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1.
Chinese Journal of Cancer Biotherapy ; (6): 1316-1321, 2018.
Article in Chinese | WPRIM | ID: wpr-801648

ABSTRACT

@#糖基化是生物体内蛋白质的基本修饰方式之一,通过影响蛋白质的折叠、运输和定位,从而参与人体多种生物学功能 的调节。研究表明,异常糖基化修饰参与生物体内多种病理生理过程,包括恶性肿瘤和一些炎症性疾病,尤其与肿瘤的转移和侵 袭密切相关。而上皮间质转化(epithelial-mesenchymal transition,EMT)指上皮细胞失去紧密连接转化为间质的复杂过程,是肿瘤 转移的重要机制之一。本文主要对蛋白质糖基化在肿瘤相关EMT的过程中所起的作用及其相关分子机制进行阐述。

2.
Biol. Res ; 48: 1-7, 2015. ilus, graf, tab
Article in English | LILACS | ID: biblio-950804

ABSTRACT

BACKGROUND: We have investigated the potential anticancer effects of karanjin, a principal furanoflavonol constituent of the Chinese medicine Fordia cauliflora, using cytotoxic assay, cell cycle arrest, and induction of apoptosis in three human cancer cell lines (A549, HepG2 and HL-60 cells). RESULTS: MTT cytotoxic assay showed that karanjin could inhibit the proliferation and viability of all three cancer cells. The induction of cell cycle arrest was observed via a PI (propidium iodide)/RNase Staining Buffer detection kit and analyzed by flow cytometry: karanjin could dose-dependently induce cell cycle arrest at G2/M phase in the three cell lines. Cell apoptosis was assessed by Annexin V-FITC/PI staining: all three cancer cells treated with karanjin exhibited significantly increased apoptotic rates, especially in the percentage of late apoptosis cells. CONCLUSION: Karanjin can induce cancer cell death through cell cycle arrest and enhance apoptosis. This compound may be effective clinically for cancer pharmacotherapy.


Subject(s)
Humans , Benzopyrans/pharmacology , Plant Extracts/pharmacology , Apoptosis/drug effects , Cell Proliferation/drug effects , Cell Cycle Checkpoints/drug effects , Fabaceae/chemistry , Antineoplastic Agents, Phytogenic/pharmacology , Benzopyrans/isolation & purification , HL-60 Cells , Hep G2 Cells , A549 Cells
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