mProX™ Human YES1 Stable Cell Line

Zhang, Ruzhen. et al. "Actin polymerization inhibition by targeting ARPC2 affects intestinal stem cell homeostasis." Burns & trauma, 2023.
In this research, the focus is on the turnover of intestinal epithelial cells driven by intestinal stem cells and the role of F-actin cytoskeleton dynamics in this process. They investigate the impact of benproperine (BPP), an anti-tumor drug, on this homeostasis. The study utilizes various methods, including fluorescence staining, flow cytometry, and organoid culture, to assess cell proliferation, differentiation, and migration. Results show that F-actin content increases during cell migration, particularly in Paneth cells, and BPP treatment affects organoid growth, cell proliferation, and gene expression related to intestinal stem cells and Paneth cell differentiation. This suggests a potential novel approach using BPP to influence intestinal epithelial cell turnover through cytoskeleton regulation.
Zhang, Ruzhen. et al. "Actin polymerization inhibition by targeting ARPC2 affects intestinal stem cell homeostasis." Burns & trauma, 2023.
Pubmed: 37849945   DOI: 10.1093/burnst/tkad038

Enokido, Takayoshi. et al. "Distinct microRNA signature and suppression of ZFP36L1 define ASCL1-positive lung adenocarcinoma." Molecular cancer research : MCR, 2023.
Achaete-scute family bHLH transcription factor 1 (ASCL1) serves as a key transcription factor in neuroendocrine differentiation and is found in roughly 10% of lung adenocarcinomas, contributing to tumor progression. The study delved into the microRNA (miRNA) patterns in ASCL1-positive lung adenocarcinomas and pinpointed several closely linked miRNAs, including miR-375, miR-95-3p/miR-95-5p, miR-124-3p, and members of the miR-17~92 family. These findings mirror the suppression of Yes1 associated transcriptional regulator (YAP1), a notable target of miR-375, observed in ASCL1-positive lung adenocarcinomas. The research also highlighted ASCL1's positive influence on miR-124-3p and miR-17~92 family members, underscoring ZFP36 ring finger protein like 1 (ZFP36L1) as a miR-124-3p target gene, while demonstrating low ZFP36L1 protein levels in ASCL1-positive lung adenocarcinomas. This study disclosed that the downregulation of ZFP36L1 by ASCL1-controlled miR-124-3p can impact gene expression, elucidating the role of ASCL1 in shaping the molecular characteristics of ASCL1-positive lung adenocarcinomas and suggesting potential clinical implications.
Enokido, Takayoshi. et al. "Distinct microRNA signature and suppression of ZFP36L1 define ASCL1-positive lung adenocarcinoma." Molecular cancer research : MCR, 2023.
Pubmed: 37801008   DOI: 10.1158/1541-7786.MCR-23-0229