EGCG sensitizes chemotherapeutic-induced cytotoxicity by targeting the ERK pathway in multiple cancer cell lines

Ran Wei, Joanna Wirkus, Zixuan Yang, Jazmin Machuca, Yasmin Esparza, Gerardo G. Mackenzie

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Epigallocatechin-3-gallate (EGCG), a major polyphenol component of green tea, presents anticancer efficacy. However, its exact mechanism of action is not known. In this study, we evaluated the effect of EGCG alone or in combination with current chemotherapeutics [gemcitabine, 5-flourouracil (5-FU), and doxorubicin] on pancreatic, colon, and lung cancer cell growth, as well as the mechanisms involved in the combined action. EGCG reduced pancreatic, colon, and lung cancer cell growth in a concentration and time-dependent manner. EGCG strongly induced apoptosis and blocked cell cycle progression. Moreover, EGCG enhanced the growth inhibitory effect of 5-FU and doxorubicin. Of note, EGCG enhanced 5-FU's and doxorubicin's effect on apoptosis, but not on cell cycle. Mechanistically, EGCG reduced ERK phosphorylation concentration-dependently, and sensitized gemcitabine, 5-FU, and doxorubicin to further suppress ERK phosphorylation in multiple cancer cell lines. In conclusion, EGCG presents a strong anticancer effect in pancreatic, colon, and lung cancer cells and is a robust combination partner for multiple chemotherapeutics as evidenced by reducing cancer cell growth, in part, by inhibiting the ERK pathway.

Original languageEnglish (US)
Article number108546
JournalArchives of Biochemistry and Biophysics
Volume692
DOIs
StatePublished - Oct 15 2020

Keywords

  • 5-FU
  • Colon cancer
  • Doxorubicin
  • Epigallocatechin-3-gallate
  • ERK
  • Gemcitabine
  • Lung cancer
  • Pancreatic cancer

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology

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