Silencing of the interferon-inducible gene Ifi204/p204 induces resistance to interferon-γ-mediated cell growth arrest of tumor cells

Yamaguchi, Hana; Hiroi, Miki; Ohmori, Yoshihiro

doi:10.1016/j.cyto.2018.06.029

Cited by 6 publications

(4 citation statements)

References 71 publications

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“…Our results suggested that overexpression of KIF20A signi cantly reversed the effect of FOXM1 inhibition on the cell killing effect of PCa to docetaxel. Besides, increasing evidence indicated that cyclinA2, cyclin D1 and cyclin E1 were positively correlated with chemotherapy resistance development whereas knockdown or depletion of them inhibited cancer cell proliferation and promote apoptosis, resulting in the enhanced sensitivity to chemotherapeutic drugs [39][40][41]. In line with them, our data revealed that depletion of FOXM1 in PCa cells downregulated their expression, but partially recovered when KIF20A was upregulated.…”

Section: Discussionsupporting

confidence: 70%

FOXM1 modulates docetaxel resistance in prostate cancer by regulating KIF20A

Yu¹,

Xu²,

wang

et al. 2020

Preprint

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Background：Resistance to docetaxel is an important factor which affects the prognosis in advanced prostate cancer (PCa). The precise mechanisms remain unclear. The transcription factor Forkhead box M1 (FOXM1), participating in cell cycle progress and cell proliferation, has been reported to affect the sensitivity of chemotherapy. The present study aims to explore the role of FOXM1 in docetaxel resistance of PCa and how FOXM1 is associated with kinesin family member 20 A (KIF20A), which has been demonstrated to promote the development of therapeutic resistance in some cancers. Methods: We monitored cell growth by MTT and colony formation assays , and cell apoptosis and cell cycle through flow cytometry. Wound-healing and transwell assays were performed to detect cell migration and invasion. The mRNA and protein expression of gene were analyzed by by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting, respectively. We determined the binding of FOXM1 on the KIF20A promoter by the ChIP assay. Tumorigenicity in nude mice was employed to assess tumorigenicity in vivo. Results: FOXM1 knockdown induced cell apoptosis and G2/M cell cycle arrest, and suppressed cell migration and invasion in docetaxel-resistant PCa cell lines (DU145-DR and VCaP-DR). The opposite trend was found in their parental cells with exogenous FOXM1 overexpression. Furthermore, thiostrepton, a specific inhibitor for FOXM1, significantly attenuated docetaxel resistance in vitro and in vivo. Additionally, we found that FOXM1 and KIF20A were consistently overexpressed and highly correlated in PCa cells and tissues. Further studies demonstrated that FOXM1 regulated the expression of KIF20A at the transcriptional level directly through a Forkhead response element (FHRE) in its promoter. Moreover, KIF20A overexpression could partially reverse the effects of FOXM1 depletion on cell proliferation, cell cycle proteins (cyclinA2, cyclinD1 and cyclinE1) and apoptosis protein (bcl-2 and PARP). Conclusions: our findings suggest that highly expressed FOXM1 may promote docetaxel resistance partly through the induction of KIF20A expression and provide insights into novel chemotherapeutic strategies for docetaxel resistance in PCa.

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Section: Discussionsupporting

confidence: 70%

FOXM1 modulates docetaxel resistance in prostate cancer by regulating KIF20A

Yu¹,

Xu²,

wang

et al. 2020

Preprint

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“…We found overexpression of KIF20A reversed FOXM1 inhibition of the cell-killing effect of docetaxel in PCa. Increasing evidence indicates cyclin A2, cyclin D1 and cyclin E1 are positively correlated with the development of chemotherapy resistance, while the knockdown or depletion of these proteins inhibits cancer cell proliferation and promotes apoptosis, increasing sensitivity to chemotherapeutic drugs [39][40][41]. Our data revealed that depletion of FOXM1 in PCa cells downregulated these proteins, while KIF20A upregulation partially restored their expression.…”

