Opata Michael M, Izevbigie Ernest B
The Laboratory of Phytoceuticals, and Cancer Prevention and Therapies Department of Biology, Jackson State University, 1400 J. R. Lynch Street, P.O Box 18540, Jackson, MS 39217, USA.
Int J Environ Res Public Health. 2006 Jun;3(2):174-9. doi: 10.3390/ijerph2006030019.
Breast cancer is the second leading cause of cancer related deaths of women in the United States. Several treatment strategies have been developed over the past decade to reduce cancer morbidity and mortality rates. While mortality rates have declined in some ethnic populations, the overall cancer incidence continues to grow. Hence, chemotherapeutic agents are needed to improve cancer treatment outcome. Previous studies show that low concentrations (microgram/ml) of water-soluble leaf extracts of a Nigerian edible plant, V. amygdalina (VA), potently retard the proliferative activities of estrogen receptor positive (ER+) human breast cancerous cells (MCF-7) cells in vitro in a concentration-dependent fashion. The anti-proliferative activities of VA are extracellular signal-regulated kinases (1/2) (ERKs (1/2))-dependent. Cell culture and animal model studies, conducted by other investigators using other plant extracts, have also revealed that plant extract components called thionins may be responsible for their anticancer activities. These thionins are believed to interact with the cells in ways that compromise membrane potential/permeability resulting in the alteration of efflux, cytosolic activities, and subsequent cell death. Therefore, we hypothesized that VA exposure may compromise cell membrane as another mode of action to elicit its anticancer activities in MCF-7 cells. The exposure of cells to VA decreased [3H]thymidine uptake in a concentration-dependent (0, 30, and 100 mug/ml VA) manner (p < 0.05) but increased [3H]thymidine release, expressed as percent of [3H]thymidine incorporated, into the medium (p < 0.05). The amount of [3H]thymidine released into the medium was 1.7, 7.4, and 11.0 % for 0, 30, and 100 mug/ml VA respectively. Thus suggesting the membranes in VA-treated cells were compromised in a concentration-dependent fashion.
乳腺癌是美国女性癌症相关死亡的第二大主要原因。在过去十年中，已经开发了几种治疗策略来降低癌症发病率和死亡率。虽然某些种族人群的死亡率有所下降，但总体癌症发病率仍在持续上升。因此，需要化疗药物来改善癌症治疗效果。先前的研究表明，尼日利亚一种可食用植物——扁桃斑鸠菊（VA）的水溶性叶提取物在低浓度（微克/毫升）时，能以浓度依赖的方式在体外有效抑制雌激素受体阳性（ER+）人乳腺癌细胞（MCF-7）的增殖活性。VA的抗增殖活性依赖于细胞外信号调节激酶（1/2）（ERKs（1/2））。其他研究人员使用其他植物提取物进行的细胞培养和动物模型研究也表明，被称为硫堇的植物提取物成分可能是其抗癌活性的原因。据信这些硫堇与细胞相互作用的方式会损害膜电位/通透性，从而导致外流、胞质活性改变以及随后的细胞死亡。因此，我们推测VA暴露可能会损害细胞膜，作为在MCF-7细胞中引发其抗癌活性的另一种作用方式。细胞暴露于VA后，[3H]胸苷摄取以浓度依赖（0、30和100微克/毫升VA）的方式降低（p<0.05），但[3H]胸苷释放增加，以掺入的[3H]胸苷百分比表示，进入培养基中（p<0.05）。对于0、30和100微克/毫升VA，释放到培养基中的[3H]胸苷量分别为1.7%、7.4%和11.0%。这表明经VA处理的细胞中的膜以浓度依赖的方式受到损害。
