BACKGROUND Cervical cancer cell function is influence by ER. Therefore, in this study, ER stress senser-ATF6, was selected for detailed research in cervical cancer. METHODS ATF6 mRNA was assessed through RT-qPCR assays. Cell transfection was to regulate ATF6 and thereafter the differential ATF6 cancer cells were divided into two groups for further functional assays. Cell viabilities were analyzed by CCK-8 and migration by Scratch. RT-qPCR examined cell death biomarkers Caspas-3 and Bcl-2. 4-PBA was utilized to inhibit ER stress. After that, ATF6, viability, migration and apoptotic proteins were scrutinized after ER inhibition. Proteins signifying EMT, autophagy and MAPK signaling pathway were checked by western bolt. Last, we inactivated the MAPK signaling to investigate into the changes in cell functions. RESULTS ATF6 presented higher expression in cervical cancer cells. Inhibited ATF6 could reduce cell viabilities and migration but promote apoptosis through suppressing Bcl-2 and increasing caspase-3. ER stress antagonist witnessed a drop in ATF6 expression, cell viability, migration and Bcl-2 but a rise in caspase-3 activation, suggesting apoptosis increase. Cell autophagy was hindered in CC cells. Knockdown of ATF6 promoted autophagy and restrained EMT and MAPK signaling pathway. Suppressed ERK1/2 obstructed cell viabilities, migration, EMT and autophagy but promoted apoptosis. CONCLUSION ATF6 might promote cell growth, migration, autophagy through ER stress and MAPK signaling in cervical cancer in vitro, indicating a potential regulatory gene in cervical cancer. However, in-depth researches are requested to enrich the knowledge of ATF6 in cervical cancer in vivo and in clinical in the future.

中文翻译：

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在宫颈癌中激活转录因子 6 通过 MAPK 通路调节细胞生长、迁移并抑制细胞凋亡和自噬。

背景子宫颈癌细胞功能受ER的影响。因此，在本研究中，ER 应力传感器-ATF6 被选择用于宫颈癌的详细研究。方法 ATF6 mRNA 通过 RT-qPCR 测定进行评估。细胞转染是为了调节ATF6，然后将分化的ATF6癌细胞分为两组进行进一步的功能测定。通过 CCK-8 分析细胞活力并通过 Scratch 分析迁移。RT-qPCR 检查了细胞死亡生物标志物 Caspas-3 和 Bcl-2。4-PBA 用于抑制内质网应激。之后，在ER抑制后仔细检查ATF6、活力、迁移和凋亡蛋白。Western bolt 检测表示 EMT、自噬和 MAPK 信号通路的蛋白质。最后，我们灭活了 MAPK 信号以研究细胞功能的变化。结果 ATF6 在宫颈癌细胞中呈高表达。被抑制的 ATF6 可以降低细胞活力和迁移，但通过抑制 Bcl-2 和增加 caspase-3 促进细胞凋亡。ER 应激拮抗剂见证了 ATF6 表达、细胞活力、迁移和 Bcl-2 的下降，但 caspase-3 激活增加，表明细胞凋亡增加。细胞自噬在 CC 细胞中受到阻碍。敲低 ATF6 促进自噬并抑制 EMT 和 MAPK 信号通路。抑制 ERK1/2 会阻碍细胞活力、迁移、EMT 和自噬，但会促进细胞凋亡。结论 ATF6 可能通过 ER 应激和 MAPK 信号在体外促进宫颈癌细胞的生长、迁移、自噬，表明在宫颈癌中是一个潜在的调控基因。然而，