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An Ω-3 fatty acid desaturase-expressing gene attenuates prostate cancer proliferation by cell cycle regulation

机译:Ω-3脂肪酸去饱和酶表达基因通过细胞周期调控减弱前列腺癌的增殖

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摘要

Previous studies have reported that Ω-6 and Ω-3 fatty acids have opposing effects on cancer development. Consuming high levels of long-chain Ω-3 polyunsaturated fatty acids (PUFAs) has been shown to reduce prostate cancer risk and increase chemotherapy sensitivity. The sdd17 gene encodes an Ω-3 fatty acid desaturase, which converts arachidonic acid into eicosapentaenoic acid (EPA). However, little is known regarding the function of the sdd17 gene in tumor cells in vitro. In the present study, prostate cancer cells were infected with the msdd17 gene, which allowed the endogenous production of Ω-3 PUFAs. The cells that expressed the msdd17 gene had high levels of long-chain Ω-3 PUFAs compared with the control cells. Expression of the msdd17 gene significantly inhibited prostate cancer cell proliferation. EPA exposure and msdd17 gene transfection each induced G2 cell cycle arrest and reduced E2F transcription factor 1 expression in prostate cancer cells. These results suggest that msdd17 gene transfection suppressed prostate cancer cell proliferation and induced G2 cell cycle arrest.
机译:先前的研究已经报道了Ω-6和Ω-3脂肪酸对癌症的发展有相反的影响。食用高水平的长链Ω-3多不饱和脂肪酸(PUFA)已显示可降低前列腺癌的风险并提高化疗敏感性。 sdd17基因编码一个Ω-3脂肪酸去饱和酶,该酶将花生四烯酸转化为二十碳五烯酸(EPA)。然而,关于sdd17基因在体外肿瘤细胞中的功能知之甚少。在本研究中,前列腺癌细胞感染了msdd17基因,该基因允许内源性产生Ω-3PUFA。与对照细胞相比,表达msdd17基因的细胞具有高水平的长链Ω-3PUFA。 msdd17基因的表达显着抑制前列腺癌细胞的增殖。 EPA暴露和msdd17基因转染均诱导前列腺癌细胞中G2细胞周期停滞并降低E2F转录因子1表达。这些结果表明msdd17基因转染抑制前列腺癌细胞增殖并诱导G2细胞周期停滞。

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