CaMKK2 Promotes the Progression of Ovarian Carcinoma through the PI3K/PDK1/Akt Axis

Author:

Chen Zhen1,Sun Xingxing2ORCID,Xia Zhiyan2,Wang Jihong2,Guo Nan3,Zhang Yi2

Affiliation:

1. Taizhou Hospital of Zhejiang Province affiliated to Wenzhou Medical University, Luqiao, Zhejiang 318050, China

2. Wuhan Economic Development Zone (Hannan) People's Hospital, The department of obstetrics and gynecology, Wuhan, Hubei 430090, China

3. Gaochun people's Hospital of Nanjing City, The department of obstetrics and gynecology, Nanjing, Jiangsu 211302, China

Abstract

Objective. To explore the functional role of Calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) in the progression of ovarian carcinoma (OC). Methods. RT-qPCR analysis and western blot were conducted to detect the mRNA and protein expression of CaMKK2, PI3K, PDK1 and Akt in OC tissues and cells, respectively. CCK-8 assay, transwell migration assay and flow cytometry were used to measure cell proliferation, migration and apoptosis, respectively. Results. CaMKK2, PI3K, PDK1 and Akt were highly expressed in OC tissues compared with the corresponding controls. CaMKK2 knockdown significantly suppressed the mRNA and protein expression of PI3K, PDK1 and Akt in HO8910 and OV90 cells. Moreover, CaMKK2 knockdown could dramatically repress cell proliferation, migration, and markedly elevate cell apoptosis in HO8910 and OV90 cells. Conclusions. CaMKK2 played a promotion role in OC progression via activating the PI3K/PDK1/Akt axis.

Funder

Independent Scientific Research Project of Wuhan Hannan District People’s Hospital

Publisher

Hindawi Limited

Subject

Applied Mathematics,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Modeling and Simulation,General Medicine

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