A pan-cancer analysis of pituitary tumor-transforming 3, pseudogene.

Autor:	Li J; The Second Affiliated Hospital of Hainan Medical University Health Management Center Haikou 570311, Hainan, China., Shaikh SN; Department of Physiology, Liaquat University of Medical and Health Sciences Jamshoro, Sindh 76090, Pakistan., Uqaili AA; Department of Physiology, Liaquat University of Medical and Health Sciences Jamshoro, Sindh 76090, Pakistan., Nasir H; Clinical and Translational Oncology, Scuola Superiore Meridionale, Naples Federico II University Napoli 80138, Italy., Zia R; Pakistan Kidney and Liver Institute and Research Lahore, Punjab 54000, Pakistan., Akram MA; University Institute of Biochemistry and Biotechnology, PMAS-Arid Agriculture University Rawalpindi 46000, Pakistan., Jawad FA; Centre of Agricultural Biochemistry and Biotechnology, University of Agriculture Faisalabad Faisalabad 38000, Pakistan., Sohail S; Registrar Ophthalmology, Al Shifa Trust Eye Hospital Rawalpindi 46000, Pakistan., AbdelGawwad MR; Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo Sarajevo 71210, Bosnia and Herzegovina., Almutairi SM; Department of Botany and Microbiology, College of Science, King Saud University P.O. 2455, Riyadh 11451, Saudi Arabia., Elshikh MS; Department of Botany and Microbiology, College of Science, King Saud University P.O. 2455, Riyadh 11451, Saudi Arabia., Jamil M; PARC Arid Zone Research Center Dera Ismail Khan 29050, Pakistan., Rasheed RA; Histology & Cell Biology Department, Faculty of Medicine, King Salman International University South Sinai, Egypt.
Jazyk:	angličtina
Zdroj:	American journal of translational research [Am J Transl Res] 2023 Aug 15; Vol. 15 (8), pp. 5408-5424. Date of Electronic Publication: 2023 Aug 15 (Print Publication: 2023).
Abstrakt:	Background: Although evidence regarding pituitary tumor-transforming 3, pseudogene (PTTG3P) involvement in human cancers has been acquired via human and animal model-based molecular studies, there is a lack of pan-cancer analysis of this gene in human tumors. Methods: Tumor-causing effects of PTTG3P in 24 human tumors were explored using The Cancer Genome Atlas (TCGA) datasets from different bioinformatics databases and applying in silico tools such as The University of ALabama at Birmingham CANcer (UALCAN), Human Protein Atlas (HPA), Kaplan Meier (KM) plotter, cBioPortal, Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), Cytoscape, Database for Annotation, Visualization, and Integrated Discovery (DAVID), Tumor IMmune Estimation Resource (TIMER), and Comparative Toxicogenomics Database (CTD). Then, via in vitro experiments, including RNA sequencing (RNA-seq) and targeted bisulfite sequencing (bisulfite-seq), expression and promoter methylation levels of PTTG3P were verified in cell lines. Results: The PTTG3P expression was overexpressed across 23 malignancies and its overexpression was further found significantly effecting the overall survival (OS) durations of the esophageal carcinoma (ESCA) and head and neck cancer (HNSC) patients. This important information helps us to understand that PTTG3P plays a significant role in the development and progression of ESCA and HNSC. As for PTTG3P functional mechanisms, this gene along with its other binding partners was significantly concentrated in "Oocyte meiosis", "Cell cycle", "Ubiquitin mediated proteolysis", and "Progesterone-mediated oocyte maturation". Moreover, ESCA and HNSC tissues having the higher expression of PTTG3P were found to have lower promoter methylation levels of PTTG3P and higher CD8+ T immune cells level. Additionally, PTTG3P expression-regulatory drugs were also explored in the current manuscript for designing appropriate treatment strategies for ESCA and HNSC with respect to PTTG3P expression. Conclusion: Our pan-cancer based findings provided a comprehensive account of the oncogenic role and utilization of PTTG3P as a novel molecular biomarker of ESCA and HNSC. Competing Interests: None. (AJTR Copyright © 2023.)
Databáze:	MEDLINE
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