Abstract
Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol molecule from green tea and is known to exhibit antioxidative as well as tumor suppressing activity. In order to examine EGCG tumor invasion and suppressing activity against adult T-cell leukemia (ATL), two HTLV-1 positive leukemia cells (HuT-102 and C91- PL) were treated with non-cytotoxic concentrations of EGCG for 2 and 4 days. Proliferation was significantly inhibited by 100 μM at 4 days, with low cell lysis or cytotoxicity. HTLV-1 oncoprotein (Tax) expression in HuT- 102 and C91-PL cells was inhibited by 25 μM and 125 μM respectively. The same concentrations of EGCG inhibited NF-kB nuclearization and stimulation of matrix metalloproteinase-9 (MMP-9) expression in both cell lines. These results indicate that EGCG can inhibit proliferation and reduce the invasive potential of HTLV-1- positive leukemia cells. It apparently exerted its effects by suppressing Tax expression, manifested by inhibiting the activation of NF-kB pathway and induction of MMP-9 transcription in HTLV-1 positive cells.
Highlights
Adult T-cell leukemia (ATL) is caused by the human T-cell lymphotropic virus type I (HTLV-1), the first human retrovirus to be isolated (Nasr et al, 2011)
In light of what was mentioned above, we tested various concentrations of EGCG on two HTLV-1-positive cell lines and we focused on the effect of EGCG on MMP activity, nuclear factor kappa B (NF-kB) DNA binding and Tax
It has been reported that EGCG induces apoptosis and cell cycle arrest in vitro in both HTLV-1 infected and noninfected malignant T-lymphocyte cell lines (Li et al, 2000; Harakeh et al; 2008)
Summary
Adult T-cell leukemia (ATL) is caused by the human T-cell lymphotropic virus type I (HTLV-1), the first human retrovirus to be isolated (Nasr et al, 2011). After a long latent period of 30-40 years, a subset of HTLV-1 carriers (only 5%) develops ATL, a chemotherapy-resistant malignancy (Kannian and Green, 2010). ATL manifests itself as an aggressive lymphoid proliferation of mature activated CD4+ cells where HTLV-1 spreads mainly through cell-to-cell transmission. Clonal proliferation of infected T cells both in vitro and in vivo is induced by the viral oncoprotein Tax which has a pleiotropic effect cell cycle progression and apoptosis (Lairmore et al, 2012). The two therapeutic strategies for ATL are hindering HTLV-1 replication and/ or inhibiting the Tax oncoprotein (Nasr et al, 2011)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
