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AKR1C1 通过调节 TWIST1 表达促进宫颈癌进展。

AKR1C1 Contributes to Cervical Cancer Progression via Regulating TWIST1 Expression.

机构信息

Department of Biochemistry and Molecular Biology, YouJiang Medical University for Nationalities, Baise City, 533000, Guangxi Zhuang Autonomous Region, China.

Department of Oncology, Affiliated Hospital of YouJiang Medical University For Nationalities, No. 18 Zhongshan 2nd Road, YouJiang District, Baise City, 533000, Guangxi Zhuang Autonomous Region, China.

出版信息

Biochem Genet. 2021 Apr;59(2):516-530. doi: 10.1007/s10528-020-10014-x. Epub 2020 Nov 10.

DOI:10.1007/s10528-020-10014-x
PMID:33170398
Abstract

Cervical cancer (CC) is a common gynecological malignancy, accounting for 10% of all gynecological cancers. Recently, targeted therapy for CC has shown unprecedented advantages. To improve CC patients' prognosis, there are still urgent needs to develop more promising therapeutic targets. Aldo-keto reductase 1 family member C1 (AKR1C1) is a type of aldosterone reductase and plays a regulatory role in a variety of key metabolic pathways. Several studies indicated that AKR1C1 was highly expressed in a series of tumors, and participated in the progression of these tumors. However, the possible effects of AKR1C1 on CC progression remain unclear. Herein, we revealed AKR1C1 was highly expressed in human CC tissues and correlated with the clinical characteristics of patients with CC. AKR1C1 could regulate the proliferation and invasion of cervical cancer cells in vitro. Further experiments showed that AKR1C1 could regulate TWIST1 expression and AKT pathway. In summary, we confirmed the involvement of AKR1C1 in CC progression, and therefore AKR1C1 may have the potential to be a molecular target for CC treatment.

摘要

宫颈癌(CC)是一种常见的妇科恶性肿瘤,占所有妇科癌症的 10%。最近,CC 的靶向治疗显示出了前所未有的优势。为了改善 CC 患者的预后,仍然迫切需要开发更有前途的治疗靶点。醛固酮还原酶 1 家族成员 C1(AKR1C1)是一种醛固酮还原酶,在多种关键代谢途径中发挥调节作用。几项研究表明,AKR1C1 在一系列肿瘤中高表达,并参与这些肿瘤的进展。然而,AKR1C1 对 CC 进展的可能影响尚不清楚。在此,我们发现 AKR1C1 在人 CC 组织中高表达,并与 CC 患者的临床特征相关。AKR1C1 可以在体外调节宫颈癌细胞的增殖和侵袭。进一步的实验表明,AKR1C1 可以调节 TWIST1 的表达和 AKT 通路。总之,我们证实了 AKR1C1 参与了 CC 的进展,因此 AKR1C1 可能有潜力成为 CC 治疗的分子靶点。

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