| 姜 霞 1，2 薛宝瑶 1 谢婷婷 1 徐晓博 1 于月 成 1.瘦素对卵巢癌细胞 SKOV3 增殖及凋亡的影响[J].现代生物医学进展英文版,2015,15(6):1019-1023. |
| 瘦素对卵巢癌细胞 SKOV3 增殖及凋亡的影响 |
| Effect of Leptin on the Proliferation and Apoptosis of Ovarian CarcinomaSKOV3 Cells* |
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| DOI： |
| 中文关键词: 卵巢癌 瘦素 增殖 凋 亡 ERK1/2 |
| 英文关键词: Ovarian cancer Leptin Proliferation Apoptosis ERK1/2 |
| 基金项目:国家自然科学基金项目（ 30872740） |
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| 中文摘要: |
| 目的： 探讨瘦素对人卵巢癌 SKOV3 细胞增殖及凋 亡的影响及其作用 机制。方法： 用 不同 浓度的瘦素(0、50、 1 00、200 ng/mL)处
理人卵巢癌 SKOV3 细胞 48 h 后， 采用 MTT 法检细胞的生长；以血清饥饿诱导细胞凋亡， 同 时给予瘦素刺激， Annexin V/PI 双染
法检测细胞凋亡的变化； western blotting 分析 p21、 cyclin D1、 Bcl-2、 Bax 蛋白的表达水平和 ERK1 /2 通路的活化情况。 结果： 瘦素
以剂量依赖性的方式促进人卵巢癌 SKOV3 细胞的增殖， 同 时抑制血清饥饿诱导的细胞凋亡。 瘦素处理可下调 p21 和上调 cyclin
D1 的表达， 抑制 促凋亡分子 Bax 的表达和上调抗凋亡分子 Bcl-2 的表达。 瘦素可诱导细胞中 ERK1/2 通路的活化， 其抑制 剂
PD98059 可明显抑制 瘦素诱导的促细胞增殖和抗凋亡作用， 同 时伴随有 cyclin D1、 Bcl-2 蛋白表达的下调和 Bax 的上调。 结论： 瘦
素可能通过活化 ERK1 /2 通路调节细胞有丝分裂进程， 进而促进卵巢癌细胞的增殖； 同 时通过调节凋亡相关蛋白 Bcl-2 和 Bax 的
表达抑制卵巢癌细胞的凋亡。 |
| 英文摘要: |
| Objective:To investigate the effect and the underlying molecular mechanism of leptin on the proliferation and
apoptosis of ovarian carcinoma SKOV3 cells.Methods:After stimulation with various doses of leptin (0, 50, 100, 200 ng/mL) for 48 h,
the cell proliferation rate was analyzed by MTT colorimetry. Serum deprivation was used to induce cell apoptosis in SKOV3 cells
stimulated with leptin. Cell apoptosis was assessed by double staining with Annexin V and propidium iodide. The expression levels of
p21, cyclin D1, Bcl-2, Bax and ERK1 /2 pathway were detected by western blotting.Results:Leptin promoted the cell proliferation and
dampened the apoptosis rates induced by serum deprivation in a dose-dependent manner. Furthermore, leptin treatment down-regulated
the expression levels of p21 , up-regulated the cyclin D1 expression. Moreover, an obvious down-regulation of Bax protein and
up-regulation of Bcl-2 was confirmed in SKOV3 cell treated with leptin. Leptin dramatically induced the activation of ERK1/2 pathway,
and blocking this pathway with its inhibitor PD98059 strikingly attenuated leptin-induced proliferation and anti-apoptosis effect in
SKOV3 cell, concomitant with the decrease of cyclin D1 and Bcl-2 expression and increase of Bax expression.Conclusion:Leptin could
promote the SKOV3 cell proliferation and inhibit the apoptosis by the activation of ERK1/2 signaling to regulate SKOV3 cell mitosis and
expression levels of apoptosis-related protein. |
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