2020
DOI: 10.1038/s41598-020-61341-3
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Author Correction: Chronic IL-1β-induced inflammation regulates epithelial-to-mesenchymal transition memory phenotypes via epigenetic modifications in non-small cell lung cancer

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Cited by 14 publications
(8 citation statements)
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“…signaling by activating multiple pathways (63)(64)(65)(66). Recently IL-1b has been shown to promote EMT via epigenetic modifications in non-small cell lung cancer (67).…”
Section: Cytokines In Cancer Metastasis and Invasionmentioning
confidence: 99%
“…signaling by activating multiple pathways (63)(64)(65)(66). Recently IL-1b has been shown to promote EMT via epigenetic modifications in non-small cell lung cancer (67).…”
Section: Cytokines In Cancer Metastasis and Invasionmentioning
confidence: 99%
“…28 TLR4 was pivotal promoter of inflammation which related NF-kB and C3 signaling, and then released TNF-α and ILs, which can induce apoptosis of osteosarcoma cells. 10,11,31,32 However, whether the role of COLEC12 for inflammation in osteosarcoma is regulated by TLR4…”
Section: F I G U R Ementioning
confidence: 99%
“…[7][8][9] TNF-α and ILs are pro-inflammatory cytokines produced by lymphocytes and macrophages, which can induce apoptosis of tumor cells and are associated with the progression of several types of tumors, including OS. 10,11 In addition, TNF-α and ILs are transcriptionally controlled by NF-kB and C3 signaling 12,13 ; therefore, searching the upstream key factors to regulate the inflammatory response may be a vital step in the treatment of osteosarcoma.…”
mentioning
confidence: 99%
“…A signal for modulation of interferon alpha and gamma signalling may reflect a reduction in the non-Type 2 component of the inflammatory CRS response ( 14 ), where persistently high levels of interferon exert detrimental effects by impairing strength and coordination of subsequent immune responses and hampering cellular function ( 15 ). These changes can contribute to the development of epithelial to mesenchymal transition characteristic of CRS ( 16 ). Moreover, high levels of Type 1 inflammatory mediators is associated with a functional defect in epithelial repair in respiratory epithelial cells ( 17 ).…”
Section: Discussionmentioning
confidence: 99%