Insulin Enhances NF-κB Activation in Luminal A T -47D Breast Cancer Cells Exposed to Low-Dose Doxorubicin

Insulin-Induced NF-κB Activation May Contribute to Doxorubicin Resistance in Luminal A T-47D Breast Cancer Cells

Findings indicate that insulin increases NF-κB activation in doxorubicin-treated T-47D breast cancer cells and may sustain NF-κB activity against the cytotoxic effects of doxorubicin.

Insulin Enhances the Viability of Doxorubicin-Treated Luminal A Breast Cancer T-47D Cells

Insulin Enhances the Viability of Doxorubicin-Exposed Luminal A Breast Cancer T-47D Cells

Breast cancer is one of the most common cancers worldwide, with a high incidence rate. Doxorubicin is a chemotherapeutic agent used in breast cancer management. Nevertheless, chemoresistance remains a major challenge in breast cancer chemotherapy. Insulin contributes to chemoresistance through its mitogenic and prosurv...

Macrophage polarization regulated by the βTrCP-NF-κB inflammatory signaling pathway is required for valproic acid’s dual role in breast tumor radiosensitivity and normal tissue radioprotection

Radiotherapy (RT) is a widely used treatment modality for breast cancer, but its broad application is limited by the risk of adverse effects, such as the potential for the tumor to develop resistance to RT. Identifying strategies that enhance RT efficacy while minimizing adverse effects is of significant clinical impor...

Neutrophil extracellular traps induce chemoresistance in human breast cancer cells through the PI3K/AKT/NF-κB pathway

Introduction Breast cancer is the most common malignancy and the leading cause of cancer-related mortality among women, and resistance to chemotherapy remains a major clinical challenge. Although doxorubicin is widely used, its efficacy is limited by chemoresistance. Neutrophil extracellular traps (NETs), web-like stru...

Association of AP-1/c-Jun with IL-6 and IL-8 expression in hepatocellular carcinoma: attenuating effects of metformin in vitro

Investigating the effects of metformin on key inflammatory cytokines involved in hepatocellular carcinoma progression, as well as on the expression of c-Jun, a key subunit of the AP-1, led to a significant reduction in the levels of IL-6 and IL-8 in HepG2 cells compared to control group.