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硬脂酰辅酶 A 去饱和酶 1 调节宫颈癌细胞的恶性进展。

Stearoyl-CoA desaturase 1 regulates malignant progression of cervical cancer cells.

机构信息

Department of Obstetrics, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China.

出版信息

Bioengineered. 2022 May;13(5):12941-12954. doi: 10.1080/21655979.2022.2079253.

Abstract

The primary regulatory gene for fatty acid synthesis, stearoyl-CoA desaturase 1 (SCD1), has been linked to the progression of several malignancies. Its role in cervical cancer remains unclear till now. This paper aimed to explore the role and mechanism of SCD1 in cervical cancer. The GEPIA database was used to perform a bioinformatics analysis of the role of SCD1 in cervical cancer staging and prognosis. The influences of SCD1 knockdown on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) progress were then investigated. Following transcription factor Kruppel like factor 9 (KLF9) was discovered to be negatively correlated with SCD1, the regulatory role of KLF9 in the effects of SCD1 on cervical cancer cells and the signaling pathway was evaluated. According to the GEPIA database, SCD1 level was associated with the cervical cancer stage, the overall survival level, and the disease-free survival level. Cell proliferation, migration, invasion, and EMT progress were all hindered when its expression was knocked down. Novelty, KLF9 reversed the effects of SCD1 on cells, as well as the Akt/glycogen synthase kinase 3β (GSK3β) signaling pathway. Together, SCD1 was negatively regulated by KLF9 and it activated the Akt/GSK3β signaling pathway to promote the malignant progression of cervical cancer cells. Developing SCD1 inhibitors offers novel ideas for the biological treatment of cervical cancer.

摘要

脂肪酸合成的主要调节基因,硬脂酰辅酶 A 去饱和酶 1(SCD1),与几种恶性肿瘤的进展有关。其在宫颈癌中的作用至今仍不清楚。本文旨在探讨 SCD1 在宫颈癌中的作用和机制。使用 GEPIA 数据库对 SCD1 在宫颈癌分期和预后中的作用进行生物信息学分析。然后研究 SCD1 敲低对细胞增殖、迁移、侵袭和上皮-间充质转化(EMT)进展的影响。发现转录因子 Kruppel 样因子 9(KLF9)与 SCD1 呈负相关后,评估了 KLF9 在 SCD1 对宫颈癌细胞的影响及其信号通路中的调节作用。根据 GEPIA 数据库,SCD1 水平与宫颈癌分期、总生存率水平和无病生存率水平相关。当表达被敲低时,细胞增殖、迁移、侵袭和 EMT 进展均受到抑制。新颖的是,KLF9 逆转了 SCD1 对细胞的作用,以及 Akt/糖原合酶激酶 3β(GSK3β)信号通路。总之,SCD1 受 KLF9 负调控,激活 Akt/GSK3β 信号通路,促进宫颈癌细胞的恶性进展。开发 SCD1 抑制剂为宫颈癌的生物治疗提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/400a/9275951/2b4eee5ee23e/KBIE_A_2079253_UF0001_OC.jpg

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