CXCL12 overexpression

The TEC score is a promising and reliable biomarker for predicting genetic mutations and prognosis in ICC patients. Enhancing the regulation of the CXCL12/CXCR4 signaling pathway may represent a potential novel therapeutic target for ICC treatment.

In multiple single cell experiments measuring effectiveness of Iberdomide in combination with Dexamethasone and an additional experiment comparing aged and untreated Vk*MYC mice with multiple myeloma (MM), key compositional patterns emerge in the murine bone marrow niche. Cell Adhesion & Migration vol. 6 220–230 (2012).

Inhibition of the STAT3 pathway using AZD9150 weakened the accelerated effects of CXCL12/CXCR7 on the growth and metastasis of esophageal cancer in vitro and in vivo. In conclusion, our research revealed that CXCL12/CXCR7 regulates EMT and other malignant processes by activating the STAT3 pathway to accelerate the growth and metastasis of esophageal cancer.

We have developed cisplatin resistant variants of mouse oral cancer cell lines (MOC1 and MOC2) to evaluate combined CXCR4 and PD-L1 blockade (AMD 3100 and Nivolumab). This model was used to determine whether CXCR4 inhibition could enhance anti-PD-L1 efficacy. Combinatorial blockade of both pathways provided better outcomes relative to anti-PD-L1 treatment and extended our understanding of immunotherapy resistance.

In in vitro and in vivo hepatocellular carcinoma mouse models it can significantly suppress primary tumor growth, prevent distant metastasis/cell migration, reduce angiogenesis, and normalize the immunosuppressive tumor microenvironment by reducing tumor-associated macrophages (TAMs) infiltration, reprogramming TAMs toward an immunostimulatory phenotype and promoting cytotoxic T cell infiltration into tumor. Although BPRCX807 treatment alone prolongs overall survival as effectively as both marketed sorafenib and anti-PD-1, it could synergize with either of them in combination therapy to further extend life expectancy and suppress distant metastasis more significantly.

Besides, SNHG1 could indirectly regulate CXCL12 expression via miR-181a-5p. We demonstrated that SNHG1 promoted MPP induced neuronal injury in neuroblastoma cells by regulating miR-181a-5p/CXCL12 axis, suggesting SNHG1 might contribute to the development of PD, which provided a novel insight into the pathogenesis and treatment of PD.