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86P - Pim1 promotes ovarian cancer growth and the Warburg effect via c-Myc-glycolysis signaling axis

Presentation Number
86P
Lecture Time
17:10 - 17:10
Speakers
  • Yong Wu (Shanghai, CN)
Session Name
Location
Foyer La Scene, Paris Marriott Rive Gauche, Paris, France
Date
05.03.2018
Time
17:10 - 18:00
Authors
  • Yong Wu (Shanghai, CN)
  • Yu Deng (Shanghai, CN)
  • Ya C. Duan (Shanghai, CN)
  • Shao J. Wang (Kunming, CN)
  • Jia J. Li (Shanghai, CN)
  • Jun Zhu (Shanghai, CN)
  • Wei W. Weng (Shanghai, CN)
  • Xiao H. Wu (Shanghai, CN)

Abstract

Background

Ovarian cancer (OC) is the second most common gynecologic malignancy, but its mortality ranks the highest in the world. Pim1, belongs to a group of constitutively activated serine/threonine kinases, has been reported in many types of cancer. Little is known about Pim1 in OC.

Methods

The protein expression of Pim1 was verified from the human protein atlas (www.proteinatlas.org), as well as ovarian cancer cell lines, and its association with survival were then analysed by bioinformatic analysis. CCK-8 assay and colony formation were used to measure cell proliferation. In order to evaluate the mechanism of Pim1 in HGSOC, Extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) and Lactate analysis were performed to find that Pim1 maintains Warburg effect via c-Myc-glycolysis signaling axis. In Vivo subcutaneous xenograft inoculation was also performed to certify its role.

Results

Silencing/overexpressing of Pim1 suppressed/promoted OC cells proliferation in vitro. Pim1 significantly influenced glycolysis by OC cells and was associated with p-c-myc protein levels and subsequent c-myc regulated key enzymes (such as PGK1, LDHA) in the glycolytic pathway. Pim1-knockdown also inhibited ovarian tumor growth in vivo. Moreover, Pim1 inhibitor SMI4a exerted chemosensitizing effects on cisplatin. Pim1 was also overexpressed in ovarian cancer and correlated with the poor overall survival of patients by bioinformatics analysis.

Conclusions

Together, these results suggest that Pim1 contributes to OC proliferation and glycolysis through p-c-myc axis, which may serve as a potential target for OC patients.

Legal entity responsible for the study

Fudan University Shanghai Cancer Center

Funding

Has not received any funding

Disclosure

All authors have declared no conflicts of interest.

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