Decreased expression of PIAS1 and PIAS3 in essential thrombocythemia patients

Hsiao, Hui‐Hua; Liu, Y.-C.; Yang, Mingyu; Tsai, Yi-Cheng; Liu, T.-C.; Chang, Chao-Sung; Lin, Sheng-Fuu

doi:10.4238/2013.november.18.10

Cited by 4 publications

(2 citation statements)

References 25 publications

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“…The high frequency point mutations in JAK2 exon 12 (G mutates into T at site 1849) are believed to lead to a valine changing into a phenylalanine at site 617 of the JAK2 kinase domain structure. This change causes instability in, and abnormal activation of, the JH2 structure and further activation of transcription in the cell proliferation gene via activation of the JAK/STAT signal transduction pathways, resulting in sustained cellular proliferation (Harrison et al, 2012;Evrot et al, 2013;Hsiao et al, 2013). In this study, we showed that the mutation was found in 44 of 68 patients with MPN (64.7%), including 24 ET, 17 PV, and 3 PMF patients.…”

Section: Discussionmentioning

confidence: 64%

Correlative study between the JAK2V617F mutation and thrombosis in patients with myeloproliferative neoplasm

et al. 2016

Genet. Mol. Res.

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ABSTRACT. In this study, we investigated the correlation between the JAK2V617F mutation and thrombosis in patients with myeloproliferative neoplasm (MPN) using real-time fluorescence quantitative PCR. The incidence of thrombus was monitored and blood and coagulation were routinely assayed in patients with MPN. The JAK2V617F mutation was found in 8/68 individuals in the control group (11.8%); it was expressed in 44/68 patients with MPN (64.7%), suggesting that the rate of this mutation was significantly higher in patients with MPN than that in the control group. Twenty-six MPN patients (38.2%) showed symptoms of thrombosis; MPN patients with thrombosis showed a significantly higher rate of the JAK2V617F mutation, were of a greater age, and had higher blood pressure than MPN patients without thrombosis. In addition, the white blood cells (WBC) (21.98 ± 1.95) and platelets (364.68 ± 97.72) were significantly higher in patients, expressing the mutated gene, with polycythemia vera than in the patients without the mutation. The WBC (32.89 ± 4.25) and hemoglobin (161.92 ± 16.19) were significantly increased in the essential thrombocythemia patients with gene mutation compared with the patients without mutation. MPN patients showed higher blood clotting ability than the control subjects; moreover, MPN patients with the JAK2V617F mutation showed higher blood clotting ability than those without the mutation. The findings of this study indicate that the JAK2V617F mutation is correlated with the incidence of thrombosis, and analysis of this mutation has important clinical significance in the diagnosis and treatment of MPN.

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Section: Discussionmentioning

confidence: 64%

Correlative study between the JAK2V617F mutation and thrombosis in patients with myeloproliferative neoplasm

et al. 2016

Genet. Mol. Res.

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“…Based on the function of PIAS3 on inhibiting cell proliferation [16] [17] and the response of STAT3 to radiation [18] [19], we will further investigate the inhibiting effect of Ad-pig3RRP-PIAS3 on metastasis which is induced by radiation in lung adenocarcinoma cells and the correlation mechanism. From a new perspective, a novel target and treatment means which combined molecular target therapy with radiotherapy will be explored in lung adenocarcinoma.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Radiation-Induced Lung Adenocarcinoma Cell Metastasis by Adenovirus of PIAS3 Overexpression Driven by Radiation-Inducible Promoter (<i>Ad-pig3RRP-PIAS3</i>)

