2021
DOI: 10.1016/j.bbrc.2021.07.086
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Set7/9 controls proliferation and genotoxic drug resistance of NSCLC cells

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Cited by 18 publications
(26 citation statements)
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“…The same overexpression pattern of SETD7 was observed in LCa vs. normal tissue (64 pairs of lung adenocarcinoma and adjacent non-tumour tissues) [67], which is in agreement with data analysed by Gu et al [32]. According to Daks et al, high SETD7 mRNA expression was associated with shorter survival probability (GSE11969-149 patients with non-small cell LCa, including 90 patients with adenocarcinomas) [63].…”
Section: Lung Cancersupporting
confidence: 83%
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“…The same overexpression pattern of SETD7 was observed in LCa vs. normal tissue (64 pairs of lung adenocarcinoma and adjacent non-tumour tissues) [67], which is in agreement with data analysed by Gu et al [32]. According to Daks et al, high SETD7 mRNA expression was associated with shorter survival probability (GSE11969-149 patients with non-small cell LCa, including 90 patients with adenocarcinomas) [63].…”
Section: Lung Cancersupporting
confidence: 83%
“…The Kontaki et al [38] and Lezina et al studies [41,65] focussed on two different processes regulated by E2F-1, and while they appear contradictory as to how SETD7 may impact E2F-1 activity, they both support SETD7 inhibition to improve sensitivity to DNA-damaging agents, which is in agreement with a more recent study by Daks et al [63] who showed that under genotoxic stress conditions induced by doxorubicin or etoposide, SETD7 knockout or knockdown, or methyltransferase activity inhibition by 2 mM (R)-PFI-2 resulted in increased sensitivity to chemotherapy with higher cell death and lower cell viability. (R)-PFI-2 also increased the sensitivity of primary-patient derived non-small LCa cells to doxorubicin, thus supporting the idea that SETD7-selective inhibitors could be used to enhance anti-cancer therapy [63]. Fu et al found that SETD7 positively regulates the activation of SHH signalling by methylating the full-length transcription activator GLI3 at K436 and K595 to improve GLI3 stability (K436) and DNA binding to the promoter regions (K595) of its downstream target GLI1.…”
Section: Lung Cancersupporting
confidence: 74%
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“…This points to Set7/9 as a potential tumor suppressor. Along with this notion, studies from several groups including ours also suggest that Set7/9 plays antiproliferative and tumor-protective roles in various cancers (7,15,56,57), including NSCLC (21,58).…”
Section: Discussionsupporting
confidence: 54%