miR-221-3p对骨髓间充质干细胞(BMSCs)共培养后宫颈癌细胞增殖和侵袭的调控作用

Hongyan Cheng, Tao Jiang
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引用次数: 0

摘要

骨髓间充质干细胞(BMSCs)影响emt相关因素。miR-221-3p参与多种肿瘤。然而,miR-221-3p是否影响与骨髓间充质干细胞共培养的宫颈癌(CC)细胞尚不清楚。将BMSCs与CC细胞共培养,转染miR-221-3p抑制剂,real - time PCR检测miR-221-3p水平、细胞增殖、凋亡活性、E-cadherin、Vimentin水平、ELISA检测TGF-β1分泌、Smad1、Smad2表达。BMSCs上调CC细胞中miR-221-3p水平,增加细胞增殖,降低细胞凋亡活性,同时降低EMT表达,增加TGF-β1分泌,增加Smad1、Smad2表达(P <0.05)。miR-221-3p抑制剂可降低BMSCs对CC细胞的作用,逆转上述变化(P <0.05)。骨髓间充质干细胞的共培养促进了CC细胞的增殖和侵袭。下调miR-221-3p可改变TGF-β1/Smad信号通路,影响CC细胞的恶性特征。
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miR-221-3p Modulates Cervical Cancer Cells Proliferation and Invasion After Co-Culture with Bone Marrow Mesenchymal Stem Cells (BMSCs)
Bone marrow-derived mesenchymal stem cells (BMSCs) affect EMT-related factors. miR-221-3p involves in several tumors. However, whether miR-221-3p affects cervical cancer (CC) cells co-cultured with BMSCs is unclear. BMSCs and CC cells were co-cultured, and transfected with miR-221-3p inhibitor followed by analysis of miR-221-3p level by real time PCR, cell proliferation, apoptosis activity, E-cadherin and Vimentin level, TGF-β1 secretion by ELISA as well as Smad1 and Smad2 expression. BMSCs upregulated miR-221-3p level in CC cells, increased cell proliferation and reduced apoptotic activity along with the decreased expression of EMT, increased TGF-β1 secretion and Smad1 and Smad2 expression (P <0.05). miR-221-3p inhibitor can reduce BMSCs’ effect on CC cells, and reverse the above changes (P <0.05). The co-culture of BMSCs promotes CC cell proliferation and invasion. Down-regulating miR-221-3p can change TGF-β1/Smad signaling pathway and affect malignant characteristics of CC cells.
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