Evidence map›Paper›PMID 26716641›Full record

ArticleOncotarget2016

Autophagy is involved in TGF-β1-induced protective mechanisms and formation of cancer-associated fibroblasts phenotype in tumor microenvironment.

Fang-Lan Liu, En-Pan Mo, Liu Yang, Jun Du, Hong-Sheng Wang, Huan Zhang, Hiroshi Kurihara, Jun Xu, Shao-Hui Cai

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Review
  3. Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Plant extract fromHeliyon · 2023
    Article
  11. Review
  12. Article
  13. Transforming growth factor-β in tumour development.Frontiers in molecular biosciences · 2022
    Review
  14. An Overview of Autophagy inFrontiers in cellular and infection microbiology · 2022
    Review
  15. Breast Cancer CAFs: Spectrum of Phenotypes and Promising Targeting Avenues.International journal of molecular sciences · 2021
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 2 institutions in 1 country.

Fang-Lan LiuPharmacy College, Jinan University, Guangzhou 510632, China.
En-Pan MoPharmacy College, Jinan University, Guangzhou 510632, China.
Liu YangPharmacy College, Jinan University, Guangzhou 510632, China.
Jun DuPharmacy College, Sun Yat-Sen University, Guangzhou 510405, China.
Hong-Sheng WangPharmacy College, Sun Yat-Sen University, Guangzhou 510405, China.
Huan ZhangPharmacy College, Jinan University, Guangzhou 510632, China.
Hiroshi KuriharaPharmacy College, Jinan University, Guangzhou 510632, China.
Jun XuPharmacy College, Jinan University, Guangzhou 510632, China.
Shao-Hui CaiPharmacy College, Jinan University, Guangzhou 510632, China.
Jinan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-β1 (TGF-β1) present in tumor microenvironment acts in a coordinated fashion to either suppress or promote tumor development. However, the molecular mechanisms underlying the effects of TGF-β1 on tumor microenvironment are not well understood. Our clinical data showed a positive association between TGF-β1 expression and cancer-associated fibroblasts (CAFs) in tumor microenvironment of breast cancer patients. Thus we employed starved NIH3T3 fibroblasts in vitro and 4T1 cells mixed with NIH3T3 fibroblasts xenograft model in vivo to simulate nutritional deprivation of tumor microenvironment to explore the effects of TGF-β1. We demonstrated that TGF-β1 protected NIH3T3 fibroblasts from Star-induced growth inhibition, mitochondrial damage and cell apoptosis. Interestingly, TGF-β1 induced the formation of CAFs phenotype in starvation (Star)-treated NIH3T3 fibroblasts and xenografted Balb/c mice, which promoted breast cancer tumor growth. In both models, autophagy agonist rapamycin increased TGF-β1-induced protective effects and formation of CAFs phenotypes, while autophagy inhibitor 3-methyladenine, Atg5 knockdown or TGF-β type I receptor kinase inhibitor LY-2157299 blocked TGF-β1 induced these effects. Taken together, our results indicated that TGF-β/Smad autophagy was involved in TGF-β1-induced protective effects and formation of CAFs phenotype in tumor microenvironment, which may be used as therapy targets in breast cancer.

Indexed as

AutophagyAnimalsApoptosisBlotting, WesternBreast NeoplasmsCell ProliferationCell Transformation, NeoplasticFemaleFibroblastsGene Expression Regulation, NeoplasticHumansImmunoenzyme TechniquesMembrane Potential, MitochondrialMiceMice, Inbred BALB CNIH 3T3 CellsProtective AgentsRNA, MessengerTransforming Growth Factor beta1autophagycancer-associated fibroblastsmitochondriaTGF-β1tumor microenvironment

Identifiers

PMID26716641
PMCPMC4826194
OpenAlexW2214896346

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.