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圆叶舞茸块茎凝集素诱导结肠癌细胞体外凋亡和生长抑制。

Kaempferia rotunda tuberous rhizome lectin induces apoptosis and growth inhibition of colon cancer cells in vitro.

机构信息

Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi 6205, Bangladesh.

Cancer Molecular Pathology, School of Medicine and Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.

出版信息

Int J Biol Macromol. 2019 Dec 1;141:775-782. doi: 10.1016/j.ijbiomac.2019.09.051. Epub 2019 Sep 7.

Abstract

Kaempferia rotunda Linn. is a plant of ginger family and has many medicinal values in traditional applications, including as antimicrobial and anticancer agents. The present study aims to examine the anticancer activity of Kaempferia rotunda tuberous rhizome lectin (KRL, MW 29 ± 1.0 kDa) against colon cancer cells SW480 and SW48. KRL inhibited 67% and 59% of SW480 and SW48 cells growth respectively at the concentration of 1.0 mg/ml. The cells growth inhibition was a dose dependent manner. KRL treatments notably inhibited the colony formation capacity of the cancer cells. The surviving fractions of SW480 and SW48 cells treated with KRL significantly (p < 0.001) reduced compared to that of control cells. Significant increment of the apoptotic cells were noted following by G/G or G/M cell cycle arrest in KRL treated SW480 and SW48 cells, respectively. Modulation of PARP1, p53, p21, Bax and Bcl2 proteins expression was observed in treated cells in comparison to that of untreated cells. Furthermore, activation of caspase-3 and caspase-9 was noted in KRL treated cells and caspase-3 and caspase-9 inhibitors pre-treated cells were shown insensitive to KRL treatment. The results implied that KRL prevents SW480 and SW48 cells proliferation by the induction of apoptosis in the mitochondrial intrinsic pathway.

摘要

蓬莪术是姜科植物,具有许多传统应用中的药用价值,包括抗菌和抗癌作用。本研究旨在研究蓬莪术块根凝集素(KRL,MW 29±1.0 kDa)对结肠癌 SW480 和 SW48 细胞的抗癌活性。KRL 在 1.0 mg/ml 的浓度下分别抑制 SW480 和 SW48 细胞生长 67%和 59%。细胞生长抑制呈剂量依赖性。KRL 处理显著抑制癌细胞的集落形成能力。与对照细胞相比,用 KRL 处理的 SW480 和 SW48 细胞的存活分数显著(p<0.001)降低。在 KRL 处理的 SW480 和 SW48 细胞中,分别观察到 G/G 或 G/M 细胞周期阻滞后凋亡细胞的显著增加。与未处理的细胞相比,在处理的细胞中观察到 PARP1、p53、p21、Bax 和 Bcl2 蛋白表达的调节。此外,在 KRL 处理的细胞中观察到 caspase-3 和 caspase-9 的激活,并且用 caspase-3 和 caspase-9 抑制剂预处理的细胞对 KRL 处理不敏感。结果表明,KRL 通过诱导线粒体内在途径的细胞凋亡来防止 SW480 和 SW48 细胞增殖。

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