Evidence map›Paper›PMID 26986571›Full record

ArticleOncology reports2016

Anticancer effect of metformin on estrogen receptor-positive and tamoxifen-resistant breast cancer cell lines.

Jinkyoung Kim, Jiyun Lee, Soon Young Jang, Chungyeul Kim, Yoojin Choi, Aeree Kim

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Targeting Estrogen Receptor for Breast Cancer.Current issues in molecular biology · 2026
    Review
  3. Metformin-Induced Receptor Turnover Alters Antibody Accumulation in HER-Expressing Tumors.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2023
    Article
  4. Article
  5. Article
  6. Metformin reverses tamoxifen resistance through theAnnals of translational medicine · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. A prospective study of type 2 diabetes, metformin use, and risk of breast cancer.Annals of oncology : official journal of the European Society for Medical Oncology · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Jinkyoung KimDepartment of Pathology, Korea University Guro Hospital, Guro-gu, Seoul 08308, Republic of Korea.
Jiyun LeeDepartment of Pathology, College of Medicine, Korea University, Seongbuk-gu, Seoul 02841, Republic of Korea.
Soon Young JangDepartment of Pathology, College of Medicine, Korea University, Seongbuk-gu, Seoul 02841, Republic of Korea.
Chungyeul KimDepartment of Pathology, Korea University Guro Hospital, Guro-gu, Seoul 08308, Republic of Korea.
Yoojin ChoiDepartment of Pathology, Korea University Guro Hospital, Guro-gu, Seoul 08308, Republic of Korea.
Aeree KimDepartment of Pathology, Korea University Guro Hospital, Guro-gu, Seoul 08308, Republic of Korea.
Korea University Medical Center · KRKorea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquisition of tamoxifen resistance (TR) during anti-estrogenic therapy using tamoxifen is a major obstacle in the treatment of estrogen receptor (ER)-positive breast cancer. As a biguanide derivative, metformin is commonly used to treat type II diabetes. It has recently emerged as a potential anticancer agent. The objective of the present study was to investigate the anticancer activity of metformin in relation to ERα expression and its signaling pathway in ERα-positive MCF-7 and MDA-MB-361 breast cancer cells as well as TR MCF-7 breast cancer cells. Metformin inhibited both protein and mRNA levels of ERα in the presence or absence of estrogen (E2) in the MCF-7, TR MCF-7 and MDA-MB-361 cells. Metformin repressed E2-inducible estrogen response element (ERE) luciferase activity, protein levels and mRNA levels of E2/ERα-regulated genes [including c-Myc, cyclin D1, progesterone receptor (PR) and pS2] to a greater degree than tamoxifen, resulting in inhibition of cell proliferation of MCF-7, TR MCF-7 and MDA-MB-361 cells. Collectively, our results suggest that one of the anticancer mechanisms of metformin could be attributable to the repression of expression and transcriptional activity of ERα. Metformin may be a good therapeutic agent for treating ERα-positive breast cancer by inhibiting the expression and function of ERα. In addition, metformin may be useful to treat tamoxifen-resistant breast cancer.

Indexed as

Antineoplastic Agents, HormonalBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmDrug SynergismEstradiolEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansInhibitory Concentration 50MCF-7 CellsMetforminTamoxifenTranscriptional ActivationAntineoplastic Agents, HormonalESR1 protein, humanEstradiolEstrogen Receptor alphaMetforminTamoxifen

Identifiers

PMID26986571
PMCPMC4811404
OpenAlexW2295697823

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.