| General information | Literature | Expression | Regulation | Mutation | Interaction |
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Basic Information |
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Gene ID | 4862 |
Name | NPAS2 |
Synonymous | MOP4|PASD4|bHLHe9;neuronal PAS domain protein 2;NPAS2;neuronal PAS domain protein 2 |
Definition | PAS domain-containing protein 4|basic-helix-loop-helix-PAS protein MOP4|class E basic helix-loop-helix protein 9|member of PAS protein 4|member of PAS superfamily 4|neuronal PAS domain-containing protein 2|neuronal PAS2 |
Position | 2q11.2 |
Gene type | protein-coding |
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Title |
Abstract |
| Silencing NPAS2 promotes cell growth and invasion in DLD-1 cells and correlated with poor prognosis of colorectal cancer. | Emerging evidences show that circadian rhythm disorder is an important factor of tumor initiation and development. Neuronal PAS domain protein2 (NPAS2), which is the largest circadian gene, has been proved to be a novel prognostic biomarker in breast cancer and non-Hodgkins lymphoma. However, the potential functions of NPAS2 in colorectal cancer are still unknown. In our present study, we detected the mRNA expressions of NPAS2 in 108 CRC patients by RT-PCR, and found that NPAS2 expression was significantly down-regulated in tumor tissues than that in NATs. Clinicopathologic analysis revealed that low expression of NPAS2 was associated with the tumor size, TNM stage and tumor distance metastasis in colorectal cancer (p<0.05). Furthermore, we effectively down-regulated NPAS2 mRNA expression by transfecting RNA interfere fragments into DLD-1 cells, and our results in vitro demonstrated that silencing NPAS2 expression could promote cell proliferation, cell invasion and increase the wound healing ability (p<0.05). However, down-regulating NPAS2 expression did not influence the apoptotic rate in DLD-1 cells (p>0.05). In conclusion, our study suggested that NPAS2, functioned as a potential tumor suppressor gene, could serve as a promising target and potential prognostic indicator for colorectal cancer. |