ArticlePloS one2011
Up-regulation of sonic hedgehog contributes to TGF-β1-induced epithelial to mesenchymal transition in NSCLC cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 63 papers.
What it found
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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.
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.
Who cites it
63 citing papers in PubMed, 126 citations in OpenAlex.
- EWS/FLI1 Characterization, Activation, Repression, Target Genes and Therapeutic Opportunities in Ewing Sarcoma.International journal of molecular sciences · 2023Review
- 3-Hydroxybenzaldehyde and 4-Hydroxybenzaldehyde enhance survival of mouse astrocytes treated with Angiostrongylus cantonensis young adults excretory/secretory products.Biomedical journal · 2021Article
- Defining the Role of GLI/Hedgehog Signaling in Chemoresistance: Implications in Therapeutic Approaches.Cancers · 2021Review
- Sulforaphane inhibits self-renewal of lung cancer stem cells through the modulation of sonic Hedgehog signaling pathway and polyhomeotic homolog 3.AMB Express · 2021Article
- HEDGEHOG/GLI Modulates the PRR11-SKA2 Bidirectional Transcription Unit in Lung Squamous Cell Carcinomas.Genes · 2021Article
- The influences of TGF-β1 upon the human adenocarcinoma cell of lung A549 and cellular immunity.Annals of translational medicine · 2020Article
- The excretory/secretory products of fifth-stage larval Angiostrongylus cantonensis induces autophagy via the Sonic hedgehog pathway in mouse brain astrocytes.PLoS neglected tropical diseases · 2020Article
- Arsenic trioxide and curcumin attenuate cisplatin-induced renal fibrosis in rats through targeting Hedgehog signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Molecular Characterization and Functional Analysis of Leucine Zipper Transcription Factor Like 1 in Zebrafish (Frontiers in physiology · 2019Article
- Radon induced mitochondrial dysfunction in human bronchial epithelial cells and epithelial-mesenchymal transition with long-term exposure.Toxicology research · 2019Article
- Epithelial-Mesenchymal Transition and Metastasis under the Control of Transforming Growth Factor β.International journal of molecular sciences · 2018Review
- Cdh1 and Pik3ca Mutations Cooperate to Induce Immune-Related Invasive Lobular Carcinoma of the Breast.Cell reports · 2018Article
- A targeted transforming growth factor-beta (TGF-β) blocker, TTB, inhibits tumor growth and metastasis.Oncotarget · 2018Article
- Targeting GLI Transcription Factors in Cancer.Molecules (Basel, Switzerland) · 2018Review
- GP73 promotes invasion and metastasis of bladder cancer by regulating the epithelial-mesenchymal transition through the TGF-β1/Smad2 signalling pathway.Journal of cellular and molecular medicine · 2018Article
- Retraction: Up-Regulation of Sonic Hedgehog Contributes to TGF-β1-Induced Epithelial to Mesenchymal Transition in NSCLC Cells.PloS one · 2018Article
- Sulforaphane reverses gefitinib tolerance in human lung cancer cells via modulation of sonic hedgehog signaling.Oncology letters · 2018Article
- Metapristone (RU486 metabolite) suppresses NSCLC by targeting EGFR-mediated PI3K/AKT pathway.Oncotarget · 2017Article
- Stimulation of IL-1β and IL-6 through NF-κB and sonic hedgehog-dependent pathways in mouse astrocytes by excretory/secretory products of fifth-stage larval Angiostrongylus cantonensis.Parasites & vectors · 2017Article
- Anti‑fibrotic effect of Sedum sarmentosum Bunge extract in kidneys via the hedgehog signaling pathway.Molecular medicine reports · 2017Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2018-10-02Duplication of/in Image · Falsification/Fabrication of Image · Investigation by Company/Institution · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Original Data and/or Images not Provided and/or not Available · · Fazlul Sarkar has institutional finding of misconduct;
- Retracted
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung cancer, especially non-small cell lung cancer (NSCLC) is the major cause of cancer-related deaths in the United States. The aggressiveness of NSCLC has been shown to be associated with the acquisition of epithelial-to-mesenchymal transition (EMT). The acquisition of EMT phenotype induced by TGF-β1in several cancer cells has been implicated in tumor aggressiveness and resistance to conventional therapeutics; however, the molecular mechanism of EMT and tumor aggressiveness in NSCLC remains unknown. METHODOLOGY/PRINCIPAL
findingsIn this study we found for the first time that the induction of EMT by chronic exposure of A549 NSCLC cells to TGF-β1 (A549-M cells) led to the up-regulation of sonic hedgehog (Shh) both at the mRNA and protein levels causing activation of hedgehog signaling. These results were also reproduced in another NSCLC cell line (H2030). Induction of EMT was found to be consistent with aggressive characteristics such as increased clonogenic growth, cell motility and invasion. The aggressiveness of these cells was attenuated by the treatment of A549-M cells with pharmacological inhibitors of Hh signaling in addition to Shh knock-down by siRNA. The inhibition of Hh signaling by pharmacological inhibitors led to the reversal of EMT phenotype as confirmed by the reduction of mesenchymal markers such as ZEB1 and Fibronectin, and induction of epithelial marker E-cadherin. In addition, knock-down of Shh by siRNA significantly attenuated EMT induction by TGF-β1. CONCLUSIONS/SIGNIFICANCE: Our results show for the first time the transcriptional up-regulation of Shh by TGF-β1, which is mechanistically associated with TGF-β1 induced EMT phenotype and aggressive behavior of NSCLC cells. Thus the inhibitors of Shh signaling could be useful for the reversal of EMT phenotype, which would inhibit the metastatic potential of NSCLC cells and also make these tumors more sensitive to conventional therapeutics.
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Registered trials
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.