Increased Jab1/COPS5 is associated with therapeutic response and adverse outcome in lung cancer and breast cancer patients

Hou, Junna; Liu, Guohong; Yuan, Yufen; Wang, Dong; Jiao, Pengfei; Liu, Xing; Pan, Yunbao

doi:10.18632/oncotarget.22146

Cited by 8 publications

(8 citation statements)

References 29 publications

(33 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, we retrospectively collected and analyzed data of 88 lung cancer and 76 breast cancer patients, and found that lung cancer patients with higher Jab1 level was less responsive to chemotherapy. Recurrent breast cancer patients had much higher Jab1 level (Hou et al, 2017 ). Both breast cancer patients and lung cancer patients with higher Jab1 level had significantly shorter disease-free survival and overall survival.…”

Section: Jab1/cops5 As Biomarker For Diagnostic and Prognosismentioning

confidence: 99%

“…Both breast cancer patients and lung cancer patients with higher Jab1 level had significantly shorter disease-free survival and overall survival. In a multivariate survival analysis, Jab1 was correlated with disease-free survival and overall survival in breast cancer (Hou et al, 2017 ). The Jab1 level was found to be a possible biomarker for clinical response to chemotherapy in lung cancer patients and for postoperative relapse in breast cancer patients who received adjuvant chemotherapy (Hou et al, 2017 ), indicating that Jab1 predicts treatment response in lung cancer and relapse in breast cancer patients.…”

Section: Jab1/cops5 As Biomarker For Diagnostic and Prognosismentioning

confidence: 99%

See 1 more Smart Citation

Jab1/COPS5 as a Novel Biomarker for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Human Cancer

et al. 2018

Self Cite

View full text Add to dashboard Cite

C-Jun activation domain-binding protein-1 (Jab1) involves in controlling cellular proliferation, cell cycle, apoptosis, affecting a series of pathways, as well as regulating genomic instability and DNA damage response (DDR). Jab1/COPS5 dysregulation contributes to oncogenesis by deactivating several tumor suppressors and activating oncogenes. Jab1 overexpression was found in many tumor types, illuminating its important role in cancer initiation, progression, and prognosis. Jab1/COPS5 has spurred a strong research interest in developing inhibitors of oncogenes/oncoproteins for cancer therapy. In this paper, we present evidences demonstrating the importance of Jab1/COPS5 overexpression in several cancer types and recent advances in dissecting the Jab1/COPS5 upstream and downstream signaling pathways. By conducting ingenuity pathway analysis (IPA) based on the Ingenuity Knowledge Base, we investigated signaling network that interacts with Jab1/COPS5. The data confirmed the important role of Jab1/COPS5 in tumorigenesis, demonstrating the potential of Jab1/COPS5 to be used as a biomarker for cancer patients, and further support that Jab1/COPS5 may serve as a potential therapeutic target in different cancers.

show abstract

Section: Jab1/cops5 As Biomarker For Diagnostic and Prognosismentioning

confidence: 99%

Section: Jab1/cops5 As Biomarker For Diagnostic and Prognosismentioning

confidence: 99%

Jab1/COPS5 as a Novel Biomarker for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Human Cancer

et al. 2018

Self Cite

View full text Add to dashboard Cite

show abstract

“…Changed genes in any cancer, including breast cancer, reflect the biological diversity of cellular phenotype and physiological function and could become important research areas for elucidating molecular mechanisms. Already, many studies have found genes or proteins strongly associated with the progress and prognosis of breast cancer, including enhancer of zeste 2 (EZH2) polycomb repressive complex 2 subunit [20] and Jab1/COPS5 [21]. In addition, the nuclear receptor-interacting protein 1 (NRIP1) and the MAPK signaling pathway can regulate the development of breast cancer cells [22].…”

Section: Introductionmentioning

confidence: 99%

Transcriptome profiling revealed multiple genes and ECM-receptor interaction pathways that may be associated with breast cancer

