Methylation-mediated silencing of protein kinase C zeta induces apoptosis avoidance through ATM/CHK2 inactivation in dedifferentiated chondrosarcoma.
Eijiro ShimadaYoshihiro MatsumotoMakoto NakagawaYosuke SusukiMakoto EndoNokitaka SetsuToshifumi FujiwaraKeiichiro IidaAkira NabeshimaKenichiro YahiroAtsushi KimuraTakeshi HiroseMasaya KanahoriRyunosuke OyamaYoshinao OdaYasuharu NakashimaPublished in: British journal of cancer (2022)
Increased DNA methylation and reduced expression of PRKCZ prevents apoptosis via inactivation of the ATM/CHK2 pathway in DDCS. Decitabine-induced expression of PRKCZ represents a promising therapy for DDCS.
Keyphrases
- dna methylation
- dna damage response
- poor prognosis
- dna damage
- protein kinase
- genome wide
- dna repair
- oxidative stress
- gene expression
- binding protein
- acute myeloid leukemia
- endoplasmic reticulum stress
- diabetic rats
- high glucose
- long non coding rna
- mouse model
- cell death
- cell cycle arrest
- drug induced
- signaling pathway