ACKR3 (Atypical Chemokine Receptor 3)

We analyzed pre- and on-treatment biopsies from patients with HR+ breast cancer treated with letrozole to induce estrogen deprivation (ED)...Finally, deletion combined with silencing of the CXCL11 receptors CXCR3 and CXCR7 in MCF7 cells impaired proliferation in response to exogenous CXCL11 and to co-culture with CD8+ T cells in estrogen-free conditions. These findings suggest that CD8+ T cell-associated CXCL11 in the TIME modulates the response of HR+ breast cancer cells to estrogen suppression.

Basal non-chemotactic, cancer cell motility was also suppressed, suggesting a role for ACKR3 in this process. The basal receptor activity in pathophysiology may provide an alternate therapeutic approach for targeting ACKR3.

SIGNIFICANCE STATEMENT: A small molecule inverse agonist of the atypical chemokine receptor 3 (ACKR3), named VUF16840, is characterized in this work. It was shown that VUF16840 was able to inhibit basal as well as ligand-induced ACKR3 activation and, moreover, inhibits the scavenging function of ACKR3.

ARRDC1 and ATP2A2 are strongly linked to BBD and BC. These findings might enhance our comprehension of the pathogenesis and progression of both BBD and BC, offering prospective biological biomarkers and therapeutic targets for clinical treatment.

The TLS/CAF-based risk model offers robust prognostic utility and highlights distinct biological and immune features between patient subgroups. These findings provide a foundation for personalized prognostic assessment and therapeutic decision-making in advanced HCC.

CXCR7 may regulate PTC cell migration and invasion through interaction with TAGLN2, primarily by activating the TGF-β/Smad2 signaling pathway. The CXCR7-TAGLN2 protein complex represents a potential novel therapeutic target for PTC.

This process can be inhibited by the drug TG-101348. We constructed a risk model with three chemokine-related genes (CRGs), which could effectively predict the prognosis of THCA. Notably, CCL17 expression had a considerable value to the risk model and may promote THCA progression by regulating the JAK-STAT pathway.

These results highlight potential cytokine and chemokine-mediated pathways involved in melanoma dermal invasion and cutaneous metastasis. While some findings did not reach statistical significance, concordant trends between in vitro and patient-derived data suggest their relevance and warrant further investigation in larger cohorts.

This dual modality addresses key challenges of inadequate internalization in conventional ADCs and cytotoxic potency in current eTPD strategies. Our findings demonstrate that DDCs provide additional optionality for developing next-generation antibody therapeutics with broader utility and improved efficacy in cancer treatment.

Finally, rescue experiments indicated that TBS6b exerts its anticancer effects primarily through targeting ACKR3. These findings establish ACKR3 as a critical target through which TBS6b mediates its anticancer activity against HCC.

CXCR1 knockdown significantly reduced cell proliferation and colony formation, while enhancing cell migration, underscoring its functional importance in OS progression. Overall, our findings suggest that the CXCR family genes are potential diagnostic and prognostic markers in OS, with implications for therapeutic targeting and further investigation into their role in OS pathogenesis.

The PARDTG - based model predicts BC survival independently. TACR1, key to immune response and drug sensitivity, could be a new therapeutic target. These results stress the importance of focusing on perioperative anesthesia - related drug targets in BC research.