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The role of Schisandrin B in inhibiting proliferation of gefitinib-resistant lung cancer cells via down-regulation of IGFBP2 expression |
SUN Lei, LAN Xiu, LYU Zhuqing, LI Weiwen. |
Department of Respiratory Medicine, the Fifth Affiliated Hospital of Wenzhou Medical University, Lishui 323000, China |
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Cite this article: |
SUN Lei,LAN Xiu,LYU Zhuqing, et al. The role of Schisandrin B in inhibiting proliferation of gefitinib-resistant lung cancer cells via down-regulation of IGFBP2 expression[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2021, 51(4): 311-314,318.
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Abstract Objective: To investigate the role of Schisandrin B (Sch B) in inhibiting proliferation of gefitinib (Gef) resistant lung cancer cells and its molecular mechanism. Methods: PC9/GR (Gefitinib resistant PC9 cells) resistant cells were domesticated with gradient concentration of Gef and maintained with 200 mmol/L Gef. The difference of IGFBP2 expression and the viability between PC9 and PC9/GR cells were analyzed. The viability, apoptosis, IGFBP2 expression and phosphorylation of AKT and mTORC1were measured with and without Sch B treatment. Lentivirus transfection to obtain IGFBP2 overexpression (OE) cells was applied to confirm the role of IGFBP2 on proliferation inhibition of Sch B in PC9/GR cells. Results: The expression of IGFBP2 in PC9/GR cells was higher than that in PC9 cells (P<0.05). After Sch B treatment, the survival rate, IGFBP2 expression and phosphorylation of AKT and mTORC1 decreased (P<0.05), whereas the apoptosis increased (P<0.05). The overexpression of IGFBP2 increased the phosphorylation of AKT and mTORC1 but alleviated the proliferation inhibition of Sch B in PC9/GR cells (P<0.05). Conclusion: Sch B induces proliferation inhibition via down-regulating expression of IGFBP2 in PC9/GR cells.
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Received: 03 June 2020
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