Author:
Zhang Zhanzhan,Zhang Aobo,Shi Yunpeng,Zhao Zijun,Zhao Zongmao
Abstract
Abstract
Background
ATP7B is a copper-transporting protein that contributes to the chemo-resistance of human cancer cells. It remains unclear what the molecular mechanisms behind ATP7B are in cancer, as well as its role in human pan-cancer studies.
Methods
Our study evaluated the differential expression of ATP7B in cancer and paracancerous tissues based on RNA sequencing data from the GTEx and TCGA. Kaplan–Meier and Cox proportional hazards regressions were used to estimate prognostic factors associated with ATP7B.The correlations between the expression of ATP7B and immune cell infiltration, tumor mutation burden, microsatellite instability and immune checkpoint molecules were analyzed. Co-expression networks and mutations in ATP7B were analyzed using the web tools. An analysis of ATP7B expression difference on drug sensitivity on tumor cells was performed using the CTRP, GDSC and CMap database.
Results
ATP7B expression differed significantly between cancerous and paracancerous tissues. The abnormal expression of ATP7B was linked to prognosis in LGG and KIRC. Infiltration of immune cells, tumor mutation burden, microsatellite instability and immunomodulators had all been linked to certain types of cancer. Cancer cells exhibited a correlation between ATP7B expression and drug sensitivity.
Conclusion
ATP7B might be an immunotherapeutic and prognostic biomarker based on its involvement in cancer occurrence and development.
Funder
National Key R & D Program Intergovernmental Cooperation on International Scientific and Technological Innovation of the Ministry of Science and Technology of China
National Natural Science Foundation of China
Special Project for the Construction of Hebei Province International Science and Technology Cooperation Base
Government funded Project on Training of outstanding Clinical Medical Personnel and Basic Research Projects of Hebei Province in the Year of 2019
Publisher
Springer Science and Business Media LLC
Subject
Genetics (clinical),Genetics
Cited by
1 articles.
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