Section: Discussionmentioning

confidence: 55%

FOXM1 modulates docetaxel resistance in prostate cancer by regulating KIF20A

Yu¹,

Xu²,

Guo

et al. 2020

Preprint

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Background: Docetaxel resistance affects prognosis in advanced prostate cancer (PCa). The precise mechanisms remain unclear. Transcription factor Forkhead box M1 (FOXM1), which participates in cell proliferation and cell cycle progression, has been reported to affect the sensitivity of chemotherapy. This study explores the role of FOXM1 in PCa docetaxel resistance and its association with kinesin family member 20 A (KIF20A), which is known to promote therapeutic resistance in some cancers.Methods: We monitored cell growth using MTT and colony formation assays, and cell apoptosis and cell cycle progression using flow cytometry. Wound-healing and transwell assays were used to detect cell invasion and migration. mRNA and protein expression were analyzed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting. We monitored FOXM1 binding to the KIF20A promoter using a ChIP assay. Tumorigenicity in nude mice was used to assess in vivo tumorigenicity.Results: FOXM1 knockdown induced cell apoptosis and G2/M cell cycle arrest, suppressing cell migration and invasion in docetaxel-resistant PCa cell lines (DU145-DR and VCaP-DR). Exogenous FOXM1 overexpression was found in their parental cells. Specific FOXM1 inhibitor thiostrepton significantly weakened docetaxel resistance in vitro and in vivo. We also found that FOXM1 and KIF20A exhibited consistent and highly correlated overexpression in PCa cells and tissues. FOXM1 also regulated KIF20A expression at the transcriptional level by acting directly on a Forkhead response element (FHRE) in its promoter. KIF20A overexpression could partially reverse the effect on cell proliferation, cell cycle proteins (cyclinA2, cyclinD1 and cyclinE1) and apoptosis protein (bcl-2 and PARP) of FOXM1 depletion.Conclusions: Our findings indicate that highly expressed FOXM1 may help promote docetaxel resistance by inducing KIF20A expression, providing insight into novel chemotherapeutic strategies for combatting PCa docetaxel resistance.

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“…We found overexpression of KIF20A reversed FOXM1 inhibition of the cell-killing effect of docetaxel in PCa. Increasing evidence indicates cyclin A2, cyclin D1 and cyclin E1 are positively correlated with the development of chemotherapy resistance, while the knockdown or depletion of these proteins inhibits cancer cell proliferation and promotes apoptosis, increasing sensitivity to chemotherapeutic drugs [38][39][40]. Our data revealed that depletion of FOXM1 in PCa cells downregulated these proteins, while KIF20A upregulation partially restored their expression.…”

Section: Discussionmentioning

confidence: 56%

FOXM1 modulates docetaxel resistance in prostate cancer by regulating KIF20A

Guo

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background Docetaxel resistance affects prognosis in advanced prostate cancer (PCa). The precise mechanisms remain unclear. Transcription factor Forkhead box M1 (FOXM1), which participates in cell proliferation and cell cycle progression, has been reported to affect the sensitivity of chemotherapy. This study explores the role of FOXM1 in PCa docetaxel resistance and its association with kinesin family member 20 A (KIF20A), which is known to promote therapeutic resistance in some cancers. Methods We monitored cell growth using MTT and colony formation assays, and cell apoptosis and cell cycle progression using flow cytometry. Wound-healing and transwell assays were used to detect cell invasion and migration. mRNA and protein expression were analyzed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting. We monitored FOXM1 binding to the KIF20A promoter using a ChIP assay. Tumorigenicity in nude mice was used to assess in vivo tumorigenicity. Results FOXM1 knockdown induced cell apoptosis and G2/M cell cycle arrest, suppressing cell migration and invasion in docetaxel-resistant PCa cell lines (DU145-DR and VCaP-DR). Exogenous FOXM1 overexpression was found in their parental cells. Specific FOXM1 inhibitor thiostrepton significantly weakened docetaxel resistance in vitro and in vivo. We also found that FOXM1 and KIF20A exhibited consistent and highly correlated overexpression in PCa cells and tissues. FOXM1 also regulated KIF20A expression at the transcriptional level by acting directly on a Forkhead response element (FHRE) in its promoter. KIF20A overexpression could partially reverse the effect on cell proliferation, cell cycle proteins (cyclinA2, cyclinD1 and cyclinE1) and apoptosis protein (bcl-2 and PARP) of FOXM1 depletion. Conclusions Our findings indicate that highly expressed FOXM1 may help promote docetaxel resistance by inducing KIF20A expression, providing insight into novel chemotherapeutic strategies for combatting PCa docetaxel resistance.

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Silencing of the interferon-inducible gene Ifi204/p204 induces resistance to interferon-γ-mediated cell growth arrest of tumor cells

Cited by 6 publications

References 71 publications

FOXM1 modulates docetaxel resistance in prostate cancer by regulating KIF20A

FOXM1 modulates docetaxel resistance in prostate cancer by regulating KIF20A

FOXM1 modulates docetaxel resistance in prostate cancer by regulating KIF20A

FOXM1 modulates docetaxel resistance in prostate cancer by regulating KIF20A

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