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PAS Domain Containing Repressor 1 (PASD1) Promotes Glioma Cell Proliferation Through Inhibiting Apoptosis In Vitro

BACKGROUND: PAS domain containing repressor 1 (PASD1), the cancer-testis antigen (CTA), has been reported to be aberrantly expressed in various cancer tissues and cancer cell lines; however, normal PASD1 expression can be detected in normal tissue, excluding testicular tissue. Moreover, PASD1 is rep...

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Detalles Bibliográficos
Autores principales: Li, Ruoyan, Guo, Mengguo, Song, Laijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6761850/
https://www.ncbi.nlm.nih.gov/pubmed/31558691
http://dx.doi.org/10.12659/MSM.916308
Descripción
Sumario:BACKGROUND: PAS domain containing repressor 1 (PASD1), the cancer-testis antigen (CTA), has been reported to be aberrantly expressed in various cancer tissues and cancer cell lines; however, normal PASD1 expression can be detected in normal tissue, excluding testicular tissue. Moreover, PASD1 is reported to be abnormally expressed in various malignant tumors. However, it remains unclear whether PASD1 participates in tumorigenesis of glioma. MATERIAL/METHODS: PASD1 expression was detected by immunohistochemistry in 155 glioma tissue specimens in this study. Furthermore, the relationship of PASD1 expression with clinicopathological features in glioma cases was statistically analyzed. In addition, PASD1 was knocked down by small interference RNA (shRNA) in glioma cell line (LN229), so as to assess the potential to use it as the target for treating glioma. RESULTS: Our findings suggested that PASD1 expression in glioma patients was extremely upregulated compared with that in normal tissue samples and cell lines. Moreover, PASD1 expression was found to be markedly correlated with gender, The World Health Organization grade and p53 expression; in addition, high PASD1 expression indicated poor prognosis for glioma patients. Additionally, downregulation of PASD1 inhibited the proliferation ability of cells and resulted in cell arrest at the G2/M phase, which was achieved through accelerating apoptosis. Furthermore, our results indicated that PASD1 downregulation could upregulate some apoptosis-modulating proteins at the same time it downregulated some cycle-regulating proteins. CONCLUSIONS: Taken together, our findings demonstrated that PASD1, an oncogene, can potentially serve as an independent prognostic factor for glioma patients.