Modulated electro-hyperthermia induced p53 driven apoptosis and cell cycle arrest additively support doxorubicin chemotherapy of colorectal cancer in vitro.
Tamas VancsikGertrud ForikaAndrea BaloghEva KissTibor KrenácsPublished in: Cancer medicine (2019)
In C26 colorectal adenocarcinoma mEHT-induced irreversible cell stress can activate both caspase-dependent apoptosis and p21waf1 mediated growth arrest pathways, likely to be driven by the upregulated nuclear p53 protein. Elevated phospho-p53(Ser15) might contribute to p53 escape from mdm2 control, which was further supported by reduced phospho-Akt(Ser473) protein levels. In combinations, mEHT could promote the uptake and significantly potentiate the cytotoxic effect of doxorubicin.
Keyphrases
- cell cycle arrest
- cell death
- pi k akt
- diabetic rats
- oxidative stress
- high glucose
- endoplasmic reticulum stress
- signaling pathway
- drug delivery
- squamous cell carcinoma
- protein protein
- locally advanced
- cell proliferation
- single cell
- amino acid
- induced apoptosis
- stem cells
- cell cycle
- rectal cancer
- mass spectrometry
- small molecule
- stress induced