CCL7 (Chemokine (C-C motif) ligand 7)

This review systematically integrates CCL7's dual roles in tumors (both pro-tumor and anti-tumor) and its stage-specific functions across inflammation (both pro-inflammatory and anti-inflammatory), fibrosis, and obesity, filling gaps in fragmented prior research. It also links the common regulatory mechanisms across multiple diseases, and puts forward specific strategies such as CCL7/CCR antagonists and combined immunotherapy, thereby providing new therapeutic strategies for the exploration and treatment of related diseases, aiming to contribute to the maintenance of human health globally.

Finally, the role of the ZBP1-CCL7/CCR1 signaling axis in promoting OSCC progression was evaluated via in vivo recombinant CCL7 protein rescue and CCR1 antagonist (BX471) intervention...This study highlights ZBP1 as crucial for OSCC progression by regulating CCL7 expression in CAFs to activate CCR1 signaling in tumor cells. This provides insights into the regulatory mechanisms within the OSCC microenvironment, offering a potential therapeutic strategy for targeted interventions.

This study provides sufficient and reliable scientific evidence for liver disease risk-related genes through multidimensional Mendelian randomization validation analysis.

Monocytes accumulate in human TNBC TDLNs, with evidence of a FRC-monocyte axis, and a TLR4 ligand signature is predictive of poor survival outcomes in TNBC patients. Thus, metastatic TNBC can reprogram lymph nodes (LNs) to facilitate PD-L1-mediated immune evasion and metastasis.

Clinically, ChREBP-SP1-choline metabolism axis expression was associated with poor clinical outcome in colorectal cancer. Thus, the study identified the interplay between tumors and TAMs via choline competition as a previously unknown immune evasion mechanism in the TME and propose ChREBP as a potential immunotherapeutic target in cancer.

Our findings indicate that CCL7 plays a promoting role in HCC growth and tumorigenesis, potentially via targeting CCR1 and CCR2 and activating the PI3K/AKT pathway.

SC-2882 is a first-in-class specific QPCTL inhibitor that induces secondary proteolytic degradation of the monocyte chemoattractants CCL2 and CCL7 (da Silva, Nature Immunology 2022) and inactivation of the "do-not-eat-me" signal CD47 (Logtenberg, Nature Medicine 2019)...Additional analysis of LME cell subpopulations by SC-RNA-seq is ongoing. Overall, these data indicate that QPCTL is a potential target in DLBCL, and that QPCTL inhibition exhibits potent anti-lymphoma effects primarily by targeting the IN-LME.

Our research identified CCL7 as a novel tumor-activator in gastric cancer pathogenesis and hypoxia-induced tumor aggravation was regulated by HIF1α/CCL7/KIAA1199 axis. The evidence may provide a novel target for gastric cancer treatment.

In MC38 cells cultured with 25 mM glucose, mRNA expression of CCL7, a chemokine recruiting DCs, was decreased compared to cells cultured with 5 mM glucose. These results suggest that the STZ-induced hyperglycemia impairs the effect of PD-1-Ab treatment on MC38 tumor growth, and is accompanied by reduced infiltration of DCs and CD8 T cells and decreased expression of CCL7 and CXCL9.

Here, we propose that a best-in-class AhR inhibitor, DA-4505, improves anti-tumor efficacy via modulation of tumor immune surveillance compared to BAY2416964, an AHR antagonist drug candidate being studied in the clinical phase. To evaluate anti-tumor effects of DA-4505 and BAY2416964, the two AhR inhibitors were dosed at 10 mg/kg once daily alone or in combination with aPD-1 (10 mg/kg) in surgical and chemotherapy models, and a PDX model (YHIM2004)...A tumor reduction was shown by treating DA-4505 alone or in combination with pembrolizumab compared to vehicle group (P<0.05)... The AhR inhibitor DA-4505 demonstrated an improvement in anti-tumor efficacy. In addition, it has shown a synergistic effect when combined with aPD-1. Discoveries from this study provide a preclinical rationale for future clinical implications in solid tumor.

High CCL7 expression was observed in human USC and HPmECC, and MDSCs migration was promoted in a CCL7 concentration-dependent manner. These results indicate that anti-tumor immunity is suppressed in USC due to increased number of tumor-infiltrating MDSCs via CCL signal.

Furthermore, higher CCR9 expressing cells showed poor response to Carboplatin upon CCR9 activation. In conclusion, our data suggest the association of distinct CC-chemokines in BrCa progression, OS, and disparate disease outcome in AA compared to EA patients implying CCR9 signaling to be a potential target for improving chemotherapeutic response.