Evidence map›Paper›PMID 35355210›Full record

ArticleMolecular biology reports2022

Metformin resistant MDA-MB-468 cells exhibit EMT-like phenotype and increased migration capacity.

Sahika Cingir Koker, Banu Yalcin, Irem Dogan Turacli

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In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

7 citing papers in PubMed, 6 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

3 authors at 1 institution in 1 country.

Sahika Cingir KokerDepartment of Medical Biology, Ufuk University, Mevlana Bulvarı 86-88, 06520, Balgat, Ankara, Turkey. sahika.koker@gmail.com.ORCID http://orcid.org/0000-0002-8529-4532
Banu YalcinONTAL, Ufuk University, Mevlana Bulvarı 86-88, 06520, Balgat, Ankara, Turkey.
Irem Dogan TuracliDepartment of Medical Biology, Ufuk University, Mevlana Bulvarı 86-88, 06520, Balgat, Ankara, Turkey.
Ufuk University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMetformin is one of the most prescribed drugs for the treatment of type II diabetes. Its anti-proliferative effect is also taken advantage for the treatment of cancer. Despite many of the studies mentioning the positive effects of metformin in inhibiting the proliferation of cancer cells, there are also studies which questions this idea as well.

methodsIn this study, we investigated the most widely studied breast cancer cell lines, ER (+) MCF7 cells, TNBC MDA-MB-231 and MDA-MB-468 cells in terms of metastatic behavior under long-term metformin treatment. MCF7, MDA-MB-231 and MDA-MB-468 cells were gained resistant to metformin starting from 0.2 to 3.2 mM.

resultsCompared to MCF7 and MDA-MB-231 cell lines, we only observed dramatic changes in MDA-MB-468 cells whose morphology has been changed towards mesenchymal like phenotype. Moreover, migration capacity of these cells was also significantly increased which were validated at both mRNA and protein levels as well as wound healing assay. In addition to EMT like phenotype and increasing migration capacity of metformin resistant MDA-MB-468 cells, they exhibited less sensitivity to PI3K inhibitor.

conclusionsAll together, our data pointed out that, metformin's effects should be questioned depending on the subtype of the breast cancer that's to be treated.

Indexed as

Diabetes Mellitus, Type 2MetforminCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansPhenotypePhosphatidylinositol 3-KinasesMetforminPhosphatidylinositol 3-KinasesBreast cancerDrug resistanceEMTMetforminPI3K inhibitor

Identifiers

PMID35355210
OpenAlexW4225899931

What OpenQuestion holds

Texttitle and abstract
Read underepoch 390

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.