Home Neoplasma 2018 Neoplasma Vol.65, No.1, p.81-88, 2018

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Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

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Neoplasma Vol.65, No.1, p.81-88, 2018

Title: KrasG12D-LOH promotes malignant biological behavior and energy metabolism of pancreatic ductal adenocarcinoma cells through the mTOR signaling pathway
Author: X. SHEN, L.G. CHANG, M.Y. HU, D. YAN, L.N. ZHOU, Y. MA, S.K. LING, Y.Q. FU, S.Y. ZHANG, B. KONG, P.L. HUANG

Abstract: Oncogenic Kras with loss of heterozygosity (LOH) is frequently detected in various tumours. However, the exact function and mechanism by which KrasG12D-LOH operates remain unclear. Therefore, the current study investigated the effect of KrasG12D-LOH on the malignant phenotype of pancreatic ductal adenocarcinoma (PDAC) cells. Our investigation revealed that KrasG12D-LOH is associated with increased proliferation, invasion and reduced apoptosis in PDAC cells. The results also exhibited enhanced glycolytic phenotype of KrasG12D-LOH PDAC cells. Hyperactive mTOR plays a significant role in the initiation and maintenance of tumors. To investigate the correlation between KrasG12D-LOH and mTOR, the mTOR signaling pathway was detected by western blot analysis. We found that KrasG12D-LOH up-regulated Akt, AMPK, REDD1 and mTOR in PDAC cells. In summary, our results demonstrated that KrasG12D-LOH promotes oncogenic Kras-induced PDAC by regulating energy metabolism and mTOR signaling pathway. These data may provide novel therapeutic perspectives for PDAC.

Keywords: KrasG12D, loss of heterozygosity, mTOR pathway, pancreatic cancer, energy metabolism
Published online: 11-Jan-2018
Year: 2018, Volume: 65, Issue: 1 Page From: 81, Page To: 88
doi:10.4149/neo_2018_170224N142
Price: 19.20 €






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