| External factors: | Lactate |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Lung cancer |
| Experiment: | SA-β-gal activity assay//Cell cycle analysis//Immunofluorescence |
| Description: | Remarkably, lactate decreased SA-β-gal activity in a dose-dependent manner.In contrast, the accumulation of γH2AX positive cells was significantly decreased upon lactate treatment.However, the majority of lactate-treated B2B/K-Ras showed a cell cycle progression though G2/M, as evident by accumulation of 4 N DNA content. |
| Target gene: | SNAIL//P16 |
| R-EF-Target gene: | Upregulation//Downregulation |
| Official symbol(s): | SNAIL//P16 |
| Target gene experiment: | qRT-PCR//Dual-Luciferase reporter assay |
| Target gene description: | Notably, lactate markedly upregulated Snail mRNA in a dose-dependent manner in both A549 and H1299 cells paralleled with obtained with Snail protein levels . Importantly, treatment with lactate attenuated p16INK4a expression activated by K-Ras oncogene. This finding is not oncogenic K-Ras specific, similar results were obtained with transfection of Activate B-Raf (V600E) and dominant negative PTEN(C124S) into B2B cells.qRT-PCR showed that lactate dose-dependently decreased p16INK4a mRNA levels in B2B cells Notably, the promoter activity of p16INK4a was significantly reduced by lactate treatment, indicating that lactate transcriptional regulate p16INK4a expression. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: