Exogenous NO induces apoptosis of hepatocellular carcinoma cells via positive p38/JNK signaling pathway and negative ERK signaling pathways

Liu, Ling; Xing, Yihao; Cao, Mengyao; Xu, Jinglei; Chen, Jingjing

doi:10.1007/s11010-020-04032-x

Cited by 5 publications

(3 citation statements)

References 39 publications

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“…ERK1/2 is involved in the regulation of various cellular processes, including cell proliferation, migration, growth, differentiation, and tumor progression (45). In addition, inactivation of p-ERK1/2 is involved in cell apoptosis induced by pharmacological intervention (46). CDC25C is a novel MAPK ERK1/2 target.…”

Section: Discussionmentioning

confidence: 99%

Luteolin potentiates low‑dose oxaliplatin‑induced inhibitory effects on cell proliferation in gastric cancer by inducing G2/M cell cycle arrest and apoptosis

Chen

Zhu

et al. 2021

Oncol Lett

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Section: Discussionmentioning

confidence: 99%

Luteolin potentiates low‑dose oxaliplatin‑induced inhibitory effects on cell proliferation in gastric cancer by inducing G2/M cell cycle arrest and apoptosis

Chen

Zhu

et al. 2021

Oncol Lett

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“…PP2A is part of the important regulators of the ERK pathway through dephosphorylating tyrosine or threonine residue, resulting in down-regulation of their activities [10]. In our previous study, we found JS-K-released NO induced cell apoptosis through inhibition of Raf/MEK/ERK signaling pathway and caused the activation of PP2A [11,12]. In the present study, we aimed to assess the inhibition of CIP2A and dephosphorylated effect of PP2A on the ERK signaling pathway in JS-K-induced apoptosis.…”

Section: Introductionmentioning

confidence: 93%

A diazeniumdiolate-based NO donor induces apoptosis by modulating the CIP2A/PP2A/ERK signaling axis

Xing

et al. 2022

Preprint

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Cancerous inhibitor of protein phosphatase 2A(CIP2A) modulates the activity of protein phosphatase 2A (PP2A). PP2A is part of the principal regulators of MAPKs through dephosphorylating tyrosine or threonine residue, resulting in down-regulation of their activities. The present study aimed to assess the inhibition of CIP2A and dephosphorylated effect of PP2A on the ERK signaling pathway in JS-K-induced apoptosis. Cells were noticeably inhibited in a time- and concentration-dependent manner after treatment with JS-K. JS-K could cause an increase in Bax, a decrease in Bcl-2, and subsequent activation of caspase cascade through the release of NO. Meanwhile, JS-K stimulated a significant decrease of CIP2A expression whereas an enhancement of PP2A expression. Furthermore, the effects of JS-K on upregulation of PP2A, downregulation of phosphorylated ERK, and activation of cleaved-caspase-3 and cleaved-PARP were enhanced in CIP2A siRNA-interfered cells. However, overexpression of CIP2A could cancel the effects of JS-K on upregulation of PP2A, downregulation of phosphorylated ERK, and activation of cleaved-caspase-3 and cleaved-PARP. In addition, dephosphorylation of MEK, ERK, Elk-1, c-Myc, and c-Fos stimulated by JS-K was declined in PP2A siRNA cells. Conversely, overexpression of PP2A could strengthen the effects of d dephosphorylation of MEK, ERK, Elk-1, c-Myc, and c-Fos stimulated by JS-K. Simultaneously, the apoptotic cells were reduced in PP2A/C siRNA cells but increased in overexpression of PP2A cells. Taking together, JS-K as a diazeniumdiolate-based NO donor induces apoptosis by modulating the CIP2A/PP2A/ERK signaling axis.

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“…PP2A is part of the important regulators of the ERK pathway through dephosphorylating tyrosine or threonine residue, resulting in down-regulation of their activities [27]. In our previous study, we found JS-K-released NO induced cell apoptosis through inhibition of Raf/MEK/ERK signaling pathway and caused the activation of PP2A [8,9]. In the present study, we aimed to assess the inhibition of CIP2A and dephosphorylated effect of PP2A on the ERK signaling pathway in JS-K-induced apoptosis.…”

Section: Introductionmentioning

confidence: 99%

A diazeniumdiolate-based NO donor induces apoptosis by modulating the CIP2A/PP2A/ERK signaling axis

Xing

et al. 2022

Preprint

Self Cite

View full text Add to dashboard Cite

Cancerous inhibitor of protein phosphatase 2A (CIP2A) modulates the activity of protein phosphatase 2A (PP2A). PP2A is part of the principal regulators of MAPKs through dephosphorylating tyrosine or threonine residue, resulting in down-regulation of their activities. The present study aimed to assess the inhibition of CIP2A and dephosphorylated effect of PP2A on the ERK signaling pathway in JS-K-induced apoptosis. Cells were noticeably inhibited in a time- and concentration-dependent manner after treatment with JS-K. JS-K could cause an increase in Bax, a decrease in Bcl-2, and subsequent activation of caspase cascade through the release of NO. Meanwhile, JS-K stimulated a significant decrease of CIP2A expression whereas an enhancement of PP2A expression. Furthermore, the effects of JS-K on upregulation of PP2A, downregulation of phosphorylated ERK, and activation of cleaved-caspase-3 and cleaved-PARP were enhanced in CIP2A siRNA-interfered cells. However, overexpression of CIP2A could cancel the effects of JS-K on upregulation of PP2A, downregulation of phosphorylated ERK, and activation of cleaved-caspase-3 and cleaved-PARP. In addition, dephosphorylation of MEK, ERK, Elk-1, c-Myc, and c-Fos stimulated by JS-K was declined in PP2A siRNA cells. Conversely, overexpression of PP2A could strengthen the effects of d dephosphorylation of MEK, ERK, Elk-1, c-Myc, and c-Fos stimulated by JS-K. Simultaneously, the apoptotic cells were reduced in PP2A/C siRNA cells but increased in overexpression of PP2A cells. Taking together, JS-K as a diazeniumdiolate-based NO donor induces apoptosis by modulating the CIP2A/PP2A/ERK signaling axis.

show abstract

Exogenous NO induces apoptosis of hepatocellular carcinoma cells via positive p38/JNK signaling pathway and negative ERK signaling pathways

Cited by 5 publications

References 39 publications

Luteolin potentiates low‑dose oxaliplatin‑induced inhibitory effects on cell proliferation in gastric cancer by inducing G2/M cell cycle arrest and apoptosis

Luteolin potentiates low‑dose oxaliplatin‑induced inhibitory effects on cell proliferation in gastric cancer by inducing G2/M cell cycle arrest and apoptosis

A diazeniumdiolate-based NO donor induces apoptosis by modulating the CIP2A/PP2A/ERK signaling axis

A diazeniumdiolate-based NO donor induces apoptosis by modulating the CIP2A/PP2A/ERK signaling axis

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