白黎蘆醇透過SIRT1蛋白表現來活化AMP-活化酵素，影響癌細胞增生

Resveratrol is a natural plant polyphenolic antioxidant compound. It functions as an agonist for estrogen receptor-mediated transcription. But other researchers have reported that resveratrol decreases cell proliferation of both estrogen receptor (ER) positive and ER negative breast cancer cells, which suggests that the interaction of resveratrol with the ER may not fully explain its inhibitory effect on proliferation. Caloric restriction (CR) reduces the incidence and progression of spontaneous and induced tumors in laboratory rodents. Resveratrol has multiple beneficial activities similar to those associated with CR, such as increased life span and delay in the onset of diseases associated with aging. One key enzyme thought to be activated during CR is the AMP-activated kinase (AMPK), a sensor of cellular energy levels. The suppression of nonessential energy expenditure by activated AMPK along with the CR mimetic and antiproliferative properties of resveratrol led us to hypothesize that the activation of AMPK could be an important component of resveratrol activity. Here, we show that resveratrol activated AMPK in both ER positive and negative breast cancer cells. The activation of AMPK suppresses downstream substrates, such as mammalian target of rapamycin and 4E-BP1 and a general decrease in mRNA translation. Moreover, we also propose that resveratrol induced the expression of Sirtuin type 1 (SIRT1) via the cellular NAD+/NADH to increase AMPK activity in cancer cells but did not require LKB1. These observations raise the possibility that resveratrol may additionally modulate cell proliferation by controlling a variety of cellular events in tumor cells through activation of AMPK, dependent of its expression of SIRT1.