Epigallocatechin gallate inhibits human tongue carcinoma cells via HK2‑mediated glycolysis.

نویسندگان

  • Feng Gao
  • Ming Li
  • Wen-Bin Liu
  • Zhong-Su Zhou
  • Rui Zhang
  • Jun-Ling Li
  • Ke-Chao Zhou
چکیده

Epigallocatechin gallate (EGCG), one of the major catechins found in green tea, was suggested to play a role as a chemopreventive agent in various human cancer models. In this study, we reported that EGCG has a profound antitumor effect on human tongue carcinoma cells by directly regulating glycolysis. EGCG dose-dependently inhibited anchorage-independent growth and short-term EGCG exposure substantially decreased EGF-induced EGF receptor (EGFR), Akt and ERK1/2 activation, as well as the downregulation of hexokinase 2 (HK2). Furthermore, inhibition of EGCG‑mediated HK2 expression was involved in Akt, but not in ERK1/2 signaling pathway suppression. Overexpression of constitutively activated Akt1 rescued inhibition of EGCG‑induced glycolysis. Moreover, EGCG inhibited HK2 expression on mitochondrial outer membrane and induced apoptosis. In summary, the results suggested that EGCG or a related analogue, may have a role in the management of human tongue carcinoma.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Deguelin inhibits non-small cell lung cancer via down-regulating Hexokinases II-mediated glycolysis

Hexokinases II (HK2) is a hub in the regulation of cancer cell glycolysis. Here we reported deguelin, a natural compound which has been studied in various tumor types, has a profound anti-tumor effect on human non-small cell lung cancer (NSCLC) via directly down-regulating of glycolysis. In NSCLC cell lines and primary NSCLC tissue, we found HK2 is overexpressed. Deguelin treatment markedly inh...

متن کامل

Green tea polyphenol epigallocatechin gallate inhibits cell signaling by inducing SOCS1 gene expression.

Therapeutic effects of green tea involve an inhibitory function of its constituent polyphenol epigallocatechin gallate (EGCG) on cell signaling. The specificity and mechanism(s) by which EGCG inhibits cell signaling have remained unclear. Here, we demonstrate that green tea and EGCG induce suppressor of cytokine signaling 1 (SOCS1) gene expression, a negative regulator of specific cell signalin...

متن کامل

STAT3 regulates glycolysis via targeting hexokinase 2 in hepatocellular carcinoma cells

Signal transducer and activator of transcription 3 (STAT3) and hexokinase 2 (HK2) are involved in hepatocellular carcinoma (HCC). Deregulation of cellular energetics involving an increase in glycolysis is a characteristic of HCC. This study examined whether STAT3 regulates HCC glycolysis through the HK2 pathway in HCC cells. Human HCC cell lines HepG2 and Hep3B cells were transfected with pcDNA...

متن کامل

Inhibitory effect of (-)-epigallocatechin and (-)-epigallocatechin gallate against heregulin beta1-induced migration/invasion of the MCF-7 breast carcinoma cell line.

Migration/invasion is involved in the multiple steps of metastasis, resulting in a poor prognosis of breast cancer. (-)-Epigallocatechin-3-gallate (EGCG) in green tea inhibits the metastasis of some cancer cell lines. Cell migration/invasion assays using Boyden chambers demonstrated that (-)-epigallocatechin (EGC), another green tea catechin, inhibited heregulin-beta1 (HRG)-induced migration/in...

متن کامل

Epigallocatechin gallate (EGCG) inhibits the sulfation of 1-naphthol in a human colon carcinoma cell line, Caco-2.

We have previously reported that epigallocatechin gallate (EGCG) strongly inhibits the in vitro phenol sulfotransferase (P-ST) activity of a human colon carcinoma cell line, Caco-2. In the present study, we examined the ability of EGCG to inhibit the sulfation of 1-naphthol in intact Caco-2 cells. Sulfation of 1-naphthol was detected in Caco-2 cells after 2 h of incubation, and was observed to ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Oncology reports

دوره 33 3  شماره 

صفحات  -

تاریخ انتشار 2015