Overexpressed DNA-binding protein inhibitor 2 as an unfavorable prognosis factor promotes cell proliferation in nasopharyngeal carcinoma

Liu, Zhen; Chen, Jing; Luo, Weiren; Yang, Huiling; Wu, Aibing; Zhen, Yan; Yu, Xiaoli; Wang, Hao; Yao, Kangde; Li, Xin; Fang, Weiyi

doi:10.1093/abbs/gms030

Cited by 6 publications

(5 citation statements)

References 35 publications

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“…The preparation of lentivirus expressing human CTGF short hairpin RNA (shRNA-1024,1047) (Table 1) was performed using the pLVTHM-GFP lentiviral RNAi expression system [16]. NPC 6–10B cells were infected with lentiviral particles containing specific or negative control vectors, and the polyclonal cells with GFP signals were selected for further experiments using FACS flow cytometry.…”

Section: Methodsmentioning

confidence: 99%

Reduced CTGF Expression Promotes Cell Growth, Migration, and Invasion in Nasopharyngeal Carcinoma

Zhen

et al. 2013

PLoS ONE

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BackgroundThe role of CTGF varies in different types of cancer. The purpose of this study is to investigate the involvement of CTGF in tumor progression and prognosis of human nasopharyngeal carcinoma (NPC).Experimental designCTGF expression levels were examined in NPC tissues and cells, nasopharynx (NP) tissues, and NP69 cells. The effects and molecular mechanisms of CTGF expression on cell proliferation, migration, invasion, and cell cycle were also explored.ResultsNPC cells exhibited decreased mRNA expression of CTGF compared to immortalized human nasopharyngeal epithelial cell line NP69. Similarly, CTGF was observed to be downregulated in NPC compared to normal tissues at mRNA and protein levels. Furthermore, reduced CTGF was negatively associated with the progression of NPC. Knocking down CTGF expression enhanced the colony formation, cell migration, invasion, and G1/S cell cycle transition. Mechanistic analysis revealed that CTGF suppression activated FAK/PI3K/AKT and its downstream signals regulating the cell cycle, epithelial-mesenchymal transition (EMT) and MMPs. Finally, DNA methylation microarray revealed a lack of hypermethylation at the CTGF promoter, suggesting other mechanisms are associated with suppression of CTGF in NPC.ConclusionOur study demonstrates that reduced expression of CTGF promoted cell proliferation, migration, invasion and cell cycle progression through FAK/PI3K/AKT, EMT and MMP pathways in NPC.

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Section: Methodsmentioning

confidence: 99%

Reduced CTGF Expression Promotes Cell Growth, Migration, and Invasion in Nasopharyngeal Carcinoma

Zhen

et al. 2013

PLoS ONE

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“…Id1 protein expression also correlates with lymph node status, indicating that increased Id expression may be related to the metastatic behaviour of human oral SCC ( Dong et al , 2010 ). Patients with increased Id2 expression levels had poorer overall survival rates than those with low Id2 levels in nasopharyngeal carcinoma ( Liu et al , 2012 ). This suggests that overexpression of Id2 protein is an unfavourable prognostic factor that indicates likely cell proliferation in nasopharyngeal carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Inhibitor of DNA binding 2 is a novel therapeutic target for stemness of head and neck squamous cell carcinoma

et al. 2017

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Background:Head and neck squamous cell carcinomas (HNSCCs) are highly lethal epithelial tumours containing self-renewal cancer stem cells (CSCs). CSCs in HNSCCs are strongly associated with tumour initiation, invasion, and chemoradiation resistance. However, the important factors regulating stemness in HNSCCs remain unclear. Here, we investigated the molecular roles and clinical significance of inhibitor of DNA binding 2 (Id2) protein to determine if it constitutes a novel therapeutic target for ablating HNSCC cells with stemness.Methods:We performed in vitro and in vivo studies of Id2 function and its effects on stemness using HNSCC cells. We also examined whether Id2 expression could be used as a prognostic indicator through immunohistochemical staining of 119 human HNSCC tumours.Results:Expression of Id2 was higher in HNSCC cells with stemness compared with differentiated HNSCC cells. Overexpression of Id2 increased proliferation, self-renewal, and expression of the putative stemness marker CD44 in HNSCC cells in vitro and in vivo. In contrast, silencing of Id2 using short hairpin RNA attenuated the stemness phenotype of HNSCC cells by reducing self-renewal, CD44 expression, cisplatin chemoresistance, and xenograft tumourigenicity. Most importantly, increased expression of Id2 was closely associated with poorer post-treatment survival rates in HNSCC patients.Conclusions:Inhibitor of DNA binding2 represents a novel and promising therapeutic target for treating and improving the clinical outcomes for patients with HNSCC.

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“…The immunohistochemically stained tissue sections were reviewed and scored independently by two pathologists without knowledge of the clinical parameters. For SOCS1 assessment , Staining intensity was graded as (0, negative; 1, weak; 2, moderate; 3, strong), and staining extent was graded as (0, 0–10%; 1, 11–50%; 2, 51–75%; >75%=3). The final score was determined by the combined staining score and proportion score (intensity score × proportion score).…”

Section: Methodsmentioning

confidence: 99%

SOCS1 is associated with clinical progression and acts as an oncogenic role in triple‐negative breast cancer

Qian

2018

IUBMB Life

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Suppressors of cytokine signaling 1 (SOCS1) is a member of SOCS family and acts as negative regulators of cytokine signaling by direct inhibition of receptor-associated janus kinases. The clinical significance and biological function of SOCS1 in variant tumor tissues and at variant tumor stages is still controversial. The aim of our study is to confirm the expression status of SOCS1 in triple-negative breast cancer (TNBC) tissues and cell lines, and explore the clinical value and biological function of SOCS1 in TNBC. In microarray data sets (GDS2250 and GDS817), we observed SOCS1 was overexpressed in TNBC tissues and cell line compared with normal mammary tissues and mammary epithelial cell line, or non-TNBC tissues and cell line. Furthermore, SOCS1 mRNA and protein overexpression were confirmed in TNBC tissues and cell lines compared with normal mammary tissues and mammary epithelial cell lines or non-TNBC tissues and cell lines. SOCS1 protein overexpression was obviously associated with advanced clinical stage, large tumor size, more lymph node metastasis, present distant metastasis, and malign histological grade. Downregulation of SOCS1 expression suppressed TNBC cells proliferation and promoted cell apoptosis. In conclusion, SOCS1 is associated with clinical progression in TNBC patients and acts as an oncogenic role in regulating TNBC cells proliferation and apoptosis. © 2018 IUBMB Life, 70(4):320-327, 2018.

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Overexpressed DNA-binding protein inhibitor 2 as an unfavorable prognosis factor promotes cell proliferation in nasopharyngeal carcinoma

Cited by 6 publications

References 35 publications

Reduced CTGF Expression Promotes Cell Growth, Migration, and Invasion in Nasopharyngeal Carcinoma

Reduced CTGF Expression Promotes Cell Growth, Migration, and Invasion in Nasopharyngeal Carcinoma

Inhibitor of DNA binding 2 is a novel therapeutic target for stemness of head and neck squamous cell carcinoma

SOCS1 is associated with clinical progression and acts as an oncogenic role in triple‐negative breast cancer

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