Ganoderma lucidum suppresses growth of breast cancer cells through the inhibition of Akt/NF-κB signaling

Ganoderma lucidum suppresses growth of breast cancer cells through the inhibition of Akt/NF-κB signaling
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DOI:
10.1207/s15327914nc4902_13
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发表时间:
2004-01-01
影响因子:
2.9
通讯作者:
Sliva, D
Sliva, D
中科院分区:
医学4区
文献类型:
--
作者:
Jiang, JH;Slivova, V;Sliva, D

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灵芝(灵芝,灵芝)是一种流行的亚洲蘑菇,已被用于超过2000年的一般促进健康,因此被称为“不朽的蘑菇。“灵芝也被用于传统中药,以预防或治疗各种疾病,包括癌症,我们以前证明,灵芝抑制乳腺癌细胞的侵袭行为,通过抑制转录因子NF-κ B。然而,灵芝对高侵袭性和转移性乳腺癌细胞生长的抑制作用的分子机制尚未完全阐明。在这里,我们发现灵芝抑制乳腺癌MDA-MB-231细胞的增殖通过下调Akt/NF-κ B信号。灵芝抑制Akt在Ser(473)上的磷酸化并下调Akt的表达,从而导致MDA-MB-231细胞中NF-κ B活性的抑制。灵芝的生物学效应表现为细胞周期停滞在G 0/G1期,这是由于NF-κ B调节的cyclin D1表达下调,随后是cdk 4的抑制。我们的研究结果表明,灵芝抑制MDA-MB-231乳腺癌细胞的生长,通过调节AktINF-kappaB信号,并可能有潜在的治疗乳腺癌的治疗用途。
Ganoderma lucidum (Reishi, Lingzhi) is a popular Asian mushroom that has been used for more than 2 millennia for the general promotion of health and was therefore called the "Mushroom of Immortality." Ganoderma lucidum was also used in traditional Chinese medicine to prevent or treat a variety of diseases, including cancer We previously demonstrated that Ganoderma lucidum suppresses the invasive behavior of breast cancer cells by inhibiting the transcription factor NF-kappaB. However the molecular mechanisms responsible for the inhibitory effects of Ganoderma lucidum on the growth of highly invasive and metastatic breast cancer cells has not been fully elucidated. Here, we show that Ganoderma lucidum inhibits proliferation of breast cancer MDA-MB-231 cells by downregulating Akt/NF-kappaB signaling. Ganoderma lucidum suppresses phosphorylation of Akt on Ser(473) and downregulates the expression of Akt, which results in the inhibition of NF-kappaB activity in MDA-MB-231 cells. The biological effect of Ganoderma lucidum was demonstrated by cell cycle arrest at G0/G1, which was the result of the downregulation of expression of NF-kappaB-regulated cyclin D1, followed by the inhibition of cdk4. Our results suggest that Ganoderma lucidum inhibits the growth of MDA-MB-231 breast cancer cells by modulating AktINF-kappaB signaling and could have potential therapeutic use for the treatment of breast cancer.