The role of glycosylation in tumor-associated epithelial-mesenchymal transition / 中国肿瘤生物治疗杂志

@#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。

Effects of karanjin on cell cycle arrest and apoptosis in human A549, HepG2 and HL-60 cancer cells

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.