ArticleMolecular neurobiology2016
TGF-β Regulates Survivin to Affect Cell Cycle and the Expression of EGFR and MMP9 in Glioblastoma.
Article in Molecular neurobiology, 2016. 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 It has been retracted, and should not be counted.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 9 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
9 citing papers in PubMed, 26 citations in OpenAlex.
- Significance of combined TGF-β1 and survivin expression on the prognosis of patients with triple-negative breast cancer.Oncology letters · 2022Article
- TGF-β1 and its signal molecules: are they correlated with the elasticity characteristics of breast lesions?BMC cancer · 2021Article
- Cell-to-cell communication mediates glioblastoma progression inBiology open · 2020Article
- Brain-Derived Neurotrophin and TrkB in Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2019Article
- The interplay between AR, EGF receptor and MMP-9 signaling pathways in invasive prostate cancer.Molecular medicine (Cambridge, Mass.) · 2018Article
- Knockdown of long non-coding RNA PVT1 induces apoptosis and cell cycle arrest in clear cell renal cell carcinoma through the epidermal growth factor receptor pathway.Oncology letters · 2018Article
- Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 editing inhibits epithelial to mesenchymal transition in ovarian cancer cells.Oncotarget · 2017Article
- TGFβ-Responsive HMOX1 Expression Is Associated with Stemness and Invasion in Glioblastoma Multiforme.Stem cells (Dayton, Ohio) · 2016Article
- Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies.Journal of Cancer · 2016Review
Corrections and comments
- Retraction · 2017-05-06Compromised Peer Review · Plagiarism of/in Article ·
- Retracted
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor beta (TGF-β) is suggestive of a molecular target for cancer therapy due to its involvement in cell cycle, differentiation, and morphogenesis. Meanwhile, survivin is identified as an apoptosis inhibitor and involved in tumorgenesis. Here, we aimed to investigate the potential associations between TGF-β and survivin in glioblastoma U87 cell line. Survivin small interfering RNA (siRNA), Western blotting, and cell cycle analysis were introduced to detect relevant proteins in TGF-β pathways. In this study, we observed a concentration- and time-dependent increase of survivin expression after treatment with TGF-β1. However, the kinase inhibitors U0126 and LY294002 inhibited the upregulation of survivin in comparison with DMSO. In addition, survivin siRNA effectively abrogated survivin expression in U87 cells, therefore affected cells' entry into the S phase of cell cycle, and then repressed the expression of epidermal growth factor receptor (EGFR) and matrix metalloproteinase 9 (MMP9) in comparison with non-transfection. In conclusion, the present study shows that TGF-β upregulates survivin expression via ERK and PI3K/AKT pathway, leading to glioblastoma cell cycle progression. Thus, the blockade of survivin will allow for the treatment of glioblastoma, partially attributing to the inhibition of EGFR and MMP9 expression.
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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.