2,6-DMBQ is a novel mTOR inhibitor that reduces gastric cancer growth in vitro and in vivo.


Journal

Journal of experimental & clinical cancer research : CR
ISSN: 1756-9966
Titre abrégé: J Exp Clin Cancer Res
Pays: England
ID NLM: 8308647

Informations de publication

Date de publication:
09 Jun 2020
Historique:
received: 22 02 2020
accepted: 28 05 2020
entrez: 11 6 2020
pubmed: 11 6 2020
medline: 5 2 2021
Statut: epublish

Résumé

Fermented wheat germ extract has been reported to exert various pharmacological activities, including anti-oxidant, anti-cell growth and cell apoptosis in various cancer cells. Although 2,6-dimethoxy-1,4-benzoquinone (2,6-DMBQ) is a benzoquinone compound and found in fermented wheat germ extract, its anticancer effects and molecular mechanism(s) against gastric cancer have not been investigated. Anticancer effects of 2,6-DMBQ were determined by MTT, soft agar, cell cycle and Annexin V analysis. Potential candidate proteins were screened via in vitro kinase assay and Western blotting. mTOR knockdown cell lines were established by lentiviral infection with shmTOR. The effect of 2,6-DMBQ on tumor growth was assessed using gastric cancer patient-derived xenograft models. 2,6-DMBQ significantly reduced cell growth and induced G1 phase cell cycle arrest and apoptosis in gastric cancer cells. 2,6-DMBQ reduced the activity of mTOR in vitro. The inhibition of cell growth by 2,6-DMBQ is dependent upon the expression of the mTOR protein. Remarkably, 2,6-DMBQ strongly reduced patient-derived xenograft gastric tumor growth in an in vivo mouse model. 2,6-DMBQ is an mTOR inhibitor that can be useful for treating gastric cancer. It has therapeutic implications for gastric cancer patients.

Sections du résumé

BACKGROUND BACKGROUND
Fermented wheat germ extract has been reported to exert various pharmacological activities, including anti-oxidant, anti-cell growth and cell apoptosis in various cancer cells. Although 2,6-dimethoxy-1,4-benzoquinone (2,6-DMBQ) is a benzoquinone compound and found in fermented wheat germ extract, its anticancer effects and molecular mechanism(s) against gastric cancer have not been investigated.
METHODS METHODS
Anticancer effects of 2,6-DMBQ were determined by MTT, soft agar, cell cycle and Annexin V analysis. Potential candidate proteins were screened via in vitro kinase assay and Western blotting. mTOR knockdown cell lines were established by lentiviral infection with shmTOR. The effect of 2,6-DMBQ on tumor growth was assessed using gastric cancer patient-derived xenograft models.
RESULTS RESULTS
2,6-DMBQ significantly reduced cell growth and induced G1 phase cell cycle arrest and apoptosis in gastric cancer cells. 2,6-DMBQ reduced the activity of mTOR in vitro. The inhibition of cell growth by 2,6-DMBQ is dependent upon the expression of the mTOR protein. Remarkably, 2,6-DMBQ strongly reduced patient-derived xenograft gastric tumor growth in an in vivo mouse model.
CONCLUSIONS CONCLUSIONS
2,6-DMBQ is an mTOR inhibitor that can be useful for treating gastric cancer. It has therapeutic implications for gastric cancer patients.

Identifiants

pubmed: 32517736
doi: 10.1186/s13046-020-01608-9
pii: 10.1186/s13046-020-01608-9
pmc: PMC7285595
doi:

Substances chimiques

Benzoquinones 0
Biomarkers, Tumor 0
Protein Kinase Inhibitors 0
MTOR protein, human EC 2.7.1.1
TOR Serine-Threonine Kinases EC 2.7.11.1
2,6-dimethyl-1,4-benzoquinone HET5TF8ZGO

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

107

Subventions

Organisme : Henan Joint Fund
ID : U1804196
Organisme : National Natural Science Foundation China
ID : 81572812
Organisme : Key program of Henan Province, China
ID : 161100510300

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Auteurs

Xueyin Zu (X)

The Pathophysiology Department, The School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450008, Henan, China.
China-US (Henan) Hormel Cancer Institute, Zhengzhou, 450008, Henan, China.

Xiaoli Ma (X)

The Pathophysiology Department, The School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450008, Henan, China.
China-US (Henan) Hormel Cancer Institute, Zhengzhou, 450008, Henan, China.

Xiaomeng Xie (X)

The Pathophysiology Department, The School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450008, Henan, China.
China-US (Henan) Hormel Cancer Institute, Zhengzhou, 450008, Henan, China.

Bingbing Lu (B)

The Pathophysiology Department, The School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450008, Henan, China.
China-US (Henan) Hormel Cancer Institute, Zhengzhou, 450008, Henan, China.

Kyle Laster (K)

China-US (Henan) Hormel Cancer Institute, Zhengzhou, 450008, Henan, China.

Kangdong Liu (K)

The Pathophysiology Department, The School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450008, Henan, China.
China-US (Henan) Hormel Cancer Institute, Zhengzhou, 450008, Henan, China.
The Affiliated Cancer Hospital, Zhengzhou University, Zhengzhou, 450008, Henan, China.
The Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450008, Henan, China.

Zigang Dong (Z)

The Pathophysiology Department, The School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450008, Henan, China. zgdong@hci-cn.org.
China-US (Henan) Hormel Cancer Institute, Zhengzhou, 450008, Henan, China. zgdong@hci-cn.org.
The Affiliated Cancer Hospital, Zhengzhou University, Zhengzhou, 450008, Henan, China. zgdong@hci-cn.org.
The Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450008, Henan, China. zgdong@hci-cn.org.
International joint research center of cancer chemoprevention, Zhengzhou, China. zgdong@hci-cn.org.

Dong Joon Kim (DJ)

The Pathophysiology Department, The School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450008, Henan, China. djkim@hci-cn.org.
China-US (Henan) Hormel Cancer Institute, Zhengzhou, 450008, Henan, China. djkim@hci-cn.org.
The Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450008, Henan, China. djkim@hci-cn.org.

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Classifications MeSH