CLIC1 (Chloride Intracellular Channel 1)

This study provides evidence supporting the association between the ITGβ1-CLIC1 axis and OSCC progression, and suggests its potential involvement in modulating the tumor immune microenvironment, indicating its promise as a therapeutic target worthy of further investigation.

This study identifies CLIC1 as a novel metabolic regulator that drives glycolytic reprogramming through direct interaction with PKM2 in gastric cancer. Targeting the CLIC1-PKM2 axis may provide a promising therapeutic strategy for metabolic intervention in GC and highlights a potential translational target for future clinical application.

Our results elucidates the key pathway through which high CLIC1 expression enhances cellular oxidative stress, subsequently promoting gastric cancer progression. Therefore, CLIC1 might function as a redox regulation therapy target and a tumor marker.

The interplay between TLSs, CLIC1 expression in tumor cells, and stromal vasculature significantly influences TNM staging parameters. Preliminary data suggest that CLIC1 CM and M patterns may promote metastasis and stromal vascularization, whereas TLS presence, particularly with certain CLIC1 patterns, may serve as a negative prognostic marker.

In summary, these findings expand our knowledge of CLIC1, confirming its oncogenic role and laying the groundwork for future development of pharmacological agents targeting this gene.

Collectively, PDAC cells elevate CLIC1 levels in a matrix-stiffness-responsive manner, bolstering the Warburg effect to drive tumor growth via ROS/HIF1α signaling. Our insights highlight opportunities for targeted therapies that concurrently address matrix properties and metabolic rewiring, with CLIC1 emerging as a promising intervention point.

CLIC family members may be candidates for potential novel cancer biomarkers due to the contrast in their expression between cancerous and healthy tissues and secretion to the interstitial fluid and blood. CLICs are investigated as potential therapeutic targets because of their involvement in cancer pathogenesis and tumor microenvironment.

Elucidating the mechanisms underlying the alterations in CLIC1 expression and structural transitions will further our understanding of its role in GSC biology. This review will highlight the role of CLIC1 in GSCs and its significance in facilitating different hallmarks of cancer.

High CLIC1 expression samples were more sensitive to camptothecin, cisplatin, doxorubicin, erlotinib, paclitaxel, rapamycin, clofarabine, tanespimycin, methotrexate, everolimus, TAK-733, trametinib and AZD8330. Single-cell analysis unveiled that CLIC1 was expressed ubiquitously in tumor cells and tumor microenvironment. Overall, CLIC1 was a promising treatment vulnerability in glioma.

Cisplatin (DDP) has been approved as a critical chemotherapy drug to treat various kinds of solid tumors...These experiments suggest that CLIC1 could alter the sensitivity of gastric cancer cells to DDP by activating autophagy. Overall, the results of this study recommend a novel mechanism of DDP resistance in gastric cancer.

As a matter of fact, CLIC1's peculiar activity and its interaction with glutathione make this protein critical for the redox equilibrium of colorectal cancer cells. Overall, the findings could be considered as a beginning point for elucidating a mechanism of action that could constitute a new milestone in anticancer research.