human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: BACKGROUND Epithelial mesenchymal transition ( EMT ) is known to be associated with chemoresistance as well as increased invasion/metastasis . However , the relationship between EMT and resistance to an epidermal growth factor receptor ( EGFR ) -targeting drug in head and neck squamous cell carcinoma ( HNSCC ) remains unknown . In this study , we investigated the acquisition of EMT by gefitinib in HNSCC cell line ( UMSCC81B ) . METHODS We isolated fibroblastoid variant ( 81B-Fb ) from gefitinib-resistant UMSCC81B-GR3 cells obtained after increasing the doses of gefitinib treatment in vitro and examined EMT and its underlying mechanism . RESULT 81B-Fb cells exhibited fibroblast-like morphology , increased motility , loss of E-cadherin , acquisition of vimentin and snail expression . In 81B-Fb cells , downregulation of EGFR , which is mediated by increased ubiquitination , and activation of downstream protein kinase B ( Akt ) , glycogen synthase kinase-beta ( GSK-3Î² ) signalling and upregulation of snail expression were observed compared with UMSCC81B cells . LY294002 , but not U0126 , suppressed foetal bovine serum or heregulin-Î²1-induced phosphorylation of Akt/GSK-3Î² and snail expression together with the inhibition of 81B-Fb cell motility . Furthermore , forced expression of EGFR resulted in partial restoration of gefitinib sensitivity and reversal of EMT . CONCLUSION These results suggest that EMT in the gefitinib-resistant cells is mediated by the downregulation of EGFR and compensatory activation of Akt/GSK-3Î²/snail pathway .
    OUTPUT:

agent
sustaining proliferative signaling;activating invasion and metastasis
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: BACKGROUND Epithelial mesenchymal transition ( EMT ) is known to be associated with chemoresistance as well as increased invasion/metastasis . However , the relationship between EMT and resistance to an epidermal growth factor receptor ( EGFR ) -targeting drug in head and neck squamous cell carcinoma ( HNSCC ) remains unknown . In this study , we investigated the acquisition of EMT by gefitinib in HNSCC cell line ( UMSCC81B ) . METHODS We isolated fibroblastoid variant ( 81B-Fb ) from gefitinib-resistant UMSCC81B-GR3 cells obtained after increasing the doses of gefitinib treatment in vitro and examined EMT and its underlying mechanism . RESULT 81B-Fb cells exhibited fibroblast-like morphology , increased motility , loss of E-cadherin , acquisition of vimentin and snail expression . In 81B-Fb cells , downregulation of EGFR , which is mediated by increased ubiquitination , and activation of downstream protein kinase B ( Akt ) , glycogen synthase kinase-beta ( GSK-3Î² ) signalling and upregulation of snail expression were observed compared with UMSCC81B cells . LY294002 , but not U0126 , suppressed foetal bovine serum or heregulin-Î²1-induced phosphorylation of Akt/GSK-3Î² and snail expression together with the inhibition of 81B-Fb cell motility . Furthermore , forced expression of EGFR resulted in partial restoration of gefitinib sensitivity and reversal of EMT . CONCLUSION These results suggest that EMT in the gefitinib-resistant cells is mediated by the downregulation of EGFR and compensatory activation of Akt/GSK-3Î²/snail pathway .
    OUTPUT:
