Repurposing of sildenafil as antitumour; induction of cyclic guanosine monophosphate/protein kinase G pathway, caspase-dependent apoptosis and pivotal reduction of Nuclear factor kappa light chain enhancer of activated B cells in lung cancer.
Amira M AboYoussefMarwa M KhalafMarina N MalakMohamed A HamzawyPublished in: The Journal of pharmacy and pharmacology (2021)
These results indicated that sildenafil markedly induces cell cycle arrest, apoptosis and inhibits the metastatic activity through activation of cyclic guanosine monophosphate/protein kinase G pathway and down-regulation of cyclin D1 and nuclear factor kappa light chain enhancer of activated B cells with downstream anti-apoptotic gene Bcl-2, which underscores the critical importance of future using sildenafil in the treatment of lung cancer.
Keyphrases
- nuclear factor
- cell cycle arrest
- cell death
- protein kinase
- toll like receptor
- pulmonary hypertension
- pulmonary arterial hypertension
- pi k akt
- binding protein
- transcription factor
- squamous cell carcinoma
- small cell lung cancer
- copy number
- signaling pathway
- genome wide
- current status
- inflammatory response
- gene expression
- immune response
- induced apoptosis
- oxidative stress
- endoplasmic reticulum stress
- cell proliferation
- genome wide identification
- cell cycle