Evidence map›Paper›PMID 40019720›Full record

ArticleBreast cancer (Tokyo, Japan)2025

Adipose-derived stem cells enhance the tumorigenic potential of pre-malignant breast epithelial cells through paracrine activation of PI3K-AKT pathway.

Qifeng Wu, Jinguang He, Tanja Herrler, Baofu Yu, Qimin Zhou, Danning Zheng, Xiaoxue Chen, Yangxuanyu Yan, Chuanchang Dai, Kai Liu and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Breast cancer (Tokyo, Japan), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Qifeng Wu *Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Jinguang He *Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Tanja Herrler *Berufsgenossenschaftliche Unfallklinik Murnau, Murnau, Germany.
Baofu YuDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Qimin ZhouDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Danning ZhengDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Xiaoxue ChenDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Yangxuanyu YanDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Chuanchang DaiDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Kai LiuDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China.
Gangming ZouGannan Medical University, Ganzhou City, Jiangxi, China.
Shengfang GeDepartment of Ophthalmology, Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai Ninth People's Hospital, Shanghai, China.
Yunbo QiaoDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China. ybqiao@shsmu.edu.cn.ORCID http://orcid.org/0000-0002-8391-5868
Qingfeng LiDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China. dr.liqingfeng@shsmu.edu.cn.
Jiao WeiDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200125, China. drweijiao@shsmu.edu.cn.

Funding

Key Research and Development Program of Jiangxi Province 20171BBG70006National Natural Science Foundation of China 81702727National Natural Science Foundation of China 81871572National Natural Science Foundation of China 82372546Natural Science Foundation of Jiangxi Province 20192BAB205063
6 · The paper itself

Abstract

backgroundAdipose-derived stem cells (ADSCs)-assisted fat grafting has emerged as a widely used procedure for breast reconstruction post mastectomy and for aesthetic augmentation. Given the limited cases of breast cancer following grafting, the oncological safety of this procedure remains controversial.

methodsThe effects of ADSCs on the oncogenic features of premalignant MCF-10AT cells were investigated using co-culture and xenograft models. We further evaluated the malignancy-promoting effect of ADSCs in a 7,12-Dimethylbenz(a)anthracene (DMBA)-induced breast cancer model. RNA-sequencing was performed on ADSCs, MCF-10AT cells, and ADSC-co-cultured MCF-10AT cells. Protein changes in ADSC/MCF-10AT co-culture medium and MCF-10AT cells were determined by proteomic analysis. Pathway inhibitors were used to investigate signaling pathways involved in the ADSC-induced oncogenic changes of MCF-10AT cells.

resultsWe found that ADSCs promoted the proliferation and migration of MCF-10AT cells, and co-injection of ADSCs increased the tumor incidence of MCF-10AT cells from 29% to 58% in nude mice. Additionally, grafted ADSCs significantly enhanced tumor incidence, growth, and distant metastasis in the DMBA-induced rats, while it could not induce tumorigenesis in normal breast tissues. Combined RNA-sequencing and proteomic analysis demonstrated that the paracrine factors secreted by ADSCs robustly activated the oncogenic PI3K-AKT signaling in MCF-10AT cells. We also revealed the auto-activated TGF-beta and Wnt pathways in co-cultured MCF-10AT cells, which may be synergistic in tumor formation and progression. As expected, blocking these pathways, especially the PI3K-AKT pathway, strongly diminished the promoting effects of ADSCs, suggesting their potential as therapeutic targets for ADSC grafting-associated breast tumors.

conclusionsOur data illustrated the synergistic effect between ADSC paracrine factors and MCF-10AT auto-activated pathways in the carcinogenesis of MCF-10AT cells through activation of the oncogenic PI3K-AKT pathway. Based on these findings, we strongly recommend pre-operative examinations for breast cancer risk factors before ADSC-associated transplantation.

Indexed as

Adipose TissueBreast NeoplasmsEpithelial CellsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktStem Cells9,10-Dimethyl-1,2-benzanthraceneAnimalsCarcinogenesisCell Line, TumorCell ProliferationCoculture TechniquesFemaleHumansMiceMice, Nude9,10-Dimethyl-1,2-benzanthracenePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAdipose-derived stem cellsBreast cancerMCF-10AT cellsPI3K–AKT pathwayTumorigenesis

Identifiers

PMID40019720
PMCPMC11993506

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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.