Gene name: | NRSN2 |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | SMMC-7721 |
Gene ID: | 80023 |
Category: | protein coding |
Phenotype: | Hepatocellular carcinoma |
Experimental category: | L |
PMID: | 26055238 |
Experiment: | Cell viability assay//SA-β-gal activity assay |
Description: | We found that when NRSN2 was overexpressed, the cellular viability of SMMC-7721 decreased and the senescent cells increased after doxorubicin treatment for 48 h . |
Target gene: | BCL-2 |
Official symbol(s): | BCL-2 |
R-AG-Target gene: | -- |
Subcategory: | Unclear |
Target gene experiment: | Western blot//qRT-PCR |
Target gene description: | Considering the increased cell viabilities and the anti-senescence/apoptosis effect after NRSN2 silencing, we examined the change of PI3K/Akt pathway, which plays an important role in tumor growth [11] and Bcl-2 family proteins, which function as a critical modulator in cell apoptosis .Meanwhile, the cleaved PARP and pro-apoptotic protein Bax was decreased, while the anti-apoptotic protein Bcl-2 was significantly increased after NRSN2 silencing. |
Regulatory pathway: | PI3K-AKT-MTOR//P53-P21 |
R-AG-Pathway: | --//-- |
Official symbol(s): | PIK3CA-AKT1-MTOR//TP53-CDKN1A |
Pathway experiment: | Western blot |
Pathway description: | Knockdown of NRSN2 led to increased (473)p-Akt levels in MHCC-LM3 cells. After silencing NRSN2 in Hep3B, we treated these transfected cells with doxorubicin, a chemotherapeutic agent which is commonly used to induce cell senescence , for 2 days and we surprisingly found that compared to the control, the levels of p53 and p21 were decreased. |
Annotation:
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