4.4 Article

Aloe-emodin suppresses esophageal cancer cell TE1 proliferation by inhibiting AKT and ERK phosphorylation

Journal

ONCOLOGY LETTERS
Volume 12, Issue 3, Pages 2232-2238

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2016.4910

Keywords

esophageal cancer; aloe-emodin; signal transduction pathway

Categories

Funding

  1. National Natural Science Foundation of China (Beijing, China) [81372269, U1304813]
  2. Science Foundation of the Henan Province of China (Zhengzhou, China) [112106000039, 13HASTIT022, 2011A310009, 12B310022, 13A310553, 14A310006]
  3. Key Science and Technology Program of Zhengzhou City (Zhengzhou, China) [141PPTGG449]

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Aberrant AKT and extracellular signal-regulated kinase (ERK) activation is often observed in various human cancers. Both AKT and ERK are important in the phosphoinositide 3-kinase/AKT and mitogen-activated protein kinase kinase/ERK signaling pathways, which play vital roles in cell proliferation, differentiation and survival. Compounds that are able to block these pathways have therefore a promising use in cancer treatment and prevention. The present study revealed that AKT and ERK are activated in esophageal cancer TE1 cells. Aloe-emodin, an anthraquinone present in aloe latex, can suppress TE1 cell proliferation and anchor-independent cell growth. Aloe-emodin can also reduce the number of TE1 cells in S phase. Protein analysis indicated that aloe-emodin inhibits the phosphorylation of AKT and ERK in a dose-dependent manner. Overall, the present data indicate that aloe-emodin can suppress TE1 cell growth by inhibiting AKT and ERK phosphorylation, and suggest its clinical use for cancer therapy.

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