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Oncol Lett. 2019 Feb;17(2):2473-2478. doi: 10.3892/ol.2018.9873. Epub 2018 Dec 28.

The role of the fat mass and obesity-associated protein in the proliferation of pancreatic cancer cells.

Author information

1
Department of Hepatobiliary Surgery, The Affiliated Jiangyin Hospital of Southeast University Medical College, Wuxi, Jiangsu 214400, P.R. China.
2
Department of Hepatic-Biliary-Pancreatic Center, Zhongda Hospital, Southeast University, Nanjing, Jiangsu 210009, P.R. China.

Abstract

Fat mass and obesity-associated (FTO) protein has been identified as a critical demethylase in regulating cellular mRNA stability by removing N6-methyladenosine (m6A) residues in mRNA. Even though the role of FTO in body energy metabolism has been well established, its role in cancer cell homeostasis remains unclear. In the present study, by using RNA interference, it was indicated that FTO is required for pancreatic cancer cell proliferation. Knockdown of FTO resulted in compromised proliferation of pancreatic cancer cells. Furthermore, DNA synthesis was compromised, followed by an increase in apoptosis in FTO small interfering RNA (siRNA)-treated cells. In terms of its underlying mechanism, FTO has been indicated to interact with MYC proto-oncogene, bHLH transcription factor and to enhance its stability by decreasing its m6A level. Therefore, the aforementioned observations indicate a novel mechanism for the regulation of pancreatic cancer cells by FTO, which may provide insight on pancreatic cancer treatment strategies.

KEYWORDS:

fat mass and obesity-associated protein; pancreatic cancer; proliferation

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