(−)-Epigallocatechingallate induces apoptosis in B lymphoma cells via caspase-dependent pathway and Bcl-2 family protein modulation

Abstract

(−)-Epigallocatechingallate (EGCG) as a representative polyphenol has attracted increasing attention due to its diversified effects, especially its potential as an agent for the prevention or treatment of certain cancers. However, the molecular mechanisms of EGCG-induced apoptosis in B lymphoma cells are unclear. The aim of this study was to investigate the effect of EGCG on proliferation and apoptosis in the B lymphoma cell lines Jeko-1 and Raji, and determine the underlying mechanisms. Cell proliferation and cytotoxicity were determined by the cell counting kit (CCK-8) assay; apoptosis was assessed by flow cytometry using the Annexin V-PE/7AAD double staining; Fas, Bcl-2 and Bax mRNA expression levels were determined by real-time PCR; caspase activity was measured by the caspase activity assay kit; the expression levels of apoptosis-associated proteins were determined by western blot analysis. We demonstrated that EGCG induced growth inhibition and apoptosis in a dose- and time-dependent manner. In agreement, EGCG upregulated the mRNA expression of Fas and Bax while downregulating Bcl-2. Protein expression levels of Bax, activated caspase-3, -7, -8, and -9, and PARP were increased, while Bcl-2 protein levels were reduced by EGCG treatment. Taken together, EGCG induces B lymphoma cell apoptosis by triggering caspase-dependent intrinsic (mitochondrial) and extrinsic (death receptor) pathways. These findings suggest that EGCG may be a potential agent for the treatment of B lymphoma.

Epigallocatechin‐3‐gallate enhances differentiation of acute promyelocytic leukemia cells via inhibition of PML‐RARα and HDAC1

“…In this study, we showed that EGCG decreased proliferation, induced apoptosis, and promoted differentiation in the promyelocytic leukemia cells via inhibition of MDR and PML‐RARα/HDAC1. EGCG was able to decrease the proliferation rate of APL cells, and this finding is consistent with previous reports on the growth inhibitory effect of EGCG in various cancer cells (Benyahia et al, ; Khan, Adhami, & Mukhtar, ; Ly et al, ; Wang et al, ). Although the obtained IC50 value for the antiproliferative effect of EGCG on leukemic cells was higher than that of ATRA, the antiproliferative effect was observed at concentrations with no obvious toxic effect on normal polymorphonuclear cells, suggesting the specificity of EGCG action in leukemic cells.…”

EGCG induces lung cancer A549 cell apoptosis by regulating Ku70 acetylation

“…Apoptosis is a complex process regulated by several molecules that function as either promoters, including Bax, Bak and caspases, or inhibitors of the cell death process such as Bcl-2, Bcl-xL and the IAP proteins (25). Studies have shown that EGCG can effectively regulate various key molecules in cell mitochondrial apoptosis pathways in other tumors as a potential antitumor substance (18,19). Our previous study showed that the long-term ingestion of green tea could effectively prevent lung cancer, in rats, induced by the carcinogen 3,4-benzopyrene (B[a]P), a process that may be related to the EGCG-mediated upregulation of P53 expression and downregulation of Bcl-2 expression (26).…”

“…EGCG has been demonstrated to act on multiple key elements in signal transduction pathways related to inhibition of carcinogen-induced mutagenesis (11,12), induction of cell cycle arrest (13), induction of apoptosis (14), inhibition of growth factor-mediated proliferation (15), inhibition of transformation (9), inhibition of angiogenesis (16) and inhibition of telomerase activity (17). It has been shown that EGCG can effectively regulate various key molecules in cell mitochondrial apoptosis pathways in other tumors as a potential antitumor substance (18,19). However, the molecular mechanisms of EGCG inducing apoptosis have not been completely elucidated in lung cancer.…”

Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis in Ec9706 and Eca109 esophageal carcinoma cells

“…Previous studies have suggested that EGCG is associated with the potential health benefits attributed to green tea consumption (21). The anticancer effect of EGCG has been explored in various tumor cells (22)(23)(24), but there are few articles concerning the anticancer effect of EGCG on esophageal cancer. In the present study, EGCG was demonstrated to suppress the viability of esophageal cancer Eca109 and Ec9706 cells via inducing apoptosis in an EGCG dose-dependent manner.…”