Background
In recent years, there have been many studies on the relationship between DLGAP5 and different types of cancers, yet there is no pan-cancer analysis of DLGAP5. Therefore, this study aims to analyze the roles of DLGAP5 in human tumors.
Methods
Firstly, we evaluated the expression level of DLGAP5 in 33 types of tumors throughout the datasets of TCGA (Cancer Genome Atlas) and GEO (Gene Expression Synthesis). Secondly, we used the GEPIA2 and Kaplan-Meier plotter to conduct Survival prognosis analysis. Additionally, cBioPortal web was utilized to analyze the genetic alteration of DLGAP5, after which we selected hepatocellular carcinoma (HCC) cell lines to define the function of DLGAP5. Last but not least, we performed immune infiltration analysis and DLGAP5-related gene enrichment analysis.
Results
DLGAP5 is highly expressed in most type of cancers, and there is a significant correlation between the expression of DLGAP5 and the prognosis of cancer patients. We have observed that DLGAP5 promotes the proliferation and invasion of hepatocellular carcinoma (HCC) cell lines. We also found that DLGAP5 expression was related with the CD8+ T-cell infiltration status in kidney renal clear cell carcinoma, uveal melanoma, and thymoma, and cancer-associated fibroblast infiltration was observed in breast invasive carcinoma, kidney renal papillary cell carcinoma and testicular germ cell tumors. In addition, enrichment analysis revealed that cell cycle- and oocyte meiosis-associated functions were involved in the functional mechanism of DLGAP5.
Conclusions
Taken together, our unpresented pan-cancer analysis of DLGAP5 provides a relatively integrative understanding of the oncogenic role of DLGAP5 in various tumors. DLGAP5 may prompt HCC cellular proliferation, invasion and metastasis. All of these provides solid basement and will promote more advanced understanding the role of DLGAP5 in tumorigenesis and development from the perspective of clinical tumor samples and cells.
Pancreatic cancer is a lethal disease with a 5-year survival less than 9%. 1 The diagnosis of pancreatic cancer is often at late stage and over 80% of patients with pancreatic cancer are not suitable for surgical resection. 2 Chemotherapy and targeted therapy are now the most widely used treatments for pancreatic cancer. However, due to the rapidly developed resistance to drugs, the survival of patients is far from satisfactory. 3 Therefore, it is imperative to uncover the underlying mechanisms responsible for tumour progression in pancreatic cancer, so as to identify promising therapeutic targets and develop more effective strategies.The ubiquitin-proteasome system (UPS), which is responsible for degrading 80%-90% of cellular proteins, is involved in multiple biological processes of cancer, including proliferation, metastasis, metabolism and drug resistance. 4 Moreover, the specificity of human UPS mainly depends on approximately 617 E3 ubiquitin ligases. Zinc finger protein 91 (ZFP91), a novel E3 ubiquitin ligase, is demonstrated to be upregulated in prostate cancer, colon cancer and pancreatic cancer. [5][6][7] It is reported that ZFP91 facilitates prostate cancer
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