Anti-RTKN2 monoclonal antibody, clone 3D3

As one of the most common malignancies in the world, lung adenocarcinoma (LUAD) is currently difficult to cure. However, the advent of precision medicine provides an opportunity to improve the treatment of lung cancer. Subtyping lung cancer plays an important role in performing a specific treatment. Here, we developed a framework that combines k-means clustering, t-test, sensitivity analysis, self-organizing map (SOM) neural network, and hierarchical clustering methods to classify LUAD into four subtypes. We determined that 24 differentially expressed genes could be used as therapeutic targets, and five genes (i.e., RTKN2, ADAM6, SPINK1, COL3A1, and COL1A2) could be potential novel markers for LUAD. Multivariate analysis showed that the four subtypes could serve as prognostic subtypes. Representative genes of each subtype were also identified, which could be potentially targetable markers for the different subtypes. The function and pathway enrichment analyses of these representative genes showed that the four subtypes have different pathological mechanisms. Mutations associated with the subtypes, e.g., epidermal growth factor receptor (EGFR) mutations in subtype 4 and tumor protein p53 (TP53) mutations in subtypes 1 and 2, could serve as potential markers for drug development. The four subtypes provide a foundation for subtype-specific therapy of LUAD.

Human osteosarcoma is the most frequent primary malignant of bone, and often occurs in adolescents. However, molecular mechanism of this disease remains unclear. In the present study, we found that the level of Rhotekin 2 (RTKN2) was up-regulated in osteosarcoma tissues and cell lines. In addition, silencing of RTKN2 of human osteosarcoma cell lines U2OS, inhibited proliferation, and induced G1 phase cell cycle arrest via reducing the level of the cyclin-dependent kinase 2 (CDK2). Furthermore, RTKN2 knockdown in the U2OS cells induced apoptosis by increasing the level of Bax and decreasing the level of Bcl2. These results suggested that RTKN2 is involved in the progression of human osteosarcoma, and may be a potential therapeutic target.