2018
DOI: 10.1080/01616412.2018.1548724
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Forced FoxO1:S249V expression suppressed glioma cell proliferation through G2/M cell cycle arrests and increased apoptosis

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Cited by 12 publications
(7 citation statements)
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“…FOXO transcription factors are critical mediators of apoptosis in cytotoxic drugs, and FOXO1 silencing attenuates intracellular reactive oxygen species levels, thereby leading to drug resistance through a downstream target ( Goto and Takano, 2009 ). Forced FOXO1 suppresses the cell growth through G2/M cell cycle arrest and increases apoptosis in glioma ( Piao et al, 2019 ), whereas silencing of DANCR could repress the ubiquitination of FOXO1 in osteoblast differentiation and reduce the amount of DANCR bound to FOXO1 ( Tang et al, 2018 ). In this study, overexpression of FOXO1 decreased the viability of U251 and U251-Eto cells, accompanied with decreased IC 50 of the drug etoposide, whereas additional treatment with overexpression of DANCR restored the cytotoxic effect induced by FOXO1.…”
Section: Discussionmentioning
confidence: 99%
“…FOXO transcription factors are critical mediators of apoptosis in cytotoxic drugs, and FOXO1 silencing attenuates intracellular reactive oxygen species levels, thereby leading to drug resistance through a downstream target ( Goto and Takano, 2009 ). Forced FOXO1 suppresses the cell growth through G2/M cell cycle arrest and increases apoptosis in glioma ( Piao et al, 2019 ), whereas silencing of DANCR could repress the ubiquitination of FOXO1 in osteoblast differentiation and reduce the amount of DANCR bound to FOXO1 ( Tang et al, 2018 ). In this study, overexpression of FOXO1 decreased the viability of U251 and U251-Eto cells, accompanied with decreased IC 50 of the drug etoposide, whereas additional treatment with overexpression of DANCR restored the cytotoxic effect induced by FOXO1.…”
Section: Discussionmentioning
confidence: 99%
“…Consistent with this finding, the results of the microarray and RT-qPCR analyses performed in the present study demonstrated that miR-640 expression was upregulated in glioblastoma. In addition, the CCK-8, BrdU (41,42) and cell adhesion (43) assays were performed to determine the molecular mechanism of miR-640 in glioblastoma cells. The results of these experiments demonstrated that overexpression of miR-640 promoted the viability, proliferation and adhesion of glioblastoma cells, while interference with miR-640 inhibited the proliferation and adhesion of these cells.…”
Section: Discussionmentioning
confidence: 99%
“…Wei et al found that artesunate may cause cell cycle arrest by downregulating the expressions of CDK (cyclin-dependent kinases), cyclin D1, and cyclin B1, thereby inhibiting the proliferation of glioma cells (Wei et al 2020). Piao et al showed that CDK1 in cells can affect the nuclear export and activity of FKHR through serine phosphorylation, thereby affecting the occurrence and development of gliomas (Piao et al 2019). However, whether such a signal network exists in thyroid cancer remains to be studied.…”
Section: Discussionmentioning
confidence: 99%