Reversal of obesity-driven aggressiveness of endometrial cancer by metformin.

Metformin endometrial cancer metabolomics obesity proliferation

Journal

American journal of cancer research
ISSN: 2156-6976
Titre abrégé: Am J Cancer Res
Pays: United States
ID NLM: 101549944

Informations de publication

Date de publication:
2019
Historique:
received: 11 09 2019
accepted: 20 09 2019
entrez: 14 11 2019
pubmed: 14 11 2019
medline: 14 11 2019
Statut: epublish

Résumé

Obesity and diabetes are associated with increased risk and worse outcomes for endometrial cancer. Metformin is a widely prescribed generic drug for the treatment of type II diabetes and metabolic syndrome and may also have anti-tumorigenic effects. Thus, we assessed the metabolic anti-tumorigenic effects of metformin in (1) human endometrial cancer cell lines under varying glucose concentrations, and (2) a novel genetically engineered mouse model of endometrioid endometrial cancer under obese and lean conditions. The effects of metformin on cytotoxicity, apoptosis, cell cycle progression, and the AMPK/mTOR/S6 and MAPK pathways were assessed in ECC-1 and Ishikawa cells under low, normal and high glucose conditions. The impact of metformin treatment on tumor growth under obese and lean conditions was evaluated using a novel LKB1 Hypoglycemic conditions significantly enhanced the sensitivity of the cells to metformin in regards to its anti-proliferative and apoptotic effects, as compared to hyperglycemic and normal glucose conditions. Metformin inhibited tumor growth in both the obese and lean mice, which metformin-induced inhibition of tumor progression in obese mice was significantly greater than in lean mice. Metabolomic profiling in endometrial cancer tissues revealed significant differences between obese- and lean-mice. Enhanced energy metabolism was seen in obese- The obese state promoted tumor aggressiveness in the LKB1

Sections du résumé

BACKGROUND BACKGROUND
Obesity and diabetes are associated with increased risk and worse outcomes for endometrial cancer. Metformin is a widely prescribed generic drug for the treatment of type II diabetes and metabolic syndrome and may also have anti-tumorigenic effects. Thus, we assessed the metabolic anti-tumorigenic effects of metformin in (1) human endometrial cancer cell lines under varying glucose concentrations, and (2) a novel genetically engineered mouse model of endometrioid endometrial cancer under obese and lean conditions.
METHODS METHODS
The effects of metformin on cytotoxicity, apoptosis, cell cycle progression, and the AMPK/mTOR/S6 and MAPK pathways were assessed in ECC-1 and Ishikawa cells under low, normal and high glucose conditions. The impact of metformin treatment on tumor growth under obese and lean conditions was evaluated using a novel LKB1
RESULTS RESULTS
Hypoglycemic conditions significantly enhanced the sensitivity of the cells to metformin in regards to its anti-proliferative and apoptotic effects, as compared to hyperglycemic and normal glucose conditions. Metformin inhibited tumor growth in both the obese and lean mice, which metformin-induced inhibition of tumor progression in obese mice was significantly greater than in lean mice. Metabolomic profiling in endometrial cancer tissues revealed significant differences between obese- and lean-mice. Enhanced energy metabolism was seen in obese-
CONCLUSIONS CONCLUSIONS
The obese state promoted tumor aggressiveness in the LKB1

Identifiants

pubmed: 31720081
pmc: PMC6834476

Types de publication

Journal Article

Langues

eng

Pagination

2170-2193

Subventions

Organisme : NIDDK NIH HHS
ID : P30 DK056350
Pays : United States
Organisme : NCI NIH HHS
ID : R37 CA226969
Pays : United States

Informations de copyright

AJCR Copyright © 2019.

Déclaration de conflit d'intérêts

None.

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Auteurs

Hui Guo (H)

Department of Gynecologic Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences Jinan, Shandong, China.
Division of Gynecologic Oncology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.
School of Medicine and Life Sciences, University of Jinan, Shandong Academy of Medical Sciences Jinan, Shandong, China.

Weimin Kong (W)

Department of Gynecologic Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University Beijing, China.

Lu Zhang (L)

Department of Gynecologic Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences Jinan, Shandong, China.

Jianjun Han (J)

Department of Surgical Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences Jinan, Shandong, China.

Leslie H Clark (LH)

Division of Gynecologic Oncology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.

Yajie Yin (Y)

Division of Gynecologic Oncology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.

Ziwei Fang (Z)

Department of Gynecologic Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University Beijing, China.

Wenchuan Sun (W)

Division of Gynecologic Oncology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.

Jiandong Wang (J)

Department of Gynecologic Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University Beijing, China.

Timothy P Gilliam (TP)

Division of Gynecologic Oncology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.

Douglas Lee (D)

Omic Insight Durham, NC, USA.

Liza Makowski (L)

Division of Hematology and Oncology, Department of Medicine, University of Tennessee Health Science Center Memphis, TN, USA.

Chunxiao Zhou (C)

Division of Gynecologic Oncology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.

Victoria L Bae-Jump (VL)

Division of Gynecologic Oncology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.

Classifications MeSH