KRAS<sup>∗</sup>-mediated repression of IRF2 results in high expression of CXCL3, which binds to CXCR2 on myeloid-derived suppressor cells and promotes their migration to the tumor microenvironment.
Reverse transcription‑quantitative PCR (RT‑qPCR) analysis of 38 paired tumor and non‑tumor tissues, and immunohistochemistry (IHC) of 212 tumor and 46 non‑tumor tissues was conducted to explore the expression of CXCL3 and its diagnostic and prognostic significance in the Guangxi Medical University CC cohort.
The KRAS<sup>∗</sup>-IRF2-CXCL3-CXCR2 axis provides a framework for patient selection and combination therapies to enhance the effectiveness of ICB therapy in CRC.
In this issue of Cancer Cell, Liao et al. demonstrate that oncogenic KRAS drives an immune suppressive program in colorectal cancer by repressing IRF2 expression, which leads to downregulation of interferon responsive genes, enhanced expression of CXCL3 and recruitment of suppressive myeloid cells, and subsequent resistance to immune checkpoint blockade.
We found that DPG strongly accelerates MH by differently regulating pro-inflammatory (CXCL1, CXCL3, CXCL5, PTGS2, IL-1β, IL-6, CCL12, CCL7) and wound healing (COL3A1, MMP9, VTN, PLAUR, SERPINE, CSF3, FGF2, FGF7, PLAT, TIMP1) genes as observed only during the recovery phase of colitis.
The treatment of PM2.5 with a strong acid at a high temperature attenuated AHR, eosinophil percentage in BALF, mRNA levels of IL-13 and CXCL3 and peribronchial inflammation.
Significant DNA hypermethylation was observed for CXCL3 and FADD gene promoters in AP lesions when compared to control tissues (P < 0.001) and among other genes (P < 0.05).
We used data from the emergency medical dispatching center of all calls for suspected stroke (SAMU 78), climatic parameters (MétéoFrance), pollution (AIRPARIF), and data from influenza epidemic surveillance networks (GROG and Sentinelles).
These results provide novel insight into the crucial role of CXCR2 in neuropathy based on CXCL3 modulation, which may become a potential therapeutic target in pain treatment.
We used data from the emergency medical dispatching center of all calls for suspected stroke (SAMU 78), climatic parameters (MétéoFrance), pollution (AIRPARIF), and data from influenza epidemic surveillance networks (GROG and Sentinelles).
However, a stratified analysis revealed that high expression of CXCL3 was associated with considerably increased mortality in the subgroup of CC patients with tumor size <5 cm (adjusted P=0.042, adjusted HR=2.298, 95% CI=1.030‑5.126) and with tumor thrombus (adjusted P=0.019, adjusted HR=5.096, 95% CI=1.306‑19.886).
In this issue of Cancer Cell, Liao et al. demonstrate that oncogenic KRAS drives an immune suppressive program in colorectal cancer by repressing IRF2 expression, which leads to downregulation of interferon responsive genes, enhanced expression of CXCL3 and recruitment of suppressive myeloid cells, and subsequent resistance to immune checkpoint blockade.
These findings suggest that CXCL3 autocrine/paracrine pathways are involved in the development of prostate cancer by regulating the expression of the target genes that are related to the progression of malignancies.
CXCL3 was reportedly associated with the invasion and metastasis of various malignancies, the role of CXCL3, however, in preeclampsia has not been fully discussed.
CXCL3 was reportedly associated with the invasion and metastasis of various malignancies, the role of CXCL3, however, in preeclampsia has not been fully discussed.