Gao¹,

Yu²,

Li³

et al. 2014

JCT

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Radiotherapy is one of important approaches for pulmonary adenocarcinoma. However, many studies have shown that radiation can also enhance the ability of tumor cells metastasis, although the lung adenocarcinoma could be killed. The increased metastasis induced by radiation is associated with the activation of STAT3 in lung adenocarcinoma cells. Based on the importance role of STAT3 in cell proliferation and survival, we can construct an adenovirus vector of PIAS3 overexpress driven by radiation-induced promoter to inhibit the activation of STAT3 specifically. In this way, when STAT3 was activated by radiation, the expression of PIAS3 will be increased at the same time; this lead to the inhibition of invasion and metastasis caused by STAT3 in lung adenocarcinoma cells. These researches are expected to develop a novel target and method for radiotherapy and molecular therapy of lung adenocarcinoma. [9], although the tumor cells can be killed. Radiation was found to activate the phosphorylation of STAT3 which resulted in the increase of invasion of A549 cells [9]. By using special inhibitor to block radiation-induced STAT3 activation, the increase of invasion and migration of A549 cell induced by radiation can be reduced significantly [10]. All above comes down to one point: STAT3 plays a key role in radiation-induced invasion and metastasis and is a potential target of therapy in lung adenocarcinoma. Keywords PIAS3-Specific STAT3 Inhibitor ProteinPIAS3 (protein inhibitor of activated STAT3) is one of PIAS (including PIAS1, PIAS2, PIAS3 and PIAS4) family members, which can inhibit STAT3 specifically [11]. As an endogenous inhibitor of STAT3, PISA3 is expressed at high level in many normal human tissues and cells, while shows a very low level or even no expression in the tumor tissues and cells. Dabric [12] found that protein expression with PIAS3 is in a low level which affected survival upon mesothelioma patients and indicated PIAS3 as having potential for development into a novel therapeutic target. When the expression of PISA3 has been silenced, the activity of STAT3 increased continuously, which resulted in the significant increasing of growth and proliferation of tumor. Our group study showed that the expression of PISA3 is in a low level, and is not affected by γ-ray radiation. As the radiation-induced activation of STAT3 plays an important role on invasion and metastasis of A549 cells, it can be inferred that PIAS3 also played a prominent role in the invasion and metastasis of lung adenocarcinoma cells via STAT3. PIG3-Radiation Sensitive GenePIG3, one of PIG family members regulated by p53 protein, participated in oxidative stress of cells and cell apoptosis pathway mediated by radiation. Our study group has drawn a conclusion that the expressions of PIG3 in mRNA and protein level were enhanced 15 to 20 times by radiation in a dose-dependent manner from 0 to 10 Gy. Other group also discovered that the PIG3 gene expression was enhanced by radiation in AHH-1 and HPBL cells [13]. These results demonstr...

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The investigation of relevancy between PIAS1 and PIAS2 gene expression and disease severity of multiple sclerosis

Kouchaki

Nikoueinejad

Akbari

et al. 2019

Journal of Immunoassay and Immunochemistry

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Decreased expression of PIAS1 and PIAS3 in essential thrombocythemia patients

Cited by 4 publications

References 25 publications

Correlative study between the JAK2V617F mutation and thrombosis in patients with myeloproliferative neoplasm

Correlative study between the JAK2V617F mutation and thrombosis in patients with myeloproliferative neoplasm

Inhibition of Radiation-Induced Lung Adenocarcinoma Cell Metastasis by Adenovirus of PIAS3 Overexpression Driven by Radiation-Inducible Promoter (<i>Ad-pig3RRP-PIAS3</i>)

The investigation of relevancy between PIAS1 and PIAS2 gene expression and disease severity of multiple sclerosis

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Decreased expression of PIAS1 and PIAS3 in essential thrombocythemia patients

Cited by 4 publications

References 25 publications

Correlative study between the JAK2V617F mutation and thrombosis in patients with myeloproliferative neoplasm

Correlative study between the JAK2V617F mutation and thrombosis in patients with myeloproliferative neoplasm

Inhibition of Radiation-Induced Lung Adenocarcinoma Cell Metastasis by Adenovirus of PIAS3 Overexpression Driven by Radiation-Inducible Promoter (&lt;i&gt;Ad-pig3RRP-PIAS3&lt;/i&gt;)

The investigation of relevancy between PIAS1 and PIAS2 gene expression and disease severity of multiple sclerosis

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Inhibition of Radiation-Induced Lung Adenocarcinoma Cell Metastasis by Adenovirus of PIAS3 Overexpression Driven by Radiation-Inducible Promoter (<i>Ad-pig3RRP-PIAS3</i>)