Growth and Differentiation Effects of Homer3 on a Leukemia Cell Line

Li, Zheng; Qiu, Huiying; Jiao, Yang; Fu, Chao; Hu, Shaoyan; Zhu, Mingzhao; Wu, Depei; Qi, Xiaofei

doi:10.7314/apjcp.2013.14.4.2525

Cited by 9 publications

(5 citation statements)

References 21 publications

(22 reference statements)

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“…There are data indicating that HOMER3 is a cancer-associated gene and may play a tumorigenic role in the esophageal squamous cell carcinoma (Shen et al 2016). These data agree with our results, but there are also data available that loss of HOMER3 is associated with acute myeloid leukemia (Li et al 2013). It is possible that these differences in functional significance of changes in HOMER3 expression level are due to the features of different tumors.…”

Section: Discussionsupporting

confidence: 90%

“…The proteins encoding by PER2, HOMER3, GADD45A, and DEK genes, also involved in cancer cell proliferation and tumor growth, are dysregulated in cancer cells (Li et al 2013;Shen et al 2016;Hacker et al 2018;Xiang et al 2018;Xiong et al 2018;Rahman et al 2019). Protein PERP controls apoptosis, the marked increase in PERP expression induces apoptosis but loss of PERP protein promotes resistance to apoptosis as well as tumorigenesis (Beaudry et al 2010;Awais et al 2016;Zhou et al 2018).…”

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confidence: 99%

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Insulin receptor substrate 1 gene expression is strongly up-regulated by HSPB8 silencing in U87 glioma cells

Hnatiuk

Tsymbal

Minchenko

et al. 2020

Endocrine Regulations

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Objective. The aim of the present investigation was to study the expression of genes encoding IRS1 (insulin receptor substrate 1) and some other functionally active proteins in U87 glioma cells under silencing of polyfunctional chaperone HSPB8 for evaluation of the possible significance of this protein in intergenic interactions. Methods. Silencing of HSPB8 mRNA was introduced by HSPB8 specific siRNA. The expression level of HSPB8, IRS1, HK2, GLO1, HOMER3, MYL9, NAMPT, PER2, PERP, GADD45A, and DEK genes was studied in U87 glioma cells by quantitative polymerase chain reaction. Results. It was shown that silencing of HSPB8 mRNA by specific to HSPB8 siRNA led to a strong down-regulation of this mRNA and significant modification of the expression of IRS1 and many other genes in glioma cells: strong up-regulated of HOMER3, GLO1, and PERP and down-regulated of MYL9, NAMPT, PER2, GADD45A, and DEK gene expressions. At the same time, no significant changes were detected in the expression of HK2 gene in glioma cells treated by siRNA, specific to HSPB8. Moreover, the silencing of HSPB8 mRNA enhanced the glioma cells proliferation rate. Conclusions. Results of this investigation demonstrated that silencing of HSPB8 mRNA affected the expression of IRS1 gene as well as many other genes encoding tumor growth related proteins. It is possible that the dysregulation of most of the studied genes in glioma cells after silencing of HSPB8 is reflected by a complex of intergenic interactions and that this polyfunctional chaperone is an important factor for the stability of genome function and regulatory mechanisms contributing to the tumorigenesis control.

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Insulin receptor substrate 1 gene expression is strongly up-regulated by HSPB8 silencing in U87 glioma cells

