Dataset related to article: "A novel insight into the anticancer mechanism of metformin in pancreatic neuroendocrine tumor cells"
- 1. Laboratory of Cellular and Molecular Endocrinology, Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy
- 2. Endocrinology and Diabetology Unit Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy ANDDepartment of Biomedical Sciences, Humanitas University, Rozzano, Italy
- 3. Laboratory of Cellular and Molecular Endocrinology, Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy andDepartment of Biomedical Sciences, Humanitas University, Rozzano, Italy
- 4. Oncology Unit, Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy
- 5. Endocrinology and Diabetology Unit Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy
- 6. Department of Pathology, Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy
- 7. Pancreas Surgery Unit, Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy
- 8. Oncology Unit, Bolzano Hospital, Bolzano, Italy
- 9. Endocrinology and Diabetology Unit, IRCCS Ospedale Maggiore Policlinico, Milano, Italy
- 10. Laboratory of Cellular and Molecular Endocrinology, Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy; Endocrinology and Diabetology Unit Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy AND Department of Biomedical Sciences, Humanitas University, Rozzano, Italy
Description
This record contains data related to article: "A novel insight into the anticancer mechanism of metformin in pancreatic neuroendocrine tumor cells."
The antidiabetic drug metformin displays anticancer properties in several neoplasms. In pituitary NETs, aryl
hydrocarbon receptor-interacting protein (AIP) is up-regulated by the somatostatin analog octreotide.
Metformin inhibited QGP-1 cell proliferation in a dose- and time-dependent manner, at concentrations similar
to those achievable in treated patients (−31 ± 12%, p < 0.05 vs basal at 100 μM). Moreover, metformin
decreased pancreatic neuroendocrine tumors (PAN-NETs) cell proliferation (−62 ± 15%, p < 0.0001 vs basal
at 10 mM), without any additive effect when combined with octreotide. Both octreotide and metformin induced
AIP up-regulation. AIP silencing abolished the reduction of mTOR phosphorylation induced by metformin and
octreotide. Moreover, metformin decreased HSP70, increased Zac1 and AhR expression; these effects were
abolished in AIP silenced QGP-1 cells.
In conclusion, metformin acts as an anticancer agent in PAN-NET cells, its activity is mediated by AIP and its
interacting proteins. These findings provide a novel insight into the antitumorigenic mechanism of metformin.
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Related works
- Is supplement to
- 10.1016/j.mce.2020.110803 (DOI)
- 32251713 (PMID)