CCL5 (Chemokine (C-C motif) ligand 5)

The findings in this study highlight the potential of a miRNA-based therapy in the treatment of, and as a biomarker for, liver cancer, something especially promising given the liver's avid uptake of RNA. Additionally, this work reveals possible causal roles in liver cancer for two unique immune cell types that are prevented by miR-146a.

Comprehensive single-cell analysis identified selective chemokine recruitment signatures supporting γδ T-cell infiltration but revealed paradoxical corecruitment of immunosuppressive populations. Patient stratification through chemokine profiling, combined with γδ T-cell enrichment and targeted chemokine antagonism, represents a rational therapeutic strategy.

Taken together, this work reveals a critical host-protective role for miR-146a in HCC that is mechanistically dependent on CCL5 and wherein tumor burden correlates with two suppressive immune populations, providing an impetus for targeting these pathways to combat HCC. Further, the correlations with tumor burden and Taa cells suggest that aging may increase HCC risk through the accumulation of CCL5-expressing Taa cells.

In 4T1 tumors, this delay was also significant compared to the equivalent treatment with GET of control pDNA. These findings support GET of pDNA encoding CCL5 combined with RT as a strategy to enhance immune-mediated tumor control.

No significant elevation was obtained with chemotherapy (5-fluorouracil, irinotecan, oxaliplatin, paclitaxel, gemcitabine or temozolomide), tyrosine kinase inhibitors sorafenib and sunitinib, or the immunostimulatory agents polyinosinic:polycytidylic acid, Mycobacterium tuberculosis antigens and diphtheria/pertussis/tetanus vaccine. Combination of the vector and CIKs obtained a strong antitumor effect in the PDAC model, although it was mainly due to vector-mediated recruitment of endogenous immune cells. We conclude that additional barriers beyond chemokine expression should be overcome in order to unleash the full potential of CIKs on solid tumors.

HDAC7 represents a promising diagnostic and therapeutic target in BCa immunotherapy. Pinocembrin, as a specific HDAC7 inhibitor, holds potential as a combination therapy agent to improve immunotherapy response in BCa.

Our study provides the first ARIMA-CNN framework for modeling gene expression and survival analysis, marking a significant innovation in integrating temporal dynamics and machine learning for biological data interpretation. This model offers deeper insights into the tumor immune microenvironment and underscores the potential for advancing precision immunotherapy strategies and identifying novel biomarkers, contributing significantly to innovative cancer management solutions.

Additionally, inhibiting G protein coupled receptor (GPCR) signaling in the BMDM ablated the anti-tumor activity suggesting that the anti-tumor activity may be dependent on the migratory ability of the BMDM. Collectively, these data show that creating hot early tumor sites by delivering anti-tumor BMDM can impact tumor growth by eliciting CD8+ T cells and NK cells, and that BMDM anti-tumor activity depends on GPCR-mediated signaling.

Notably, Palbociclib emerged as a potential therapeutic agent targeting the novel discovered biomarker CCL5...In conclusion, our findings highlight five hub genes as prognostic markers that could stratify GBM patients with different immune landscapes and levels of drug sensitivity. Furthermore, experimental results suggest that low CCL5 expression could alleviate T cell exhaustion and represent a promising therapeutic target, offering new strategies for improving GBM prognosis.

Functional assays demonstrated that CCL5 promoted CCR1+ macrophage migration, an effect suppressed by both the CCR1 antagonist BX471 and CCL5-neutralizing antibody...Together, our findings establish the CCL5/CCR1 axis as a key mediator of tumor-macrophage crosstalk in DA, supporting immune evasion and chemoresistance via suppression of macrophage-induced apoptosis. Targeting this axis may represent a promising therapeutic strategy to enhance the efficacy of conventional chemotherapy in DA.

Such approaches have the potential to offer novel preventive and therapeutic options for patients diagnosed with BC. Further clinical studies are required to confirm the effects of FDOJ treatment on immune function and BC outcomes.

CAF-derived CCL5 enhanced aerobic glycolysis in breast cancer cells by up-regulating IP3R expression, which in turn promoted their metastasis.