mProX™ Human LIFR Stable Cell Line

Chandrasekar, Bysani. et al. "Empagliflozin Reverses Oxidized LDL-Induced RECK Suppression, Cardiotrophin-1 Expression, MMP Activation, and Human Aortic Smooth Muscle Cell Proliferation and Migration." Mediators of inflammation, 2023.
Persistent oxidative stress and inflammation are key factors in the development of vascular proliferative diseases, manifested through the proliferation and migration of smooth muscle cells (SMCs). The presence of oxidatively modified low-density lipoproteins (OxLDL) further increases oxidative stress levels, inflammatory responses, and the activation of matrix metallopeptidases (MMPs), leading to SMC migration, proliferation, and changes in phenotype. Reversion-inducing cysteine-rich protein with Kazal motifs (RECK), a membrane-anchored MMP inhibitor, has been identified as a potential target for inhibiting this process. Empagliflozin, an SGLT2 inhibitor, has been found to have pleiotropic cardiovascular protective effects, including antioxidant and anti-inflammatory effects. This study aimed to determine (i) the effect of OxLDL on RECK expression, (ii) the potential of ectopic RECK expression to reverse OxLDL-induced SMC migration and proliferation, and (iii) whether pretreatment with empagliflozin could counteract the effects of OxLDL on RECK suppression, MMP activation, and SMC migration, proliferation, and differentiation. The findings demonstrate that pathophysiological levels of OxLDL promote SMC migration and proliferation via activation of NF-κB.
Chandrasekar, Bysani. et al. "Empagliflozin Reverses Oxidized LDL-Induced RECK Suppression, Cardiotrophin-1 Expression, MMP Activation, and Human Aortic Smooth Muscle Cell Proliferation and Migration." Mediators of inflammation, 2023.
Pubmed: 37830075   DOI: 10.1155/2023/6112301

Zhao, Chunlong. et al. "Discovery of Novel Fedratinib-Based HDAC/JAK/BRD4 Triple Inhibitors with Remarkable Antitumor Activity against Triple Negative Breast Cancer." Journal of medicinal chemistry, 2023.
In recent research, the potential of multitarget HDAC inhibitors that can block the BRD4-LIFR-JAK1-STAT3 signaling pathway simultaneously for treatment of TNBC and other solid tumors has been identified. This study specifically focuses on the rational design, synthesis, and biological evaluation of novel Fedratinib-based multitarget HDAC inhibitors. Results show that among the compounds tested, compound 17 demonstrates promising inhibitory activity against HDAC and TNBC cells. These findings suggest that compound 17 may hold promise as a potential treatment for TNBC and other solid tumors.
Zhao, Chunlong. et al. "Discovery of Novel Fedratinib-Based HDAC/JAK/BRD4 Triple Inhibitors with Remarkable Antitumor Activity against Triple Negative Breast Cancer." Journal of medicinal chemistry, 2023.
Pubmed: 37796543   DOI: 10.1021/acs.jmedchem.3c01242