LCK (LCK Proto-Oncogene, Src Family Tyrosine Kinase)

FLCK may extend diagnostic sensitivity beyond IgG-based assays and aid in the integrative evaluation of cerebrospinal fluid biomarkers. Prospective studies should evaluate their prognostic value and specificity across neuroinflammatory and infectious diseases.

Moreover, we explore therapeutic strategies targeting palmitoylation, such as the use of selective palmitoyltransferase inhibitors, the design of palmitoylation-deficient CAR-T cells, and the development of nanotechnology-based delivery platforms. By incorporating cross-cancer insights, we propose that palmitoylation is a promising regulatory axis for reprogramming the PDAC immune microenvironment and overcoming resistance to immunotherapy.

From cell lines-based functional assays to bioinformatic analysis, this study demonstrated that clinical potential of ARHGAP6 as a novel biomarker of AML.

This study illuminated the "epigenetic-immune axis" as a central regulatory mechanism driving ECCC metastasis. DNA methylation systematically silenced immune response genes by targeting ETS1-binding sites and TCR signalling components, thus reconstructing the immunosuppressive TME to facilitate metastasis. The development of the metastatic risk score model and identification of LCK as a potential therapeutic target provide valuable strategies for precision treatment decisions and advancing targeted epigenetic-immune therapies in ECCC.

Likewise, p56lck phosphorylation of the antigen receptor immunoreceptor tyrosine-based activation motifs (ITAMs) and key CD28 tyrosine motifs ensures the functionality and the survival of CARs, while their phospho-targets are also inhibited by PD-1, a key component of the immune checkpoint blockade. This review covers historic and current elements of our knowledge of CD4/CD8-p56lck-induced activation events and their importance to the development of CAR T-cell immunotherapies.

Unlike inhibitors and inhibitor-based PROTACs, these MGDs engage LCK in regions distal to the ATP binding site and thus their activities in T-ALL are not affected by gate-keeper LCK mutations that drive resistance to inhibitor-based therapeutics. Taken together, our data underscore the potential of LCK-targeting MGDs as a strategy to overcome kinase inhibitor resistance in T-ALL, highlighting a potentially generalizable strategy in cancer therapy.

Additionally, NFKB1 may positively regulate IL1A, providing a rationale for further in vivo and clinical studies. In conclusion, our study demonstrates the potential role of IL 1A in the prognosis of RCC and establishes a theoretical foundation for subsequent in vivo and clinical investigations.

It also increased the level of TNF-α in the serum and decreased IL-6, implying an enhanced immune response. In conclusion, the combined asiaticoside and anti-PD-L1 treatment enhances the anti-HCC effect in vivo by promoting LCK activation to regulate T cells.

Finally, dysregulation of the signature genes was confirmed in LC cell lines by Western blot, and PPARG knockdown significantly reduced the expression of the immunosuppressive cytokines IL6, TGFB1, TGFB2 and VEGFC by qRT-PCR and ELISA. We have developed a UbRGs-based signature for LC prognostic evaluation that is valuable in clinical application, indicative of the immune microenvironment and beneficial for individualized treatment guidance.

TIGIT serves as a biomarker in SCLC, with its high expression indicating favorable prognosis and treatment response. These effects may be due to TIGIT's unique immune landscape and its association with other immune checkpoints.

In Caco-2 cells, GPE mitigated TNFα-induced monolayer permeabilization, decreased tight junction (TJ) protein levels, enhanced cellular oxidant production, activated redox-sensitive signaling, i.e., NF-κB and ERK1/2, and increased NOX1 and MLCK mRNA levels, the latter being a key regulator of monolayer permeability. The above findings suggest that GPE may protect against HFD-induced obesity and associated metabolic dysfunction (insulin resistance and NAFLD) by modulating intestinal barrier integrity and related endotoxemia.

CXCL10 likely regulates CXCR4, LCK, CCR7, and other genes involved in pathways such as cytokine-cytokine receptor interactions, HIV-1 infection, and Epstein-Barr virus infection. This study offers insights into the co-pathogenic mechanisms of UC and NSOI, providing a foundation for further mechanistic research and therapeutic development.