Molecular characterization and integrative genomic analysis of a panel of newly established penile cancer cell lines
| Autor: | Zai Shang Li, Fangjian Zhou, Zi Ke Qin, Zhuo Wei Liu, Kang bo Huang, Wenlin Huang, Ting Yu Liu, Qiang Hua Zhou, Jie Ping Chen, Chuang Zhong Deng, Kai Yao, Ranyi Liu, Hui Han |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male Cancer Research DNA Copy Number Variations Carcinogenesis Immunology Mice Nude Tumor initiation Biology Article Metastasis 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine CDKN2A Cell Movement Cell Line Tumor medicine Penile cancer Animals Humans Neoplasm Invasiveness HRAS lcsh:QH573-671 Penile Neoplasms Cell Proliferation lcsh:Cytology Cell growth Cancer Cell Biology Genomics medicine.disease ErbB Receptors 030104 developmental biology Cell culture 030220 oncology & carcinogenesis Mutation Cancer research Androgens Microsatellite Repeats |
| Zdroj: | Cell Death & Disease Cell Death and Disease, Vol 9, Iss 6, Pp 1-14 (2018) |
| ISSN: | 2041-4889 |
| Popis: | Cell line models are essential tools to study the molecular mechanisms underlying tumor initiation and progression. There are limited treatment options for penile squamous cell carcinoma (PSCC), accounting for 1–2% of male tumors in developing countries, and limited progress in preclinical research in PSCC due to lacking available models with identified genomic characteristics. Here, biological and molecular characteristics and whole-genomic alterations were analyzed in a panel of PSCC cell lines newly established in our laboratory. These cell lines were all human papillomavirus (HPV)-negative, epithelial-like, immortalized, and tumorigenic in nude mice, whereas they displayed different proliferation, migration and invasion capacities in vitro, and tumorigenic ability in nude mice. They were all cisplatin sensitive, anti-EGFR therapy resistant, and androgen irresponsive. Whole-genomic sequecing analysis revealed that transition mutations (C:G>T:A and T:A>C:G) were the most common substitution types in these cell lines, whereas ERCC5, TP53, PTH1, CLTCL1, NOTCH2, MAP2K3, CDK11A/B, USP6, ADCH5, BCLAF1, CDKN2A, FANCD2, HRAS, and NOTCH1 were the most frequently altered genes. Amplifications of MYC, PLAG1, NCOA2, RUNX1T1, COX6C, and EGFR and losses of FBXW7, TET2, XPC, and FANCE were frequently observed in cell lines. The exomic variations between cell lines and their corresponding cancer tissues were highly consistent. Genetic variations were mainly involved in the MAPK, Jak-STAT, TGF-beta, Notch, and apoptosis signaling pathways. Conclusively, these panel of PSCC cell lines established in our laboratory harbor some common or specific biological characteristics and genomic variations, and they may serve as optimal models to investigate the molecular mechanisms underlying the progression, metastasis, relapses, and treatment resistance of PSCC and to develop effective treatment strategy. |
| Databáze: | OpenAIRE |
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