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陈涛, 李雄伟, 孙晓东. 拉帕替尼和紫杉醇在食管癌细胞中的抗肿瘤活性及其作用机制[J]. 肿瘤防治研究, 2021, 48(1): 19-23. DOI: 10.3971/j.issn.1000-8578.2021.20.0579
引用本文: 陈涛, 李雄伟, 孙晓东. 拉帕替尼和紫杉醇在食管癌细胞中的抗肿瘤活性及其作用机制[J]. 肿瘤防治研究, 2021, 48(1): 19-23. DOI: 10.3971/j.issn.1000-8578.2021.20.0579
CHEN Tao, LI Xiongwei, SUN Xiaodong. Synergistic Antitumor Activity and Mechanism of Lapatinib and Paclitaxel in Esophageal Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2021, 48(1): 19-23. DOI: 10.3971/j.issn.1000-8578.2021.20.0579
Citation: CHEN Tao, LI Xiongwei, SUN Xiaodong. Synergistic Antitumor Activity and Mechanism of Lapatinib and Paclitaxel in Esophageal Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2021, 48(1): 19-23. DOI: 10.3971/j.issn.1000-8578.2021.20.0579

拉帕替尼和紫杉醇在食管癌细胞中的抗肿瘤活性及其作用机制

Synergistic Antitumor Activity and Mechanism of Lapatinib and Paclitaxel in Esophageal Cancer Cells

  • 摘要:
    目的 探讨拉帕替尼、紫杉醇和拉帕替尼联合紫杉醇对食管癌EC109细胞的抗肿瘤活性及作用机制。
    方法 MTT法检测拉帕替尼(1、2、4、8 μmol/L)、紫杉醇(5、10、20、40 μg/L)及联合使用对食管癌EC109细胞增殖的影响;分别检测拉帕替尼2 μmol/L、紫杉醇10 μg/L及联合使用对EC109细胞的侵袭、周期、凋亡和EGFR、HER2及其下游信号通路的影响。
    结果 MTT结果显示:拉帕替尼联合紫杉醇可协同抑制EC109细胞增殖,联合作用指数均大于1.15;拉帕替尼联合紫杉醇组发生侵袭的细胞数62.0±9.5个,明显少于拉帕替尼152.4±16.1个和紫杉醇组103.6±12.7个(P < 0.05);拉帕替尼联合紫杉醇组G2/M期细胞((43.4±3.1)%),高于拉帕替尼((20.3±2.5)%)和紫杉醇组((26.6±2.8)%)(P < 0.05);拉帕替尼联合紫杉醇组的细胞凋亡率为(47.3±8.4)%,高于拉帕替尼((12.7±2.3)%)和紫杉醇组((21.4±5.2)%)(P < 0.05);Western blot结果显示:拉帕替尼联合紫杉醇可协同抑制磷酸化EGFR、HER2及AKT蛋白的表达。
    结论 拉帕替尼联合紫杉醇通过抑制食管癌细胞EC109的增殖和侵袭、阻滞细胞周期、诱导细胞凋亡、抑制EGFR、HER2下游信号通路的转导发挥协同抗肿瘤活性。

     

    Abstract:
    Objective To investigate the anti-tumor activity and mechanism of lapatinib, paclitaxel and their combination on esophageal cancer cells EC109.
    Methods MTT assay was used to detect the effects of lapatinib (1, 2, 4, 8 μmol/L), paclitaxel (5, 10, 20, 40 μg/L) and their combination on the proliferation of esophageal cancer cells EC109. We tested the effects of 2 μmol/L lapatinib, 10 μg/L paclitaxel and their combination on the invasion, cell cycle, apoptosis and EGFR, HER2 and downstream signaling pathways of EC109 cells.
    Results Lapatinib combined with paclitaxel synergistically inhibited the proliferation of EC109 cells, and the combined action index was greater than 1.15. The number of invaded cells in the combination group (62.0±9.5) was significantly less than those in the lapatinib group (152.4±16.1) and the paclitaxel group (103.6±12.7) (P < 0.05). G2/M cells in the combination group ((43.4±3.1)%) was higher than those in lapatinib group ((20.3±2.5)%) and paclitaxel group ((26.6±2.8)%) (P < 0.05). The apoptosis rate of the combination group was (47.3±8.4)%, higher than those of lapatinib ((12.7±2.3)%) and paclitaxel group ((21.4±5.2)%) (P < 0.05). Lapatinib combined with paclitaxel could synergistically inhibit the expression of phosphorylated EGFR, HER2 and AKT proteins.
    Conclusion Lapatinib combined with paclitaxel exert synergistic antitumor activity by synergistically inhibiting the proliferation and invasion of esophageal cancer cell line EC109, arresting cell cycle, inducing apoptosis and inhibiting the transduction of EGFR/HER downstream signaling pathway.

     

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