LncRNA TUC338通过激活EGFR/PI3K/AKT 信号通路促进肺癌细胞的增殖、迁移和侵袭

目的 探讨长链非编码RNATUC338（lncRNA TUC338）对非小细胞肺癌（NSCLC）细胞增殖、迁移、侵袭及表皮生长因子受体（EGFR）/磷酸肌醇3激酶（PI3K）/丝氨酸/苏氨酸蛋白激酶（AKT）通路的影响。方法 收集2019年7月—2021年6月我院胸外科手术切除的37例NSCLC患者肺癌组织与癌旁组织标本，RT-qPCR检测组织标本及NSCLC细胞中lncRNA TUC338表达；对NCI-H157细胞进行干预，将si-TUC338、si-NC、pcDNA-TUC338、pcDNA-NC质粒转染细胞及EGFR与PI3K双重抑制剂MTX-211（MTX-211）、pcDNA-TUC338与MTX-211共同处理细胞，CCK-８法检测细胞增殖，Transwell小室法检测细胞迁移与侵袭，Western blot检测细胞周期蛋白D1（cyclin D1）、基质金属蛋白酶2（MMP-2）、MMP-9蛋白及EGFR、PI3K、AKT相关蛋白表达。结果 LncRNA TUC338在肺癌组织与细胞中高表达；抑制lncRNA TUC338表达可显著抑制NCI-H157细胞增殖、迁移与侵袭及EGFR/PI3K/AKT通路激活（P＜0.05）；过表达lncRNA TUC338可促进NCI-H157细胞增殖、迁移与侵袭及EGFR/PI3K/AKT激活（P＜0.05）。结论 LncRNA TUC338在肺癌中呈高表达，可能通过激活EGFR/PI3K/AKT信号通路促进肺癌NCI-H157细胞增殖、迁移与侵袭。

LncRNA TUC338 promotes the proliferation, migration and invasion of lung cancer cells by activating EGFR/PI3K/AKT signaling pathway

Objective To investigate the effects and regulatory mechanisms of long non-coding RNA (lncRNA) TUC338 on the proliferation, migration and invasion and epidermal growth factor receptor (EGFR)/phosphoinositide 3 kinase (PI3K)/serine/threonine protein kinase (AKT) of non-small cell lung cancer cells. Methods From July 2019 to June 2021, lung cancer tissue and paracancerous tissue specimens resected from 37 patients with NSCLC by thoracic surgery in Suining Central Hospital were collected. RT-qPCR was used to detect the expression of lncRNA TUC338 in tissue specimens and NSCLC cells. NCI-H157 cells were intervened, and si-TUC338, si-NC, pcDNA-TUC338, pcDNA-NC plasmids were transfected into cells. EGFR and PI3K dual inhibitor MTX-211 inhibitor (MTX-211). pcDNA-TUC338 and MTX-211 were co-treated Cells. CCK-8 assay was used to detect cell proliferation. Transwell chamber assay was used to detect cell migration and invasion. Western blot was used to detect cyclin D1 (cyclin D1), matrix metalloproteinase 2 (MMP-2), MMP-9 protein and EGFR. The phosphoinositide 3 kinase (PI3K), serine/threonine protein kinase (AKT) related protein expression were detected respectively. Results LncRNA TUC338 was highly expressed in lung cancer tissues and cells. Inhibiting the expression of lncRNA TUC338 could significantly inhibit the proliferation, migration and invasion of NCI-H157 cells and the activation of EGFR/PI3K/AKT pathway (P<0.05). Over-expression of lncRNA TUC338 could promote NCI-H157 cells proliferation, migration and invasion and EGFR/PI3K/AKT activation (P<0.05).Conclusion LncRNA TUC338 is highly expressed in lung cancer, which may promote the proliferation, migration and invasion of lung cancer NCI-H157 cells by activating the EGFR/PI3K/AKT signaling pathway.