Eriocalyxin B inhibits proliferation and induces apoptosis through downregulation of Bcl-2 and activation of caspase-3 in human bladder cancer cells

Abstract

Eriocalyxin B inhibits proliferation and induces apoptosis through down -regulation of Bcl-2 and activation of caspase-3 in human bladder cancer cells Bangladesh Journal of Pharmacology Research Article IntroductionNatural products provide many promising sources of potential anti-cancer agents and several lead structures in the past decades, which were originally isolated from plants such as paclitaxel, camptothecin, vinca alkaloids, and etoposide have potential application in cancer chemotherapy, therefore, plants are considered as one of the most vital sources for the development of novel anti-cancer drugs (Amin et al., 2009;Cragg and Newman, 2005). Diterpenoids constitute a vast class of isoprenoid natural products, which are found mainly in plants and fungi and also been found in marine organisms and insects as well (Garcia et al., 2007;Hanson, 2004). Eriocalyxin B (EriB) is a natural entkaurene diterpene compound isolated from Isodon eriocalyx var. laxiflora, a herb of the Labiatae family distributed in the South-West China and has been reported to have wide spectrum of biological effects, including anti-inflammatory and antibacterial agent in local folk medicine (Ikezoe et al., 2003;Wang et al., 2007). Furthermore, EriB has anti-proliferative effect and induced apoptosis in cancer cells such as ovarian cancer (Leizer et al., 2010), pancreatic adenocarcinoma (Li et al., 2012) and leukemia (Wang et al., 2007;Zhang et al., 2010). However, the cytotoxic effects of EriB on bladder cancer and its mechanism were still unknown.Bladder cancer is an increasingly common and potentially lethal malignancy (Ploeg et al., 2009 AbstractEriocalyxin B (EriB) has been shown to possess promising anti-cancer potential against various cancer cells. However, its effect against bladder cancer cells remained unexplored. In this study, for the first time, we investigated the effects of EriB on cell proliferation, cell cycle, and apoptosis in bladder cancer T24 cells. In order to examine the effects of EriB on cell proliferation, cell cycle, and apoptosis, we performed MTT assay, flow cytometric analysis and Western blot. The results revealed that EriB decreased the cell viability of T24 cells. Flow cytometric analysis demonstrated that EriB markedly induced apoptosis of T24 cells and arrested cell cycle at G2/M phase in a dose-dependent manner. Further characteriza-tion showed that EriB involved in the down-regulation of Bcl-2 and activation of caspase-3 before culminating in apoptosis in EriB-treated T24 cells. These in vitro results suggested that EriB should be further examined for in vivo activity in human bladder cancer. This ork is li e sed u der a Creati e Co o s Attri utio 3.0 Li e se. You are free to opy, distri ute a d perfor the ork. You ust attri ute the ork i the a er spe ified y the author or li e sor. Article Info

Eriocalyxin B Inhibits Adipogenesis in 3T3-L1 Adipocytes by Cell Cycle Arrest

“…Eriocalyxin B has been documented to possess a variety of pharmacological activities, which has the effects of antiinflammatory, antiproliferative, anti-angiogenic, and the most common activity is anti-cancer [29,35,36]. In this work, we reported that eriocalyxin B is capable of inhibiting adipocyte differentiation.…”

“…Many studies show that MCE is a prerequisite for differentiation of 3T3-L1 preadipocytes into adipocytes. A study demonstrated that Eriocalyxin B markedly arrested cell cycle at G2/M phase in a dosedependent manner [29]. CDKs are serine/threonine kinases that control cell cycle progression.…”

Enhanced cytotoxic potential of Orthosiphon stamineus extract in MCF-7 cells through suppression of nucleolin and bcl2

“…Down-regulation of bcl2 leads to the release of cytochrome c from mitochondria to the cytosol, resulting in cell death. Eriocalyxin B inhibits the proliferation and induces apoptosis through downregulation of bcl2 (Rasul et al, 2013). Studies examined that the cellular levels of cytochrome c, caspase 3, PARP, p53, bax, bcl2 and β-actin expression after baicalein treatment.…”