Rac1b, an alternative splice form of Rac1, has been previously shown to be upregulated in colon and breast cancer cells, suggesting an oncogenic role for Rac1b in these cancers. Our analysis of NSCLC tumor and matched normal tissue samples indicates Rac1b is upregulated in a significant fraction of lung tumors in correlation with mutational status of K-ras. To directly assess the oncogenic potential of Rac1b in vivo, we employed a mouse model of lung adenocarcinoma, in which the expression of Rac1b can be conditionally activated specifically in the lung. While expression of Rac1b alone is insufficient to drive tumor initiation, the expression of Rac1b synergizes with an oncogenic allele of K-ras resulting in increased cellular proliferation and accelerated tumor growth. Finally, we show that in contrast to our previous findings demonstrating a requirement for Rac1 in K-ras-driven cell proliferation, Rac1b is not required in this context. Given the partially overlapping spectrum of downstream effectors regulated by Rac1 and Rac1b, our findings further delineate the signaling pathways downstream of Rac1 that are required for K-ras driven tumorigenesis.

Bright lights: Fullerene-silica hybrid nanoparticles have bright photoluminescence, high photostability, and low cytotoxicity, which are assets for bioimaging agents. The origin of the photoluminescence of the nanoparticle is the C-O-Si bond (see picture).

A porous metal–organic framework (MOF), Fe4(μ3-O)2(BTB)8/3(DMF)2(H2O)2·(DMF)10(H2O)2 (1) (BTB = benzene-1,3,5-tribenzoate, DMF = N,N-dimethylformamide) has two interpenetrating 3D frameworks composed of fused cages and shows a stronger affinity for CO2 than most other known highly porous MOFs. The unique tetranuclear iron–oxo clusters act as 8-connectors, which are linked by 3-connecting BTBs, to give a partially augmented the net (using the symbolism of O’Keeffe and co-workers). The underlying implications for (3,8)-coordinated networks are also discussed in relation to the framework structure of 1.