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A green tea polyphenol, epigalocatechin-3-gallate, induces apoptosis of human hepatocellular carcinoma, possibly through inhibition of Bcl-2 family proteins.
J Hepatol. 2006 Jun; 44(6):1074-82.JH

Abstract

BACKGROUND/AIMS

A major polyphenol of green tea, epigallocatechin-3-gallate (EGCG), has previously been shown to induce cell-cycle arrest and apoptosis in various cancers. However, little is known about its effects on hepatocellular carcinomas (HCCs).

METHODS

Four HCC cell lines, HLE, HepG2, HuH-7 and PLC/PRF/5, were treated with EGCG or vehicle. Cell viability was assessed by trypan blue staining and WST-8 assay. Cell-cycle, apoptosis and apoptosis-related proteins in HLE cells were evaluated by flow cytometry and Western blotting. The effect of EGCG was also studied in vivo using a xenograft model. The effect of co-treatment with EGCG and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was also assessed.

RESULTS

EGCG inhibited the growth of all HCC cell lines at concentrations of 50-100 microg/ml. In HLE cells, EGCG induced apoptosis but not cell-cycle arrest and appears to have down-regulated Bcl-2alpha and Bcl-xl by inactivation of NF-kappaB. Oral administration of EGCG showed similar effects in HLE xenograft tumors. Co-treatment with EGCG and TRAIL synergistically induced apoptosis in HLE cells.

CONCLUSIONS

EGCG induced apoptosis in HLE cells, both in vitro and in vivo. Moreover, it enhanced TRAIL-induced apoptosis. Therefore, EGCG treatment may be useful for improving the prognosis of HCCs.

Authors+Show Affiliations

Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan. liverresearch2004@yahoo.co.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16481065

Citation

Nishikawa, T, et al. "A Green Tea Polyphenol, Epigalocatechin-3-gallate, Induces Apoptosis of Human Hepatocellular Carcinoma, Possibly Through Inhibition of Bcl-2 Family Proteins." Journal of Hepatology, vol. 44, no. 6, 2006, pp. 1074-82.
Nishikawa T, Nakajima T, Moriguchi M, et al. A green tea polyphenol, epigalocatechin-3-gallate, induces apoptosis of human hepatocellular carcinoma, possibly through inhibition of Bcl-2 family proteins. J Hepatol. 2006;44(6):1074-82.
Nishikawa, T., Nakajima, T., Moriguchi, M., Jo, M., Sekoguchi, S., Ishii, M., Takashima, H., Katagishi, T., Kimura, H., Minami, M., Itoh, Y., Kagawa, K., & Okanoue, T. (2006). A green tea polyphenol, epigalocatechin-3-gallate, induces apoptosis of human hepatocellular carcinoma, possibly through inhibition of Bcl-2 family proteins. Journal of Hepatology, 44(6), 1074-82.
Nishikawa T, et al. A Green Tea Polyphenol, Epigalocatechin-3-gallate, Induces Apoptosis of Human Hepatocellular Carcinoma, Possibly Through Inhibition of Bcl-2 Family Proteins. J Hepatol. 2006;44(6):1074-82. PubMed PMID: 16481065.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A green tea polyphenol, epigalocatechin-3-gallate, induces apoptosis of human hepatocellular carcinoma, possibly through inhibition of Bcl-2 family proteins. AU - Nishikawa,T, AU - Nakajima,T, AU - Moriguchi,M, AU - Jo,M, AU - Sekoguchi,S, AU - Ishii,M, AU - Takashima,H, AU - Katagishi,T, AU - Kimura,H, AU - Minami,M, AU - Itoh,Y, AU - Kagawa,K, AU - Okanoue,T, Y1 - 2005/12/28/ PY - 2005/07/25/received PY - 2005/10/27/revised PY - 2005/11/17/accepted PY - 2006/2/17/pubmed PY - 2006/8/12/medline PY - 2006/2/17/entrez SP - 1074 EP - 82 JF - Journal of hepatology JO - J Hepatol VL - 44 IS - 6 N2 - BACKGROUND/AIMS: A major polyphenol of green tea, epigallocatechin-3-gallate (EGCG), has previously been shown to induce cell-cycle arrest and apoptosis in various cancers. However, little is known about its effects on hepatocellular carcinomas (HCCs). METHODS: Four HCC cell lines, HLE, HepG2, HuH-7 and PLC/PRF/5, were treated with EGCG or vehicle. Cell viability was assessed by trypan blue staining and WST-8 assay. Cell-cycle, apoptosis and apoptosis-related proteins in HLE cells were evaluated by flow cytometry and Western blotting. The effect of EGCG was also studied in vivo using a xenograft model. The effect of co-treatment with EGCG and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was also assessed. RESULTS: EGCG inhibited the growth of all HCC cell lines at concentrations of 50-100 microg/ml. In HLE cells, EGCG induced apoptosis but not cell-cycle arrest and appears to have down-regulated Bcl-2alpha and Bcl-xl by inactivation of NF-kappaB. Oral administration of EGCG showed similar effects in HLE xenograft tumors. Co-treatment with EGCG and TRAIL synergistically induced apoptosis in HLE cells. CONCLUSIONS: EGCG induced apoptosis in HLE cells, both in vitro and in vivo. Moreover, it enhanced TRAIL-induced apoptosis. Therefore, EGCG treatment may be useful for improving the prognosis of HCCs. SN - 0168-8278 UR - https://www.unboundmedicine.com/medline/citation/16481065/A_green_tea_polyphenol_epigalocatechin_3_gallate_induces_apoptosis_of_human_hepatocellular_carcinoma_possibly_through_inhibition_of_Bcl_2_family_proteins_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0168-8278(05)00818-4 DB - PRIME DP - Unbound Medicine ER -