Project description:Analysis of TE-1 cells following knockdown of EI24 and control vector. Etoposide induced 2.4 kb transcript (EI24), also known as p53-induced gene 8 (PIG8), is located on human chromosome 11q23. Serving as a p53 responsive pro-apoptotic factor, EI24 plays a pivotal role in inhibiting cell growth and activating autophagy and is associated with drug resistance. Results provide insight into the role of EI24 in cell proliferation and drug resistance of ESCC cells.
Project description:Analysis of EC109 cells following overexpression of EI24 and control vector. Etoposide induced 2.4 kb transcript (EI24), also known as p53-induced gene 8 (PIG8), is located on human chromosome 11q23. Serving as a p53 responsive pro-apoptotic factor, EI24 plays a pivotal role in inhibiting cell growth and activating autophagy and is associated with drug resistance. Results provide insight into the role of EI24 in cell proliferation and drug resistance of ESCC cells.
Project description:Analysis of ZR-75-1 cells folowing knockdown of EI24 (P53-Induced Gene 8) and control vector. As a p53 response gene, EI24 is known to controlling cell growth, apoptosis, and autophagy. Results provide insight into the role of EI24 in epithelial-to-mesenchymal Parental ZR-75-1 cells, ZR-75-1 cells with shGFP knockdown (control), Two independent clone of knockdown of EI24 in ZR-75-1. All samples are perfomed in duplicate. Total 8 samples exist.
Project description:Analysis of ZR-75-1 cells folowing knockdown of EI24 (P53-Induced Gene 8) and control vector. As a p53 response gene, EI24 is known to controlling cell growth, apoptosis, and autophagy. Results provide insight into the role of EI24 in epithelial-to-mesenchymal
Project description:To understand the difference of protein expression between paired esophageal squamous cell carcinoma (ESCC) and adjacent normal tissues, we collected 10 paired ESCC and normal tissues from surgical resected specimems for high-throughput proteomic experiments. From comparative analysis, the dysregulated signaling pathways in ESCC could be uncovered.