AGR2 overexpression

These effects were partly reversed by AGR2 overexpression and AKT activation. Our findings demonstrated that quercetin inhibits cholesterol metabolism and cisplatin resistance in CAL27 cells by modulating the AGR2/AKT/SREBP2 axis.

Patients with AGR2 low expression could be suitable for combination treatment with immune checkpoint inhibitor agents and TGF-β blockers. Therefore, this study provides a theoretical foundation for developing a strategy for personalized immunotherapy to patients with breast cancer.

Mechanically, AFAP1-AS1 sequestered the miR-653-5p and blocked the inhibition of miR-653-5p to AGR2 and stepwise upregulated AGR2 overexpression in LUAD gefitinib resistant cells, resulting gefitinib resistance in LUAD. AFAP1-AS1 promotes gefitinib-resistance LUAD cells through a previously unrecognized miR-653-5p/AGR2 axis, suggesting targeting AFAP1-AS1/miR-653-5p/AGR2 axis might be a promising way for LUAD intervention.

AGR2 is highly expressed in UPR-active CSCs and drug-resistant GB cells, and its repression leads to apoptosis, via multiple pathways.

Finally, we performed the GSEA analysis and found that AGR2 was negatively related to IL-17 and NF-kβ signaling pathways. AGR2 was finally determined as the most important prognostic biomarker in BRCA bone metastasis, and it may play a vital role in cancer progression by regulating IL-17 and NF-kB signaling pathways.

In this review, we summarize the already known roles and mechanisms of action of the AGR family proteins in digestive diseases, their expression in the healthy digestive tract, and in digestive oncology. At last, we discuss the potential diagnostic and therapeutic implications underlying the biology of AGR proteins.

EIF5A2 knockdown inhibited the biological process of cervical cancer cells through modulation of AGR2. The in-depth investigation of the molecular mechanism of EIF5A2 in cervical cancer cells provides new strategies for the prevention and treatment of clinical malignancies.

AGR2 expression was detected in several glioma primary cell lines, both AGR2 and GRp78 were co-localized in tissues and cell lines.It has been linked to drug resistance, a series of cytotoxic studies were conducted to evaluate the link between AGR2 expression and drug resistance founding that AGR2 is significantly expressed in surviving cells.siRNA against AGR2 Exome 2 exhibited the greatest inhibitory impact, demonstrating the significance of its existence.Using double hits results in significant survival inhibition.When siRNA for AGR2 was used in conjunction with Temozolomide or Irinotecan, there was a substantial change in cell density compared to drugs alone,surviving cells are those that express AGR2. Conclusion AGR2 was highly expressed in high-grade GBM and meningioma. It’s one of the CSC markers in the CNS system tumours and part of the UPR machinery.AGR2 expression was shown in the remaining survival cells following drug treatments or using siRNA, indicating AGR2 importance for cell proliferation and survival.Targeting, blocking AGR2 using antibodies and peptides is one way to eliminate cancer in the brain, among other cancer types.

In response to these drugs, particularly doxorubicin, tumor cells can enter into senescence...All these results showed that AGR2 expression in sera and tumors of breast cancer patients is a marker of tumor progression and metastasis occurrence. They also showed that its overexpression regulates CIS escape via activation of the mTOR/AKT signaling pathway.

The results of this study indicated that LINC01857 was highly expressed in HCC, and it could improve HCC cell proliferation and reduce apoptosis via competitively binding to miR-197-3p, promoting AGR2 and upregulating the AKT and ERK pathways.

ERGI and AGR2 change indicate favorable modulation by acolbifene and appear to provide independent information. Conclusions These results suggest that change in expression of benign breast AGR2 might be a useful addition to change in expression of other classic estrogen response genes in evaluating the potential of novel SERMs such as acolbifene compared to standard SERMs like tamoxifen in early phase prevention trials.

Our study suggests participation of multiple genetic mechanisms, general and specific of each subtype, in the thrombogenesis of AGC patients. If validated, these genetic risk factors, individually or as molecular signatures, could contribute to improve capacity to predict individual thrombotic risk in these patients.