Evidence map›Paper›PMID 36604141›Full record

ArticleActa biochimica et biophysica Sinica2022

Caveolin-1-deficient fibroblasts promote migration, invasion, and stemness via activating the TGF-β/Smad signaling pathway in breast cancer cells.

Qingyun Huang, Longyuan Wu, Yi Wang, Xinyu Kong, Xinhua Xiao, Qiyuan Huang, Miao Li, Yujia Zhai, Fuxiu Shi, Ruichen Zhao and 2 more

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Qingyun HuangDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Longyuan WuDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Yi WangDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Xinyu KongDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Xinhua XiaoThe First Affiliated Hospital, Nanchang University, Nanchang 330006, China.
Qiyuan HuangDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Miao LiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Yujia ZhaiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Fuxiu ShiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Ruichen ZhaoDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Junpei ZhongDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Lixia XiongDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, China.
Nanchang University · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) represent one of the main components in the tumor stroma and play a key role in breast cancer progression. Transforming growth factor-β (TGF-β) has been established to mediate breast cancer metastasis by regulating the epithelial-mesenchymal transition (EMT) and stemness of cancer cells. Caveolin-1 (CAV-1) is a scaffold protein of caveolae that is related to the proliferation and metabolism of cancer cells. It is now well demonstrated that CAV-1 deficiency in the tumor stroma is positively correlated with distant metastasis, but the mechanism remains unclear. Here, we explore whether CAV-1-deficient fibroblasts play an essential role in the EMT and stemness of breast cancer cells (BCCs) through TGF-β signaling. We establish a specific small interfering RNA (siRNA) to inhibit CAV-1 expression in fibroblasts and coculture them with BCCs to investigate the effect of CAV‑1-deficient fibroblasts and the tumor microenvironment on breast cancer progression. This study refreshingly points out that CAV-1 deficiency in fibroblasts enhances TGF-β1 secretion and then activates the TGF-β1/Smad signaling pathway of BCCs, thus promoting the metastasis and stemness of BCCs. Collectively, our findings indicate an unexpected role of CAV-1 deficiency in fibroblasts and the tumor microenvironment as a permissive factor, which is regulated by the TGF-β1 signaling pathway in BCCs.

Indexed as

Breast NeoplasmsCaveolin 1Cell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleFibroblastsHumansSignal TransductionTransforming Growth Factor betaTransforming Growth Factor beta1Tumor MicroenvironmentCAV1 protein, humanCaveolin 1Transforming Growth Factor betaTransforming Growth Factor beta1breast neoplasmscancer-associated fibroblastscaveolin 1epithelial-mesenchymal transitiontransforming growth factor-β

Identifiers

PMID36604141
PMCPMC9827800
OpenAlexW4304759491

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.