. These findings require further validation through wet-lab experiments and prospective clinical studies to support clinical translation.

In conclusion, CLIC6 can serve as a key biomarker for various cancers, and its expression level is related to the tumor immune microenvironment and the outcomes in selected cancers; further validation is warranted. Our research on CLIC6 in BRCA has revealed new potential for tumor treatment strategies targeting this marker.

The different expression patterns of CLICs in HNSCC patients' tissues and blood serum suggest that they may play an essential role in HNSCC pathogenesis and serve as biomarkers for HNSCC detection.

A prognostic signature composed of CDCP1, CLIC6, FURIN, KRT6A, MFI2, and P2RY13, based on PANR-DEGs, provides a theoretical framework and reference for further LUAD research.

Further analysis uncovered significant associations between our ITH-based signature and specific cancer hallmarks, genetic alterations, and clinicopathological features. Our findings not only establish a practical prognostic tool but also provide novel insights into the intricate relationship between tumor heterogeneity and the microenvironment, highlighting potential therapeutic targets for personalized breast cancer treatment.

We developed a PRMTs-related prognostic model for assessing prognosis and immunotherapy responses in LUAD. This model was vital for developing more personalized and effective treatment plans for LUAD patients.

The gene signature we constructed can well predict the prognosis as well as the treatment response of BC patients. In addition, our predicted small-molecule complexes provide an important reference for personalized treatment of breast cancer patients.

Moreover, CLIC6 mitigates hepatic oxidative damage via the Janus tyrosine kinase 1/signal transducer and activator of the transcription pathway, attenuates c-Jun N-terminal kinase (JNK) phosphorylation, and modulates apoptosis-related proteins, effectively hindering HCC development. CLIC6 demonstrates potent antitumor effects in HCC through inhibition of proliferation, promotion of apoptosis, modulation of cytokine levels, regulation of immune cell balance, and attenuation of oxidative stress pathways.

We developed a risk model with excellent predictive efficacy based on MPTdn and revealed that BCL2A1, SCUBE2, NPY1R and CLIC6 could be used as the biomarkers, laying a solid foundation for investigations of therapeutic targets of breast cancer.

In summary, this study identified TPPP3, MUC4 and CLIC6 as lactate-associated clinical modelling indicators linked to NPC, providing a foundation for advancing diagnostic and therapeutic strategies for this malignancy.

The induction of cell death by ATP appears to play a protective role in BC progression. These findings carry significant implications for the implementation of personalized and tailored treatment strategies for BC patients.