Evidence map›Paper›PMID 27765901›Full record

ArticleOncotarget2016

A FASN-TGF-β1-FASN regulatory loop contributes to high EMT/metastatic potential of cisplatin-resistant non-small cell lung cancer.

Li Yang, Fuquan Zhang, Xin Wang, Ying Tsai, Kuang-Hsiang Chuang, Peter C Keng, Soo Ok Lee, Yuhchyau Chen

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 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.1field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
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  8. Article
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  16. The Interplay Between TGF-β Signaling and Cell Metabolism.Frontiers in cell and developmental biology · 2022
    Review
  17. Article
  18. Novel Insights on Lipid Metabolism Alterations in Drug Resistance in Cancer.Frontiers in cell and developmental biology · 2022
    Review
  19. Increased Expression of LIPC Is Associated with Aggressive Phenotype of Borrmann Type 4 Gastric Cancer.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2021
    Article
  20. Article
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.

Li YangDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Fuquan ZhangDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Xin WangDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Ying TsaiDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Kuang-Hsiang ChuangDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Peter C KengDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Soo Ok LeeDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Yuhchyau ChenDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
University of Rochester · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin-resistant A549CisR and H157CisR cell lines were developed by treating parental A549 (A549P) and H157 (H157P) cells. These cisplatin-resistant cells showed slight growth retardation, but exhibited higher epithelial-mesenchymal transition (EMT) and increased metastatic potential compared to parental cells. We observed a highly up-regulated fatty acid synthase (FASN) level in A549CisR and H157CisR cells compared to parental cells and the up-regulation of FASN was also detected in A549P and H157P cells after short time treatment with cisplatin, suggesting that the high level of FASN in cisplatin-resistant cells may be from the accumulated cellular responses during cisplatin-resistance developmental process. We next investigated whether the inhibition of FASN by using a specific FASN inhibitor, cerulenin, can influence growth and EMT/metastatic potential of A549CisR and H157CisR cells. There was slight growth inhibition, but significantly reduced EMT/metastatic potential in cisplatin-resistant cells upon inhibitor treatment. The in vitro result was further investigated in orthotopic xenograft mouse models established with luciferase-tagged H157P and H157CisR cells. Mice were injected with cerulenin or vehicle after tumors were developed. No significant tumor regression was detected at the end of cerulenin treatment, but IHC staining showed higher expression of EMT/metastasis markers in H157CisR cell-derived tumors than H157P cell-derived tumors, and showed dramatic reduction of these markers in tumor tissues of cerulenin-treated mice, confirming the in vitro results. In mechanism dissection studies, we revealed the existence of the FASN-TGF-β1-FASN positive loop in A549CisR and H157CisR cells, but not in parental cells, which is believed to augment the FASN function in cisplatin-resistant cells.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorCisplatinFatty Acid Synthase, Type IFemaleHumansLung NeoplasmsMiceTransforming Growth Factor beta1Antineoplastic AgentsCisplatinFASN protein, humanFatty Acid Synthase, Type ITransforming Growth Factor beta1cisplatin-resistanceEMTfatty acid synthase (FASN)non-small cell lung cancerTGF-β1

Identifiers

PMID27765901
PMCPMC5342435
OpenAlexW2478866869

What OpenQuestion holds

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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.