【摘要】：目的探討逆轉(zhuǎn)miR-155對宮頸癌Caski細胞生長、侵襲及耐藥性的影響。方法應用EGF處理宮頸癌Caski細胞,構建體外腫瘤細胞上皮間質(zhì)轉(zhuǎn)化模型,通過穩(wěn)定高表達miR-155觀察其對宮頸癌Caski細胞生長、體外侵襲、遷移能力及對順鉑化療敏感性的影響。通過轉(zhuǎn)染anti-miR-155以低表達miR-155,觀察其對宮頸癌Caski細胞生長、體外侵襲、遷移能力的影響。結(jié)果高表達miR-155能夠促進TP53表達,抑制Smad2和CCND1表達;但單純低表達miR-155并不能抑制E-cadherin表達及促進細胞增殖、侵襲和轉(zhuǎn)移的能力。結(jié)論miR-155可以抑制CCND1表達,調(diào)控細胞周期,抑制Caski細胞的增殖;miR-155高表達可以促進Caski細胞對順鉑的化療敏感性。
[Abstract]:Objective to investigate the effect of reversing miR-155 on the growth, invasion and drug resistance of cervical cancer Caski cells. Methods Cervical cancer Caski cells were treated with EGF, and the epithelial interstitial transformation model of tumor cells was established in vitro. The effects of miR-155 on the growth, invasion, migration and chemosensitivity to cisplatin of cervical cancer Caski cells were observed by stably high expression of miR-155. The effects of anti-miR-155 transfection on the growth, invasion and migration of cervical cancer Caski cells were observed by low expression of miR-155,. Results overexpression of miR-155 could promote the expression of TP53 and inhibit the expression of Smad2 and CCND1, but the low expression of miR-155 could not inhibit the expression of E-cadherin and the ability of cell proliferation, invasion and metastasis. Conclusion miR-155 can inhibit the expression of CCND1, regulate cell cycle and inhibit the proliferation of Caski cells, and the high expression of miR-155 can promote the chemosensitivity of Caski cells to cisplatin.
【作者單位】： 鄭州人民醫(yī)院婦科;
【分類號】：R737.33

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