Abnormal expression pattern of the ASPP family of proteins in human non-small cell lung cancer and regulatory functions on apoptosis through p53 by iASPP

Li, Shijun; Guangxia, Shi; Yuan, Hong; Zhou, Tao; Zhang, Qiuping; Zhu, Hong; Wang, Xiaoyan

doi:10.3892/or.2012.1778

Cited by 14 publications

(16 citation statements)

References 13 publications

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“…ASPP2 is commonly considered a tumor suppressor, and its expression is often reduced in malignant tumors [14, 24, 25]. However, inconsistent with previous reports, our results indicated that ASPP2 expression was significantly increased in ESCCs as compared with noncancerous tissues, suggesting that ASPP2 might be involved in ESCC tumorigenesis.…”

Section: Discussioncontrasting

confidence: 93%

Prognostic values of apoptosis-stimulating P53-binding protein 1 and 2 and their relationships with clinical characteristics of esophageal squamous cell carcinoma patients: a retrospective study

et al. 2017

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BackgroundEsophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related death, and new prognostic biomarkers are urgently needed. Apoptosis-stimulating P53-binding protein 1 (ASPP1) and 2 (ASPP2) have been reported to play important roles in the development, progression, metastasis, and prognosis of cancers, but their roles in ESCC have not been elucidated. In this study, we examined the expression of ASPP1 and ASPP2 in ESCC to evaluate their prognostic values.MethodsThe protein expression of ASPP1, ASPP2, and P53 in 175 specimens of ESCC was detected using immunohistochemical staining; their expression in cancerous and noncancerous tissues was scored according to the staining intensity and the percentage of stained cells. The associations of ASPP1, ASPP2, and P53 with clinicopathologic parameters, overall survival (OS), and disease-free survival (DFS) were analyzed.ResultsThe protein expression levels of ASPP2 and P53 were significantly higher in cancerous tissues than in paired noncancerous tissues (P < 0.001), whereas the expression levels of ASPP1 in the two groups were similar. In ESCCs, ASPP1 expression was significantly associated with histological differentiation (P = 0.002) and invasive depth (P = 0.014); ASPP2 expression was associated with age (P = 0.029) and histological differentiation (P < 0.001); and P53 expression was associated with age (P = 0.021) and tumor size (P = 0.040). No correlations were found between ASPP1, ASPP2, and P53 expression. Survival analysis revealed that high ASPP2 expression was significantly associated with increased 5-year OS (P = 0.001) and DFS rates (P = 0.010) and that high P53 expression was significantly associated with a reduced 5-year DFS rate of ESCC patients (P = 0.015). Multivariate Cox analysis indicated that ASPP2 was an independent predictor of OS [hazard ratio (HR): 0.541, 95% confidence interval (CI) 0.363–0.804] and DFS (HR: 0.599, 95% CI 0.404–0.888) of ESCC patients and that P53 was an independent predictor of DFS (HR: 2.161, 95% CI 1.100–4.245).ConclusionsASPP1 might be involved in the progression of ESCC, and ASPP2 was a potential prognostic biomarker of ESCC and should be evaluated in future studies.

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Section: Discussioncontrasting

confidence: 93%

Prognostic values of apoptosis-stimulating P53-binding protein 1 and 2 and their relationships with clinical characteristics of esophageal squamous cell carcinoma patients: a retrospective study

et al. 2017

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“…Downregulation of the expression of iASPP by shRNA inhibited proliferation and induced apoptosis of p53-defective prostate cancer cells. Existing data regarding the involvement of iASPP in tumor metastasis also suggests thatit may have potential as a therapeutic target [6, 13]. …”

Section: Introductionmentioning

confidence: 99%

MicroRNA-124 Regulates the Proliferation of Colorectal Cancer Cells by TargetingiASPP

Liu

Zhao

Yao

et al. 2013

BioMed Research International

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MicroRNAs are a class of small, noncoding RNAs that function as critical regulators of gene expression by targeting mRNAs for translational repression or degradation. In this study, we demonstrate that expression of microRNA-124 (miR-124) is significantly downregulated in colorectal cancer tissues and cell lines, compared to the matched adjacent tissues. We identified and confirmed inhibitor of apoptosis-stimulating protein of p53 (iASPP) as a novel, direct target of miR-124 using target prediction algorithms and luciferase reporter gene assays. Overexpression of miR-124 suppressed iASPP protein expression, upregulated expression of the downstream signaling molecule nuclear factor-kappa B (NF-κB), and attenuated cell viability, proliferation, and colony formation in SW480 and HT-29 colorectal cancer cells in vitro. Forced overexpression of iASPP partly rescued the inhibitory effect of miR-124 on SW480 and HT29 cell proliferation. Taken together, these findings shed light on the role and mechanism of action of miR-124, indicate that the miR-124/iASPP axis can regulate the proliferation of colorectal cancer cells, and suggest that miR-124 may serve as a potential therapeutic target for colorectal cancer.

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“…Thus, TP53BP1 has a role in checkpoint signaling during mitosis, enhances TP53-mediated transcriptional activation and plays a role in the response to DNA damage [18,19]. TP53BP2 is a member of the ASPP (apoptosis-stimulating protein of p53) family of TP53 interacting proteins which are down regulated in tumor tissues and is required for the induction of apoptosis by TP53-family proteins [16]. TP53BP2 protein promotes DNA binding and transactivation of TP53-family proteins on the promoters of pro-apoptotic genes.…”

Section: Introductionmentioning

confidence: 99%

Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells

Minchenko¹,

Danilovskyi²,

Kryvdiuk³

et al. 2014

Fiziol Zh

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Acute L-glutamine deprivation affects the expression of tP53-related protein genes in u87 glioma cells We have studied the effect of acute L-glutamine deprivation on the expression of tumor protein 53 (TP53)related genes such as TOPORS (topoisomerase I binding, arginine/serine-rich, E3 ubiquitin protein ligase), TP53BP1 (TP53 binding protein 1), TP53TG1 (TP53 inducible gene 1), SESN1 (p53 regulated PA26 nuclear protein), NME6 (NME/NM23 nucleoside diphosphate kinase 6), and ZMAT3 (zinc finger, Matrin-type 3) in glioma cells with ERN1 knockdown. It was shown that blockade of ERN1 function in U87 glioma cells is induced the expression of RYBP and SESN1 genes, but decreased the expression of TP53BP1, TP53TG1, TOPORS, NME6, genes. Moreover, the expression levels of RYBP, SESN1, TP53BP1, and ZMAT3 genes is increased in control glioma cells by L-glutamine deprivation condition but blockade of ERN1 signaling enzyme function significantly enhances this effect on the expression all of these genes. At the same time, the ERN1 knockdown eliminates the response TP53TG1 and TOPORS genes to L-glutamine deprivation condition. Results of this investigation clearly demonstrate that the expression most of genes encoding TP53-related factors depends upon acute L-glutamine deprivation condition as well as upon ERN1, the major signaling system of the endoplasmic reticulum stress.

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Abnormal expression pattern of the ASPP family of proteins in human non-small cell lung cancer and regulatory functions on apoptosis through p53 by iASPP

Cited by 14 publications

References 13 publications

Prognostic values of apoptosis-stimulating P53-binding protein 1 and 2 and their relationships with clinical characteristics of esophageal squamous cell carcinoma patients: a retrospective study

Prognostic values of apoptosis-stimulating P53-binding protein 1 and 2 and their relationships with clinical characteristics of esophageal squamous cell carcinoma patients: a retrospective study

MicroRNA-124 Regulates the Proliferation of Colorectal Cancer Cells by TargetingiASPP

Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells

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