Betulin inhibits lung carcinoma proliferation through activation of AMPK signaling.

Tumour Biol

Department of Pneumology, Huaihe Hospital of Henan University, Baobei Road No. 8, 475000, Kaifeng, Henan Province, China.

Published: November 2014

AI Article Synopsis

  • - Betulin is a natural triterpene found in birch tree bark and has been shown to make up to 30% of the dry weight of its extracts.
  • - The study investigated betulin's ability to inhibit growth and proliferation in lung carcinoma cells (A549 and NCI-292) using specific assays, showing significant effects on cell cycle regulators.
  • - At a molecular level, betulin was linked to the activation of AMP kinase and the suppression of mTOR signaling; inhibiting AMPK signaling reduced its antiproliferative effects, suggesting a potential role for betulin in lung cancer treatment and prevention.

Article Abstract

Betulin (lup-20(29)-ene-3β, 28-diol) is an abundant, naturally occurring triterpene. It is commonly isolated from the bark of birch trees and forms up to 30% of the dry weight of the extractive. In the present study, we revealed its antiproliferative effects and mechanisms using two lung carcinoma cells (A549 and NCI-292). By 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and bromodeoxyuridine (BrdU) incorporation assays, we found that betulin could efficiently inhibit cell growth and proliferation. Besides, several key genes of cell-cycle regulators were also affected by betulin treatment. At the molecular level, our results demonstrated that treatment with betulin was also associated with activation of AMP kinase and inhibition of mTOR/p70S6K/pS6 signaling in these cells. In agreement, inhibition of AMPK signaling largely reversed the antiproliferative roles of betulin. Taken together, these data provide evidence for a mechanism that may contribute to the antineoplastic effects of betulin and justify further work to explore its potential roles in lung cancer prevention and treatment.

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Source
http://dx.doi.org/10.1007/s13277-014-2426-7DOI Listing

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