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Nfe2l1- silenced insulinoma cells acquire aggressiveness and chemoresistance
Journal article   Open access   Peer reviewed

Nfe2l1- silenced insulinoma cells acquire aggressiveness and chemoresistance

Jingqi Fu, Hongzhi Zheng, Qi Cui, Chengjie Chen, Simeng Bao, Jing Sun, Lu Li, Bei Yang, Huihui Wang, Yongyong Hou, …
Endocrine-related cancer, Vol.25(3), pp.185-200
03/2018
DOI: 10.1530/ERC-17-0458
PMID: 29203613
url
https://doi.org/10.1530/ERC-17-0458View
Published (Version of record) Open Access

Abstract

The transcription factor nuclear factor erythroid 2-like 1 (NFE2L1 or NRF1) is involved in various critical cell processes such as maintenance of ubiquitin-proteasome system and regulation of the cellular antioxidant response. We previously determined that pancreatic β-cell-specific -knockout mice had hyperinsulinemia and that silencing of in mouse islets or MIN6 insulinoma β-cells induced elevated basal insulin release and altered glucose metabolism. Hypoglycemia is a major issue with aggressive insulinomas, although a role of NFE2L1 in this pathology is not defined. In the present work, we studied the tumorigenicity of deficient insulinoma MIN6 cells ( -KD) and sensitivity to chemotherapy. -KD cells grew faster and were more aggressive than Scramble cells In a mouse allograft transplantation model, insulinomas arising from -KD cells were more aggressive and chemoresistant. The conclusion was amplified using streptozotocin (STZ) administration in an allograft transplantation model in diabetic Akita background mice. Furthermore, -KD cells were resistant to damage by the chemotherapeutic drugs STZ and 5-fluorouracil, which was linked to binding of hexokinase 1 with mitochondria, enhanced mitochondrial membrane potential and closed mitochondrial potential transition pore. Overall, both and data from -KD insulinoma cells provided evidence of a previously un-appreciated action of NFE2L1 in suppression of tumorigenesis. silencing desensitizes insulinoma cells and derived tumors to chemotherapeutic-induced damage, likely via metabolic reprograming. These data indicate that NFE2L1 could potentially play an important role in the carcinogenic process and impact chemosensitivity, at least within a subset of pancreatic endocrine tumors.
Animals Antineoplastic Agents - therapeutic use Apoptosis Cell Line, Tumor Drug Resistance, Neoplasm Fluorouracil - therapeutic use Gene Silencing Insulin-Secreting Cells - metabolism Insulinoma - drug therapy Insulinoma - genetics Insulinoma - metabolism Insulinoma - pathology Membrane Potential, Mitochondrial Mice Mice, Inbred C57BL Mice, Mutant Strains NF-E2-Related Factor 1 - genetics NF-E2-Related Factor 1 - metabolism Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Streptozocin - therapeutic use

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