Hnatiuk

Tsymbal

Minchenko

et al. 2020

Endocrine Regulations

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“…HOMER3 is overex6pressed in acute myeloid leukemia (AML), and decreased expression of HOMER3 is associated with poor prognosis in AML (27,28). Li et al (29) further reported that forced expression of HOMER3 in K562 cells could inhibit proliferation, influence the cell cycle, and affect apoptosis induced by As2O3 via inhibition of Bcl-2 expression. However, the roles of FSCN1 and HOMER3 were previously unclear in esophageal carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Identification of candidate target genes of genomic aberrations in esophageal squamous cell carcinoma

et al. 2016

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Abstract. The aim of the present study was to identify the candidate target genes of genomic aberrations in esophageal squamous cell carcinoma (ESCC). Array comparative genomic hybridization (CGH) and quantitative polymerase chain reaction were applied to analyze the copy number changes and expression level of candidate genes, respectively. Integrative analysis revealed that homozygous deletions of cyclin-dependent kinase inhibitor (CDKN) 2A and CDKN2B and gains of fascin actin-bundling protein 1 (FSCN1) and homer scaffolding protein 3 (HOMER3) occurred frequently in ESCC. The results demonstrated that the homozygous deletion of CDKN2A or CDKN2B was significantly associated with lymph node metastasis. Notably, the expression of CDKN2A and CDKN2B was lower in dysplasia than in normal esophageal epithelium. We also observed that the copy number increase of FSCN1 was significantly associated with pT, pN and pStage, and that the gain of HOMER3 was significantly linked with pN and pStage. We further revealed that FSCN1 and HOMER3 were overexpressed in ESCC, and that their overexpression was correlated with copy number increase. In conclusion, CDKN2A, CDKN2B, FSCN1 and HOMER3 are candidate cancer-associated genes and may play a tumorigenic role in ESCC.

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“…In addition, Homer protein 3 (HOMER3), a member of HOMER, together with WW domain binding protein 2 (WBP2) plays a significant role in glioma invasion [ 45 ]. For instance, in leukemia, HOMER3 inhibits expression of Bcl2 thus influencing the cell cycle [ 46 ]. Activity-regulated cytoskeleton associated protein (ARC) causes the internalization of AMAPR from the postsynaptic membrane hence regulating the synapse strength.…”

Section: Discussionmentioning

confidence: 99%

Validation of the functions and prognostic values of synapse-associated proteins in lower-grade glioma

et al. 2021

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Synapse and synapse associated proteins (SAPs) play critical roles in various neurodegeneration diseases and brain tumors. However, in lower-grade gliomas (LGG), SAPs have not been explored systematically. Herein, we are going to explore SAPs expression profile and its clinicopathological significance in LGG which can offer new insights to glioma therapy. In this study, we integrate a list of SAPs that covered 231 proteins with synaptogenesis activity and post synapse formation. The LGG RNA-seq data were downloaded from GEO, TCGA and CGGA database. The prognosis associated SAPs in key modules of PPI (protein-protein interaction networks) was regarded as hub SAPs. Western blot, quantitative reverse transcription PCR (qRT-PCR) and immunochemistry results from HPA database were used to verify the expression of hub SAPs. There were 68 upregulated SAPs and 44 downregulated SAPs in LGG tissue compared with normal brain tissue. Data from function enrichment analysis revealed functions of differentially expressed SAPs in synapse organization and glutamatergic receptor pathway in LGGs. Survival analysis revealed that four SAPs, GRIK2, GABRD, GRID2 and ARC were correlate with the prognosis of LGG patients. Interestingly, we found that GABRD were upregulated in LGG patients with seizures, indicating that SAPs may link to the pathogenesis of seizures in glioma patients. The four-SAPs signature was revealed as an independent prognostic factor in gliomas. Our study presented a novel strategy to assess the prognostic risks of LGGs, based on the expression of SAPs.

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Growth and Differentiation Effects of Homer3 on a Leukemia Cell Line

Cited by 9 publications

References 21 publications

Insulin receptor substrate 1 gene expression is strongly up-regulated by HSPB8 silencing in U87 glioma cells

Insulin receptor substrate 1 gene expression is strongly up-regulated by HSPB8 silencing in U87 glioma cells

Identification of candidate target genes of genomic aberrations in esophageal squamous cell carcinoma

Validation of the functions and prognostic values of synapse-associated proteins in lower-grade glioma

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