NETO2 promotes progression of prostate cancer by inhibiting the cellular senescence pathway
Abstract Purpose: Prostate cancer (PCa) has become the most frequently occurring cancer among western men, due to the rapid progression of tumor, late events will inevitably occur, which leads to poor prognosis of patients. Therefore, it is of great significance to explore the molecular mechanism of tumor progression.Methods: Herein, we conducted a transcriptomic analysis using public database to search for key genes that affect PCa progression. The correlation between gene expression and clinical pathological parameters and patient prognosis were examined, and it was verified in clinical samples. Next, we established cell lines by RNA interference, and studied its biological function by MTS, EdU, colony formation, wound-healing and transwell assay. The impact of gene on tumor growth was examined in nude mice xenograft model. Finally, high-throughput sequencing and signal pathway analysis were used to explore the molecular mechanism of gene action.Results: By combining clinical samples with public databases, we found that NETO2 expression was markedly elevated in tumors especially in metastatic tumors compared with normal tissues, and the expression level of NETO2 was closely associated with the clinical pathological parameters and prognosis of the patients. Functionally, NETO2 drove PCa cell proliferation, migration and invasion in vitro, and promoted growth of PCa cells in vivo. Moreover, through transcriptome high-throughput sequencing and experimental verification, our data demonstrate that NETO2 inhibits PCa cellular senescence via modulating p53-p21 pathway.Conclusions: Our results indicate that NETO2 plays an oncogenic role in PCa, which provides a new idea for clinical diagnosis and treatment of refractory PCa..
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Preprint| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
ResearchSquare.com - (2022) vom: 26. Mai Zur Gesamtaufnahme - year:2022 |
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| Sprache: |
Englisch |
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| Beteiligte Personen: |
Liu, Yangzhou [VerfasserIn] |
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| Links: |
Volltext [kostenfrei] |
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| doi: |
10.21203/rs.3.rs-1682664/v1 |
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| funding: |
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XRA03610132X |
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| 520 | |a Abstract Purpose: Prostate cancer (PCa) has become the most frequently occurring cancer among western men, due to the rapid progression of tumor, late events will inevitably occur, which leads to poor prognosis of patients. Therefore, it is of great significance to explore the molecular mechanism of tumor progression.Methods: Herein, we conducted a transcriptomic analysis using public database to search for key genes that affect PCa progression. The correlation between gene expression and clinical pathological parameters and patient prognosis were examined, and it was verified in clinical samples. Next, we established cell lines by RNA interference, and studied its biological function by MTS, EdU, colony formation, wound-healing and transwell assay. The impact of gene on tumor growth was examined in nude mice xenograft model. Finally, high-throughput sequencing and signal pathway analysis were used to explore the molecular mechanism of gene action.Results: By combining clinical samples with public databases, we found that NETO2 expression was markedly elevated in tumors especially in metastatic tumors compared with normal tissues, and the expression level of NETO2 was closely associated with the clinical pathological parameters and prognosis of the patients. Functionally, NETO2 drove PCa cell proliferation, migration and invasion in vitro, and promoted growth of PCa cells in vivo. Moreover, through transcriptome high-throughput sequencing and experimental verification, our data demonstrate that NETO2 inhibits PCa cellular senescence via modulating p53-p21 pathway.Conclusions: Our results indicate that NETO2 plays an oncogenic role in PCa, which provides a new idea for clinical diagnosis and treatment of refractory PCa. | ||
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| 700 | 1 | |a Ma, Yuxiang |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Zuomin |e verfasserin |4 aut | |
| 700 | 1 | |a Pan, Jinyou |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Jiamin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Mingda |e verfasserin |4 aut | |
| 700 | 1 | |a Lin, Jingwei |e verfasserin |4 aut | |
| 700 | 1 | |a Cai, Yingxin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Zhigang |e verfasserin |4 aut | |
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