et al. 2019

View full text Add to dashboard Cite

Background Exploration of the genes with abnormal expression during the development of breast cancer is essential to provide a deeper understanding of the mechanisms involved. Transcriptome sequencing and bioinformatics analysis of invasive ductal carcinoma and paracancerous tissues from the same patient were performed to identify the key genes and signaling pathways related to breast cancer development. Methods Samples of breast tumor tissue and paracancerous breast tissue were obtained from 6 patients. Sequencing used the Illumina HiSeq platform. All. Only perfectly matched clean reads were mapped to the reference genome database, further analyzed and annotated based on the reference genome information. Differentially expressed genes (DEGs) were identified using the DESeq R package (1.10.1) and DEGSeq R package (1.12.0). Using KOBAS software to execute the KEGG bioinformatics analyses, enriched signaling pathways of DEGs involved in the occurrence of breast cancer were determined. Subsequently, quantitative real time PCR was used to verify the accuracy of the expression profile of key DEGs from the RNA-seq result and to explore the expression patterns of novel cancer-related genes on 8 different clinical individuals. Results The transcriptomic sequencing results showed 937 DEGs, including 487 upregulated and 450 downregulated genes in the breast cancer specimens. Further quantitative gene expression analysis was performed and captured 252 DEGs (201 downregulated and 51 upregulated) that showed the same differential expression pattern in all libraries. Finally, 6 upregulated DEGs (CST2, DRP2, CLEC5A, SCD, KIAA1211, DTL) and 6 downregulated DEGs (STAC2, BTNL9, CA4, CD300LG, GPIHBP1 and PIGR), were confirmed in a quantitative real time PCR comparison of breast cancer and paracancerous breast tissues from 8 clinical specimens. KEGG analysis revealed various pathway changes, including 20 upregulated and 21 downregulated gene enrichment pathways. The extracellular matrix–receptor (ECM-receptor) interaction pathway was the most enriched pathway: all genes in this pathway were DEGs, including the THBS family, collagen and fibronectin. These DEGs and the ECM-receptor interaction pathway may perform important roles in breast cancer. Conclusion Several potential breast cancer-related genes and pathways were captured, including 7 novel upregulated genes and 76 novel downregulated genes that were not found in other studies. These genes are related to cell proliferation, movement and adhesion. They may be important for research into breast cancer mechanisms, particularly CST2 and CA4. A key signaling pathway, the ECM-receptor interaction signal pathway, was also identified as possibly involved in the development of breast cancer. Electronic supplementary material The online version of this article (10.1186/s11658-019-0162-0) contains supplementary material, which is available to authorized user...

show abstract

“…The role of CAV1 in gastric cancer remains controversial 33 . The oncogenic role of COPS5 34 , MRE11 35 , RICTOR 36 , CHEK1 37 , CLDN7 38 , EIF4EBP1 39 , EPPK1 40 , ITGA2 41 , MAP2K1 42 , RPS6KA1 43 , TFRC 44 have been reported in different cancer types. Specifically EIF4EBP1 were overexpressed in GC 45 and MAP2K1 has been identified to be associated with GC by different studies 46 .…”

Section: Discussionmentioning

confidence: 99%

Comprehensive profiling of JMJD3 in gastric cancer and its influence on patient survival

Xia

Xiao

et al. 2019

Sci Rep

View full text Add to dashboard Cite

Histone methylation is thought to control the regulation of genetic program and the dysregulation of it has been found to be closely associated with cancer. JMJD3 has been identified as an H3K27 demethylase and its role in cancer development is context specific. The role of JMJD3 in gastric cancer (GC) has not been examined. In this study, JMJD3 expression was determined. The prognostic significance of JMJD3 and its association with clinical parameters were evaluated. JMJD3 dysregulation mechanism and targets were analyzed. The effect of JMJD3 mutation was determined by functional study. Results showed that JMJD3 was overexpressed in different patient cohorts and also by bioinformatics analysis. High JMJD3 expression was correlated with shortened overall survival in patients with GC and was an independent prognosis predictor. Genetic aberration and DNA methylation might be involved in the deregulation of JMJD3 in GC. Downstream network of JMJD3 was analyzed and several novel potential targets were identified. Furthermore, functional study discovered that both demethylase-dependent and demethylase-independent mechanisms were involved in the oncogenic role of JMJD3 in GC. Importantly, histone demethylase inhibitor GSK-J4 could reverse the oncogenic effect of JMJD3 overexpression. In conclusion, our study report the oncogenic role of JMJD3 in GC for the first time. JMJD3 might serve as an important epigenetic therapeutic target and/or prognostic predictor in GC.

show abstract

Increased Jab1/COPS5 is associated with therapeutic response and adverse outcome in lung cancer and breast cancer patients

Cited by 8 publications

References 29 publications

Jab1/COPS5 as a Novel Biomarker for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Human Cancer

Jab1/COPS5 as a Novel Biomarker for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Human Cancer

Transcriptome profiling revealed multiple genes and ECM-receptor interaction pathways that may be associated with breast cancer

Comprehensive profiling of JMJD3 in gastric cancer and its influence on patient survival

Contact Info

Product

Resources

About