Evidence map›Paper›PMID 30936596›Full record

ArticleIranian journal of medical sciences2019

Induction of Apoptosis by a Combination of 2-Deoxyglucose and Metformin in Esophageal Squamous Cell Carcinoma by Targeting Cancer Cell Metabolism.

Abbas Shafaee, Jalil Pirayesh Islamian, Davoud Zarei, Mohsen Mohammadi, Kazem Nejati-Koshki, Alireza Farajollahi, Seyed Mahmoud Reza Aghamiri, Mohammad Rahmati Yamchi, Behzad Baradaran, Mohammad Asghari Jafarabadi

Open access · greenAbstract read
In one paragraph

Article in Iranian journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Abbas ShafaeeDepartment of Radiology-Faculty of Paramedicine- Tabriz University of Medical Sciences, Tabriz, Iran.
Jalil Pirayesh IslamianDepartment of Medical Physics, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Davoud ZareiDepartment of Medical Radiation Science, School of Paramedicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohsen MohammadiDepartment of Medical Radiation Science, School of Paramedicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Kazem Nejati-KoshkiDepartment of Medical Biotechnology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Alireza FarajollahiDepartment of Medical Physics, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Seyed Mahmoud Reza AghamiriDepartment of Radiation Medicine, Faculty of Nuclear Engineering, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad Rahmati YamchiDepartment of Medical Biotechnology, Faculty of Advanced Medical Sciences, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Behzad BaradaranImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammad Asghari JafarabadiDepartment of Statistics and Epidemiology, Tabriz University of Medical Sciences, Tabriz, Iran.
Tabriz University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRZanjan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBoth mitochondrial dysfunction and aerobic glycolysis are signs of growing aggressive cancer. If altered metabolism of cancer cell is intended, using the glycolysis inhibitor (2-deoxyglucose (2DG)) would be a viable therapeutic method. The AMP-activated protein kinase (AMPK), as a metabolic sensor, could be activated with metformin and it can also launch a p53-dependent metabolic checkpoint and might inhibit cancer cell growth.

methodsAfter treatment with 5 mM metformin and/or 500 µM 2DG, the TE1, TE8, and TE11 cellular viability and apoptosis were assessed by MTT, TUNEL, and ELISA methods. The changes in p53 and Bcl-2 genes expression levels were examined using real-time PCR method. Data were analyzed by Kruskal-Wallis test using the SPSS 17.0 software.

resultsMetformin and 2DG, alone and in combination, induced apoptosis in the cell lines. Real-time PCR revealed that metformin induced apoptosis in TE8 and TE11 cells by activating p53, down-regulating Bcl-2 expression. The induced apoptosis by 2DG raised by metformin and the combination modulated the expression of Bcl-2 protein in all cell lines and it was more effective in TE11 cell line.

conclusionMetformin induced apoptosis in ESCC by down-regulating Bcl-2 expression, and up-regulating p53 and induced apoptosis increased by 2-deoxy-d-glucose. Thus, the combination therapy is an effective therapeutic strategy for esophageal squamous cell carcinoma.

Indexed as

2-Deoxy-D-GlucoseApoptosisEsophageal carcinomaMetformin

Identifiers

PMID30936596
PMCPMC6423430
OpenAlexW2906770778

What OpenQuestion holds

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LicenceCC BY-NC-SA
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.