Combination of pristimerin and paclitaxel additively induces autophagy in human breast cancer cells via ERK1/2 regulation.

Combination of pristimerin and paclitaxel additively induces autophagy in human breast cancer cells via ERK1/2 regulation. Mol Med Rep. 2018 Sep 14;: Authors: Lee Y, Na J, Lee MS, Cha EY, Sul JY, Park JB, Lee JS Abstract Pristimerin, a quinonemethide triterpenoid, has demonstrated anticancer activity against a number of types of cancer, including breast cancer. However, its mechanism of action remains unclear. The present study investigated the autophagy‑induced anticancer efficacy of pristimerin on MDA‑MB‑231 human breast cancer cells. Pristimerin inhibited the growth of these cells in a concentration‑dependent manner. Treatment with pristimerin dose‑dependently induced an increase of light chain 3B (LC3‑II), whereas autophagy inhibitor 3‑methyladenine (3‑MA) inhibited pristimerin‑induced LC3‑II accumulation and cytotoxic effects. Autophagy was also activated by paclitaxel as observed by an elevated LC3‑II level. Although 24 µM paclitaxel induced autophagy without cytotoxicity, combined with pristimerin it additively induced cell growth inhibition and autophagy induction. Autophagy induction was measured with an autophagy detection kit and LC3‑II levels were monitored by western blot analysis. Treatment with 3‑MA inhibited LC3‑II accumulation and cell death induced by a combination of paclitaxel and pristimerin. Pristimerin and paclitaxel inhibited extracellular signal‑regulated kinase (ERK)1/2/p90RSK...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research