Gene name: | SCN9A |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | HEC |
Experiment: | SA-β-gal activity assay//RT-qPCR//Knockdown |
Description: | As expected, inducing the oncogenic stress (+4-OHT) resulted in proliferation arrest, as demonstrated by their reduced ability to form colonies and by the decrease in the level of the proliferation marker KI67,while it led to an increase in the SA-β-Gal activity and in the expression of two SASP components IL8 and IL6,both major hall-marks of senescence. Strikingly, the knockdown of SCN9A in HEC-TM cells overcame all of the hallmarks of senescence induced by an oncogenic stress. |
Target gene: | NF-KB |
Official symbol(s): | NF-KB |
R-AG-Target gene: | -- |
Subcategory: | Unclear |
Target gene experiment: | qRT-PCR//Immunofluorescence |
Target gene description: | We examined whether or not the inhibition of NF-KB transcription factors, either by constitutively expressing a stabilized version of IKBA (mIKBA), a well-known inhibitor of NF-KB, or by knocking down the expression of RELA, the main subunit of the NF-KB transcription factors, blocked the induction of SCN9A during OIS. Both approaches significantly reduced the induction of SCN9A following an oncogenic stress at the mRNA, as well as at the protein levels. |
Regulatory pathway: | CA-RB-E2F |
R-AG-Pathway: | -- |
Official symbol(s): | Regulation of retinoblastoma protein |
Pathway experiment: | qRT-PCR//Live calcium imaging |
Pathway description: | The inhibition of Rb by E7 prevented the repression of mitotic genes induced by plasma membrane depolarization and blocked plasma membrane depolarization-induced senescence.We observed increased calcium after plasma membrane depolarization in HEC-T cells. |
Annotation:
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