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

Zhen Chen | Zendy; Xingxing Sun | Zendy; Zhiyan Xia | Zendy; Jihong Wang | Zendy; Nan Guo | Zendy; Yi Zhang | Zendy

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

Author(s) -

Zhen Chen,

Xingxing Sun,

Zhiyan Xia,

Jihong Wang,

Nan Guo,

Yi Zhang

Publication year - 2022

Publication title -

computational and mathematical methods in medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.462

H-Index - 48

eISSN - 1748-6718

pISSN - 1748-670X

DOI - 10.1155/2022/7187940

Subject(s) - protein kinase b , pi3k/akt/mtor pathway , gene knockdown , cell growth , protein kinase a , biology , apoptosis , microbiology and biotechnology , cancer research , chemistry , kinase , phosphorylation , signal transduction , biochemistry

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.

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