Abstract
Genistein, the predominant isoflavone found in soy products, has exerted its anticarcinogenic effect in many different tumor types in vitro and in vivo. Accumulating evidence in recent years has strongly indicated the existence of cancer stem cells in gastric cancer. Here, we showed that low doses of genistein (15 μM), extracted from Millettia nitida Benth var hirsutissima Z Wei, inhibit tumor cell self-renewal in two types of gastric cancer cells by colony formation assay and tumor sphere formation assay. Treatment of gastric cancer cells with genistein reduced its chemoresistance to 5-Fu (fluorouracil) and ciplatin. Further results indicated that the reduced chemoresistance may be associated with the inhibition of ABCG2 expression and ERK 1/2 activity. Furthermore, genistein reduced tumor mass in the xenograft model. Together, genistein inhibited gastric cancer stem cell-like properties and reduced its chemoresistance. Our results provide a further rationale and experimental basis for using the genistein to improve treatment of patients with gastric cancer.
Highlights
IntroductionIt has been demonstrated that genistein functions as a promising chemopreventive agent to inhibit carcinogenesis through the modulation of genes that intimately related to the regulation of programmed cell death and cell cycle [4,5]
Soy isoflavones have been identified as dietary components contributing to relatively lower rates of different types of cancer in Asian counties including China
It has been demonstrated that genistein functions as a promising chemopreventive agent to inhibit carcinogenesis through the modulation of genes that intimately related to the regulation of programmed cell death and cell cycle [4,5]
Summary
It has been demonstrated that genistein functions as a promising chemopreventive agent to inhibit carcinogenesis through the modulation of genes that intimately related to the regulation of programmed cell death and cell cycle [4,5]. A number of reports have demonstrated the inhibiting carcinogenesis by genistein through the modulation of multiple regulatory pathways in the mammary tumor model, including programmed cell death, cell cycle, angiogenesis and metastasis. The potential inhibitory of genistein on the gastric cancer cell stem-like properties is still unclear. Our results demonstrated that gastric cancer cells treated with genistein inhibited the gastric cancer cell stem-like properties, such as self-renewal ability, drug resistance and tumorigenicity, which are associated with the decreased expression of stemness-related genes and the drug resistance gene ABCG2
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