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Interleukin-22 enhances chemoresistance of lung adenocarcinoma cells to paclitaxel.
Human Cell ( IF 4.3 ) Pub Date : 2020-05-25 , DOI: 10.1007/s13577-020-00373-3
Zhiliang Huang 1, 2 , Yu Gao 2, 3 , Dianchen Hou 1
Affiliation  

The chemoresistance of tumors is the main barrier to cancer treatment. Interleukin-22 (IL-22) plays an important role in the chemoresistance of multi-cancers; however, the roles of IL-22 in the paclitaxel resistance of lung adenocarcinoma cells remain to be investigated. The present study aims to investigate the potential mechanisms of IL-22 enhancing the chemoresistance of lung adenocarcinoma cells to paclitaxel. We cultured A549, H358, and A549/PTX cell lines. qRT-PCR and western blot assays were performed to examine the mRNA and/or protein levels of IL-22 in A549, A549/PTX, H358, and H358/PTX. Moreover, cells were transfected with IL-22 siRNA1, IL-22 siRNA2, and siRNA NC, and treated with paclitaxel, and the proliferation rate of lung adenocarcinoma cells was evaluated by MTT assay. Flow cytometry was conducted to determine the apoptosis rate of lung adenocarcinoma cells. The results showed that the expression of IL-22 in lung adenocarcinoma tissues was higher than that in normal tissues, and the expression of IL-22 was higher in A549/PTX and H358/PTX compared with A549 and H358 cells. Meanwhile, the expression of IL-22 was strongly correlated with smoking history and TMN stage, as well. Furthermore, IL-22 siRNA inhibited the proliferation and promoted the apoptosis of A549/PTX and H358/PTX cells, and IL-22 siRNA also suppressed the expression levels of AKT and Bcl-2 and increased the expression levels of Bax and cleaved caspase 3. To sum up, IL-22 may mediate the chemosensitivity of lung adenocarcinoma cells to paclitaxel through inhibiting the AKT signaling pathways.

中文翻译:

白介素-22增强了肺腺癌细胞对紫杉醇的化学耐药性。

肿瘤的化学抗性是癌症治疗的主要障碍。白介素-22(IL-22)在多癌的化学耐药中起重要作用;然而,IL-22在肺腺癌细胞的紫杉醇耐药性中的作用仍有待研究。本研究旨在探讨IL-22增强肺腺癌细胞对紫杉醇耐药的潜在机制。我们培养了A549,H358和A549 / PTX细胞系。进行qRT-PCR和蛋白质印迹测定以检查A549,A549 / PTX,H358和H358 / PTX中IL-22的mRNA和/或蛋白质水平。此外,将细胞用IL-22 siRNA1,IL-22 siRNA2和siRNA NC转染,并用紫杉醇处理,并通过MTT法评价肺腺癌细胞的增殖率。进行流式细胞术以确定肺腺癌细胞的凋亡率。结果表明,肺腺癌组织中IL-22的表达高于正常组织,与A549和H358细胞相比,A549 / PTX和H358 / PTX中IL-22的表达较高。同时,IL-22的表达也与吸烟史和TMN分期密切相关。此外,IL-22 siRNA抑制A549 / PTX和H358 / PTX细胞的增殖并促进其凋亡,IL-22 siRNA还抑制AKT和Bcl-2的表达,并增加Bax和caspase 3的表达。综上所述,IL-22可能通过抑制AKT信号通路来介导肺腺癌细胞对紫杉醇的化学敏感性。结果表明,肺腺癌组织中IL-22的表达高于正常组织,与A549和H358细胞相比,A549 / PTX和H358 / PTX中IL-22的表达较高。同时,IL-22的表达也与吸烟史和TMN分期密切相关。此外,IL-22 siRNA抑制A549 / PTX和H358 / PTX细胞的增殖并促进其凋亡,IL-22 siRNA还抑制AKT和Bcl-2的表达,并增加Bax和caspase 3的表达。综上所述,IL-22可能通过抑制AKT信号通路来介导肺腺癌细胞对紫杉醇的化学敏感性。结果显示,肺腺癌组织中IL-22的表达高于正常组织,与A549和H358细胞相比,A549 / PTX和H358 / PTX中IL-22的表达较高。同时,IL-22的表达也与吸烟史和TMN分期密切相关。此外,IL-22 siRNA抑制A549 / PTX和H358 / PTX细胞的增殖并促进其凋亡,IL-22 siRNA还抑制AKT和Bcl-2的表达,并增加Bax和caspase 3的表达。综上所述,IL-22可能通过抑制AKT信号通路来介导肺腺癌细胞对紫杉醇的化学敏感性。与A549和H358细胞相比,A549 / PTX和H358 / PTX中IL-22的表达更高。同时,IL-22的表达也与吸烟史和TMN分期密切相关。此外,IL-22 siRNA抑制A549 / PTX和H358 / PTX细胞的增殖并促进其凋亡,IL-22 siRNA还抑制AKT和Bcl-2的表达,并增加Bax和caspase 3的表达。综上所述,IL-22可能通过抑制AKT信号通路来介导肺腺癌细胞对紫杉醇的化学敏感性。与A549和H358细胞相比,A549 / PTX和H358 / PTX中IL-22的表达更高。同时,IL-22的表达也与吸烟史和TMN分期密切相关。此外,IL-22 siRNA抑制A549 / PTX和H358 / PTX细胞的增殖并促进其凋亡,IL-22 siRNA还抑制AKT和Bcl-2的表达,并增加Bax和caspase 3的表达。综上所述,IL-22可能通过抑制AKT信号通路来介导肺腺癌细胞对紫杉醇的化学敏感性。
更新日期:2020-05-25
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