mProX™ Human NEK9 Stable Cell Line

Joschua Ohnmacht, Alexander. et al. "The pharmacoepigenomic landscape of cancer cell lines reveals the epigenetic component of drug sensitivity." Communications biology, 2023.
The study focuses on the correlation between DNA methylation and cancer development and treatment response. Despite various efforts to understand this relationship, there is still a lack of epigenetic biomarkers to accurately predict the effectiveness of treatment. To address this issue, a comprehensive analysis of 721 cancer cell lines treated with 453 anti-cancer compounds was conducted across 22 cancer types. As a result, it was found that DNA methylation plays a significant role in predicting drug sensitivity through the regulation of gene expression. Additionally, the study highlights the potential of epigenetic biomarkers in refining patient stratification and advancing precision oncology.
Joschua Ohnmacht, Alexander. et al. "The pharmacoepigenomic landscape of cancer cell lines reveals the epigenetic component of drug sensitivity." Communications biology, 2023.
Pubmed: 37558831   DOI: 10.1038/s42003-023-05198-y

Lu, Guofang. et al. "Cancer associated fibroblast derived SLIT2 drives gastric cancer cell metastasis by activating NEK9." Cell death & disease, 2023.
Cancer-associated fibroblasts (CAFs) possess significant secretory properties that profoundly influence the pro-metastatic environment within tumors. A recent investigation unveiled the role of SLIT2, an axon guidance protein secreted by CAFs, in promoting gastric cancer (GC) metastasis by binding to the roundabout guidance receptor 1 (ROBO1) in two GC cell lines, AGS and MKN45. Mass-spectrometry analysis uncovered an interaction between ROBO1 and NEK9, a serine/threonine kinase, which was further intensified by SLIT2. Domain analysis highlighted the importance of NEK9's kinase domain in binding to ROBO1's intracellular domain (ICD) and its direct phosphorylation of tripartite motif containing 28 (TRIM28) and cortactin (CTTN) in AGS and MKN45 cells. TRIM28 functioned as a transcriptional elongation factor, facilitating CTTN activation. Bioinformatics analysis and experimental validation identified TRIM28's regulation of STAT3 and NF-κB p100, with a collaborative transcription of CTTN by STAT3 and NF-κB p100 observed in AGS and MKN45. Consequently, CAF-derived SLIT2 increased CTTN expression and phosphorylation, leading to cytoskeletal reorganization and GC cell metastasis. Metastatic GC lesions exhibited elevated levels of NEK9, TRIM28, and CTTN compared to non-cancerous tissues and primary cancer lesions, as confirmed through IHC and Multiplex IHC analysis. Patient data analysis revealed a correlation between increased NEK9, TRIM28, and CTTN levels and decreased overall survival in GC patients. These findings underscore the interplay between CAFs and cancer cells mediated by SLIT2/ROBO1 and inflammatory signaling, with potential implications for biomarker identification and GC therapy.
Lu, Guofang. et al. "Cancer associated fibroblast derived SLIT2 drives gastric cancer cell metastasis by activating NEK9." Cell death & disease, 2023.
Pubmed: 37443302   DOI: 10.1038/s41419-023-05965-z