Differential regulation and synthetic lethality of exclusive RB1 and CDKN2A mutations in lung cancer.

Genetic alterations in lung cancer are distinctly represented in non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma (SCLC). Mutation of the RB1 and CDKN2A genes, which are tightly associated with cell cycle regulation, is exclusive to SCLC and NSCLC cells, respectively. Through the systematic analysis of transcriptome and proteome datasets for 318 cancer cell lines, we characterized differential gene expression and protein regulation in RB1-mutant SCLC and CDKN2A-mutant NSCLC. Many of the genes and proteins associated with RB1-mutant SCLC cell lines belong to functional categories of gene expression and transcription, whereas those associated with CDKN2A-mutant NSCLC cell lines were enriched in gene sets of the extracellular matrix and focal adhesion. These results indicate that the loss of RB1 and CDKN2A function induces distinctively different signaling cascades in SCLC and NSCLC cells. In addition, knockdown of the RB1 gene in CKDN2A-mutant cell lines (and vice versa) synergistically inhibits cancer cell proliferation. The present study on the exclusive role of RB1 and CDKN2A mutations in lung cancer subtypes demonstrates a synthetic lethal strategy for cancer regulation.

Observation of highly reproducible resistive-switching behavior from solution-based ZnO nanorods.

The authors report upon highly reproducible, unipolar resistive-switching random access memory with narrow voltage distributions using Au/ZnO nanorods/Au structures. The ZnO nanorods resistive switching layer was prepared by a simple spin-coating process on a sol-gel seed layer, and from its size confinement effect, this device showed narrow set/reset voltage distributions and low voltage operations compared with Au/ZnO thin film/Au structures. With this electrical uniformity, the device exhibited good reliabilities such as long retention (> 70000 sec) and high endurance (> 5000 cycles).