Evidence map›Paper›PMID 32934344›Full record

ArticleBritish journal of cancer2020

OXPHOS-dependent metabolic reprogramming prompts metastatic potential of breast cancer cells under osteogenic differentiation.

Yangling Hu, Weimin Xu, Hui Zeng, Zilong He, Xiao Lu, Daming Zuo, Genggeng Qin, Weiguo Chen

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  6. Metabolism in Tumour-Induced Bone Disease.Current osteoporosis reports · 2026
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  14. Metabolic reprogramming in bone metastasis of human cancers.Frontiers in cell and developmental biology · 2025
    Review
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  16. Article
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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

8 authors at 2 institutions in 1 country.

Yangling Hu *Department of Radiology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China.
Weimin Xu *Department of Radiology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China.
Hui ZengDepartment of Radiology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China.
Zilong HeDepartment of Radiology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China.
Xiao LuDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Daming ZuoInstitute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, 510515, Guangzhou, China.
Genggeng QinDepartment of Radiology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China. zealotq@smu.edu.cn.ORCID http://orcid.org/0000-0002-7563-3924
Weiguo ChenDepartment of Radiology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China. chenweiguo1964@21cn.com.ORCID http://orcid.org/0000-0003-1552-0511
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicrocalcification is one of the most reliable clinical features of the malignancy risk of breast cancer, and it is associated with enhanced tumour aggressiveness and poor prognosis. However, its underlying molecular mechanism remains unclear.

methodsClinical data were retrieved to analyse the association between calcification and bone metastasis in patients with breast cancer. Using multiple human breast cancer cell lines, the osteogenic cocktail model was established in vitro to demonstrate calcification-exacerbated metastasis. Migration and invasion characteristics were determined by wound healing and transwell migration. mRNA and protein expression were identified by quantitative PCR and western blotting. Metabolic alterations in breast cancer cells were evaluated using Seahorse Analyser.

resultsThe osteogenic differentiation of human breast cancer cells activated the classical TGF-β/Smad signalling pathway and the non-canonical MAPK pathway, which, in turn, exacerbated the progression of epithelial-mesenchymal transition (EMT). The metabolic programme switched to enhancing mitochondrial oxidative phosphorylation (OXPHOS) upon osteogenic differentiation. Rotenone was used to inhibit the OXPHOS complex during osteogenesis to block mitochondrial function, consequently reversing the EMT phenotype.

conclusionsThis study provides important insights into the mechanisms involved in breast cancer bone metastasis, and outlines a possible strategy to intervene in OXPHOS for the treatment of breast tumours.

Indexed as

Oxidative PhosphorylationBreast NeoplasmsCalcinosisCell DifferentiationCellular ReprogrammingEpithelial-Mesenchymal TransitionFemaleHumansNeoplasm InvasivenessOsteogenesis

Identifiers

PMID32934344
PMCPMC7686370
OpenAlexW3087514165

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.