ArticleTechnology in cancer research & treatment2018
Study on Attenuating Angiogenesis and Epithelial-Mesenchymal Transition (EMT) of Non-Small Cell Lung Carcinoma (NSCLC) by Regulating MAGEC2.
Article in Technology in cancer research & treatment, 2018. 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 It has been retracted, and should not be counted.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 4 papers.
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.
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
4 citing papers in PubMed.
- Cancer/Testis Antigens as Targets for RNA-Based Anticancer Therapy.International journal of molecular sciences · 2023Review
- The effects of anti-PD-L1 monoclonal antibody on the expression of angiogenesis and invasion-related genes.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- Emerging roles of the MAGE protein family in stress response pathways.The Journal of biological chemistry · 2020Review
- MAGEC2 Correlates With Unfavorable Prognosis And Promotes Tumor Development In HCC Via Epithelial-Mesenchymal Transition.OncoTargets and therapy · 2019Article
Corrections and comments
- Retraction · 2023-12-18Concerns/Issues about Image · Concerns/Issues about Third Party Involvement · Duplication of/in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Investigation by Third Party · Manipulation of Images · Paper Mill · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/E44A65A14C31A61585FF65E3F4403A
- Retracted
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the role of MAGE family member C2 in angiogenesis and epithelial-mesenchymal transition of non-small cell lung carcinoma.
methodsThe Cancer Genome Atlas data set was analyzed to filter the highly expressed gene melanoma antigen family C2 in non-small cell lung carcinoma. Quantitative reverse transcription-polymerase chain reaction was performed to verify the overexpression of melanoma antigen family C2 in non-small cell lung carcinoma cell lines. Melanoma antigen family C2 complementary DNA and short hairpin RNA (shRNA) were transfected into SK-MES-1 cells to regulate melanoma antigen family C2 expression. Cell Counting Kit-8 assay, flow cytometry, wound healing assay, and Transwell assay were performed to investigate the effect of melanoma antigen family C2 on proliferation, apoptosis, migration, and invasion of SK-MES-1 cell line. Western blot was used to detect the expression of epithelial-mesenchymal transition markers. Enzyme-linked immunosorbent assay was performed to investigate the secretion of vascular endothelial growth factor, and tube formation assay was conducted to explore the effect of melanoma antigen family C2 on angiogenesis ability of the tumor. Tumor xenograft on nude mice and immunohistochemical/hematoxylin and eosin staining were also performed to detect the influence of melanoma antigen family C2 on growth and metastasis of non-small cell lung carcinoma cells.
resultsMelanoma antigen family C2 was highly expressed in non-small cell lung carcinoma cells; melanoma antigen family C2 promoted the expression of epithelial-mesenchymal transition-related proteins as well as enhance the secretion of vascular endothelial growth factor and promote angiogenesis; melanoma antigen family C2 promoted proliferation, migration, and invasion and suppressed apoptosis of non-small cell lung carcinoma cells. It could also facilitate growth and metastasis of non-small cell lung carcinoma in vivo.
conclusionMelanoma antigen family C2 was a critical factor of angiogenesis and epithelial-mesenchymal transition in non-small cell lung carcinoma.
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