Evidence map›Paper›PMID 32472219›Full record

ArticleCell biology and toxicology2021

UCP1 regulates ALDH-positive breast cancer stem cells through releasing the suppression of Snail on FBP1.

Fuchuang Zhang, Bingjie Liu, Qiaodan Deng, Dandan Sheng, Jiahui Xu, Xueyan He, Lixing Zhang, Suling Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Cell biology and toxicology, 2021. 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
1.4field-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, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Pleiotropic effects of DCLK1 in cancer and cancer stem cells.Frontiers in molecular biosciences · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Regulation of cancer stem cells in triple negative breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2021
    Review
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

8 authors at 1 institution in 1 country.

Fuchuang ZhangKey Laboratory of Breast Cancer in Shanghai, The Shanghai Key Laboratory of Medical Epigenetics, Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College, Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences, Cancer Institutes, Fudan University, Shanghai, 200032, China.
Bingjie LiuKey Laboratory of Breast Cancer in Shanghai, The Shanghai Key Laboratory of Medical Epigenetics, Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College, Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences, Cancer Institutes, Fudan University, Shanghai, 200032, China.
Qiaodan DengKey Laboratory of Breast Cancer in Shanghai, The Shanghai Key Laboratory of Medical Epigenetics, Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College, Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences, Cancer Institutes, Fudan University, Shanghai, 200032, China.
Dandan ShengKey Laboratory of Breast Cancer in Shanghai, The Shanghai Key Laboratory of Medical Epigenetics, Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College, Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences, Cancer Institutes, Fudan University, Shanghai, 200032, China.
Jiahui XuKey Laboratory of Breast Cancer in Shanghai, The Shanghai Key Laboratory of Medical Epigenetics, Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College, Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences, Cancer Institutes, Fudan University, Shanghai, 200032, China.
Xueyan HeKey Laboratory of Breast Cancer in Shanghai, The Shanghai Key Laboratory of Medical Epigenetics, Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College, Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences, Cancer Institutes, Fudan University, Shanghai, 200032, China.
Lixing ZhangKey Laboratory of Breast Cancer in Shanghai, The Shanghai Key Laboratory of Medical Epigenetics, Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College, Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences, Cancer Institutes, Fudan University, Shanghai, 200032, China. zhanglixing601@163.com.
Suling LiuKey Laboratory of Breast Cancer in Shanghai, The Shanghai Key Laboratory of Medical Epigenetics, Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College, Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences, Cancer Institutes, Fudan University, Shanghai, 200032, China. suling@fudan.edu.cn.
Fudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uncoupling protein 1 (UCP1) has been implicated in ameliorating metabolic related disorders, of which most symptoms are risk factors for breast cancer. Here, we found that UCP1 was obviously downregulated in basal-like breast cancer (BLBC) and was positively correlated with improved survival. However, the underlying regulatory mechanisms remain largely unknown. Our studies showed that UCP1 inhibited tumor progression via suppressing aldehyde dehydrogenase (ALDH)-positive breast cancer stem cell (BCSC) population in BLBC. Furthermore, we found that UCP1 induced the upregulation of fructose bisphosphatase 1 (FBP1) which was previously blocked by Snail overexpression, and UCP1 decreased ALDH-positive BCSCs via FBP1-dependent metabolic rewiring, which could be reversed by Snail overexpression. In addition, breast cancer cells co-cultured with UCP1-deficient adipocytes had increased proportion of ALDH-positive BCSCs, indicating a potential protection role of UCP1 in tumor microenvironment. These results suggested that UCP1 suppressed BCSCs through inhibiting Snail-mediated repression of FBP1, and that upregulation of UCP1 might be a previously undescribed therapeutic strategy for combating breast cancer. Graphical abstract.

Indexed as

AdipocytesAldehyde DehydrogenaseBreast NeoplasmsCarcinogenesisCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleFructose-BisphosphataseGlycolysisHumansNeoplasm InvasivenessNeoplastic Stem CellsSnail Family Transcription FactorsSurvival AnalysisAldehyde DehydrogenaseFBP1 protein, humanFructose-BisphosphataseSnail Family Transcription FactorsUncoupling Protein 1BCSCBreast cancerFBP1UCP1

Identifiers

PMID32472219
OpenAlexW3030285854

What OpenQuestion holds

Textmetadata
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.