Department of Allergy, Pulmonary and Critical Care Medicine, Gachon University, Gil Medical Center, Incheon, 21565, Republic of Korea.
Gachon Medical Research Institute, Gachon University Gil Medical Center, Incheon, 21565, Republic of Korea.
BMC Complement Altern Med. 2019 Nov 15;19(1):312. doi: 10.1186/s12906-019-2725-z.
Cervical cancer is the second-leading cause of cancer-related mortality in females. Coix lacryma-jobi L. var. ma-yuen (Rom.Caill.) Stapf ex Hook. f. is the most widely recognized medicinal herb for its remedial effects against inflammation, endocrine system dysfunctions, warts, chapped skin, rheumatism, and neuralgia and is also a nourishing food.
To investigate the activity of Coix lacryma-jobi sprout extract (CLSE) on cell proliferation in human cervical cancer HeLa cells, we conducted a Cell Counting Kit-8 (CCK-8) assay. Flow-cytometric analysis and western blot analysis were performed to verify the effect of CLSE on the regulation of the cell cycle and apoptosis in HeLa cells.
We observed that CLSE significantly inhibited cell proliferation. Furthermore, CLSE dose-dependently promoted cell cycle arrest at the sub-G1/ S phase in HeLa cells, as detected by bromodeoxyuridine (BrdU) staining. The cell-cycle-arrest effects of CLSE in HeLa cells were associated with downregulation of cyclin D1 and cyclin-dependent kinases (CDKs) 2, 4, and 6. Moreover, CLSE induced apoptosis, as determined by flow-cytometric analysis and nuclear DNA fragmentation with Annexin V/propidium iodide (PI) and 4'6'-diamidino-2-phenylindole (DAPI) staining. Induction of apoptosis by CLSE was involved in inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) and upregulation of the apoptotic proteins p53, cleaved poly (ADP-ribose) polymerase (PARP), cleaved caspase-3, and cleaved caspase-8. Finally, we observed that CLSE inactivated the phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) pathways.
CLSE causes cell cycle arrest and apoptotic cell death through inactivation of the PI3K/AKT pathway in HeLa cells, suggesting it is a viable therapeutic agent for cervical cancer owing to its anticancer effects.
宫颈癌是女性癌症相关死亡的第二大主要原因。薏苡（Coix lacryma-jobi L. var. ma-yuen （Rom.Caill.） Stapf ex Hook. f.）是最被广泛认可的药用植物，具有抗炎、内分泌系统功能障碍、疣、皲裂皮肤、风湿和神经痛的治疗效果，也是一种滋养食品。
为了研究薏苡芽提取物（CLSE）对人宫颈癌 HeLa 细胞增殖的活性，我们进行了细胞计数试剂盒-8（CCK-8）检测。通过流式细胞术分析和蛋白质印迹分析验证了 CLSE 对 HeLa 细胞细胞周期和凋亡调控的影响。
我们观察到 CLSE 显著抑制细胞增殖。此外，CLSE 以剂量依赖的方式促进 BrdU 染色的 HeLa 细胞在亚 G1/S 期的细胞周期停滞。CLSE 在 HeLa 细胞中的细胞周期停滞作用与细胞周期蛋白 D1 和细胞周期蛋白依赖性激酶（CDKs）2、4 和 6 的下调有关。此外，CLSE 通过流式细胞术分析和 Annexin V/碘化丙啶（PI）和 4'6'-二脒基-2-苯基吲哚（DAPI）染色的核 DNA 片段化确定诱导凋亡。CLSE 诱导的凋亡涉及抗凋亡蛋白 B 细胞淋巴瘤 2（Bcl-2）的抑制和凋亡蛋白 p53、裂解多聚（ADP-核糖）聚合酶（PARP）、裂解半胱天冬酶-3 和裂解半胱天冬酶-8 的上调。最后，我们观察到 CLSE 使磷酸肌醇 3-激酶（PI3K）和蛋白激酶 B（AKT）通路失活。
CLSE 通过在 HeLa 细胞中使 PI3K/AKT 通路失活导致细胞周期停滞和凋亡细胞死亡，表明其具有抗癌作用，是治疗宫颈癌的一种可行的治疗药物。
