These findings underscore the role of environmental exposures in shaping tumor biology and offer a mechanistic basis for the poorer prognosis observed in smokers with breast cancer.
Finally, we reported a specific polypeptide antagonist of α9 nAChR, GeXIVA[1,2] and exerted good anti-tumor effects in tumor-bearing mice of TNBC, which indicated a great potential of GeXIVA[1,2] to be further studied as a novel targeted therapy for TNBC. This study provides a scientific basis for establishing α9 nAChR as a novel therapeutic target for TNBC, which is worthy of further development in the future.
8 months ago
Journal
|
GPX4 (Glutathione Peroxidase 4) • SLC7A11 (Solute Carrier Family 7 Member 11) • CHRNA9 (Cholinergic Receptor Nicotinic Alpha 9 Subunit)
These findings highlight IGF1R as a promising therapeutic target for reducing stemness and metastasis in TNBC patients exposed to environmental nicotine.
Ultimately, the immune microenvironment and enrichment pathways were analyzed among individuals categorized as high-risk and low-risk. The predictable ion homeostasis-associated 15 gene signature established in this study predicts overall survival outcomes in patients with KIRC, to some extent helping clinicians to select personalized treatment regimens.
1 year ago
Journal
|
SAA1 (Serum Amyloid A1) • PDK4 (Pyruvate Dehydrogenase Kinase 4) • ABCB6 (ATP Binding Cassette Subfamily B Member 6 (Langereis Blood Group)) • CHRNA9 (Cholinergic Receptor Nicotinic Alpha 9 Subunit) • EDNRB (Endothelin Receptor Type B) • TNFSF11 (TNF Superfamily Member 11) • ANGPTL3 (Angiopoietin Like 3)
Collectively, our study established the links between genetic variations in α9-nAChR and smoking exposure in promoting breast tumor development. This emphasizes the need to consider gene-environment interactions carefully while developing effective breast cancer prevention and treatment strategies.
Similarly, the mRNA expression levels of STAT3, IL-6, and TNF-α, which are crucial factors in the STAT3 pathway, were elevated in glioma tissues compared to paracancerous tissues. CHRNA9 is a potential prognostic marker and immunotherapy target for glioma, with its mechanism of action potentially linked to the STAT3 pathway.
The coal particle exposure could induce the change of oxidative stress response, inflammatory response and EMT related markers, down-regulate the AChE enzymatic activity, and interfere the mRNA expression levels of AChRs in A549 cells. The addition of exogenous AChE recombinant protein could reverse the above effects to a certain extent.
Available drugs such as duloxetine provide only modest benefits against oxaliplatin-induced neuropathy. In wildtype mice treated with oxaliplatin, quantitated circulating T-cells remained unaffected by RgIA4. Together, these results show that RgIA4 requires both chrna9 and CD3 T-cells to exert its protective effects against acute cold-allodynia produced by oxaliplatin.
We investigated their prognostic significance in lung cancer patients and found CHRNA7 to be an independent prognostic factor. Overall, the results obtained from this preliminary study warrant a large cohort-based analysis that may ultimately lead to potential patient-specific stratification biomarkers predicting cancer-treatment outcomes.