Find Paper, Faster
Example:10.1021/acsami.1c06204 or Chem. Rev., 2007, 107, 2411-2502
Down-regulation of PTTG1 suppresses PDGF-BB-induced proliferation, migration and extracellular matrix production of airway smooth muscle cells (ASMCs) by regulating PI3K/AKT/mTOR signaling pathway
Molecular & Cellular Toxicology  (IF1.08),  Pub Date : 2021-07-27, DOI: 10.1007/s13273-021-00155-4
Guodong Cheng, Xiaowei Liu, Ping Li, Yan Li


To investigate the biological functions and the molecular mechanisms of PTTG1 in PDGF-BB-induced ASMCs.


QPCR and western blotting were used to detect PTTG1 levels in PDGF-BB-induced ASMCs. MTT, BrdU incorporation, cell apoptosis and cell invasion assays were performed to evaluate the effect of PTTG1 on cell proliferation, invasion and apoptosis, respectively. Western blotting was also used to assess the extracellular matrix and PI3K/AKT/mTOR signaling pathway components in PDGF-BB-induced ASMCs.


PTTG1 was highly expressed in PDGF-BB-induced ASMCs. The depletion of PTTG1 suppressed the proliferation and motility of PDGF-BB-induced ASMCs. The data further showed that PTTG1 ablation stimulated cell apoptosis, and inhibited the production of extracellular matrix by PDGF-BB-induced ASMCs. Mechanically, PTTG1 depletion inhibited the PI3K/AKT/mTOR signaling pathway, thereby inhibiting proliferation, motility, and extracellular matrix production.


PTTG1 could serve as a promising molecular target for the treatment of asthma.