NF-κB–mediated chemoresistance in breast cancer cells

Anticancer agent CHS 828 suppresses nuclear factor‐κB activity in cancer cells through downregulation of IKK activity

“…36 Many chemotherapeutic agents have been shown to induce NF-B activity during the treatment, which led to an induction of antiapoptotic proteins, thereby decreasing the sensitivity of the cancer cells toward the treatment. 9,21,23,25,[37][38][39][40][41][42][43][44][45][46][47] Therefore, a combination of chemotherapeutic treatment and inhibition of the NF-B activity could be beneficial for the patient. In line with this, mice bearing HT-1080 tumors expressing the superrepressor form of I B␣ exhibited an increased sensitivity toward treatment with the chemotherapeutic compound camptothecin.…”

Inhibition of Inhibitor of Nuclear Factor-κB Phosphorylation Increases the Efficacy of Paclitaxel in in Vitro and in Vivo Ovarian Cancer Models

“…Although adjuvant approaches in combination with paclitaxel have been reported for lung cancer (30), prostate cancer (31), pancreatic cancer (32), and breast cancer (33), there have been no reports about an adjuvant approach in combination with paclitaxel for ovarian cancer. In addition, in vitro models were used in previous reports, and there have been no reports using in vivo models.…”

“…It has been reported that intrinsically or constitutively activated NF B may be critical in the development of drug resistance in cancer cells (29). Therefore, several agents that are able to inhibit NF B function might be considered as an adjuvant approach in combination with paclitaxel for lung cancer (30), prostate cancer (31), pancreatic cancer (32), and breast cancer (33).…”

Nuclear Factor-κB Activation: A Question of Life or Death

“…The activation of PKC operates directly in a death receptor dependent manner in PancTuI cells and pancreatic tumor cells, protecting them from anti-CD95 and TRAIL-mediated apoptosis by preventing the loss of DeltaPsim and cytochrome c release, as well as by the induction of NF-κB (Trauzold et al, 2001). Pharmacologic or molecular inhibition of the NF-κB pathway blocked cell survival in MCF-7 APO+ cells, while only molecular inhibition induced cytotoxicity in the APO-cells (Weldon et al, 2001). TGF-α protected gastric mucosal cells against apoptosis that is induced by serum depletion or sodium butyrate in a dose-dependent manner.…”