The interplay between IQGAP1 and small GTPases in cancer metastasis.

The metastatic spread of tumor cells to distant anatomical locations is a critical cause for disease progression and leads to more than 90 % of cancer-related deaths. IQ motif-containing GTPase-activating protein 1 (IQGAP1), a prominent regulator in the cancer metastasis process, is a scaffold protein that interacts with components of the cytoskeleton. As a critical node within the small GTPase network, IQGAP1 acts as a binding partner of several small GTPases, which in turn function as molecular switches to control most cellular processes, including cell migration and invasion. Given the significant interaction between IQGAP1 and small GTPases in cancer metastasis, we briefly elucidate the role of IQGAP1 in regulating cancer metastasis and the varied interactions existing between IQGAP1 and small GTPases. In addition, the potential regulators for IQGAP1 activity and its interaction with small GTPases are also incorporated in this review. Overall, we comprehensively summarize the role of IQGAP1 in cancer tumorigenicity and metastasis, which may be a potential anti-tumor target to restrain cancer progression.

Generation of a Murine Model for c-MYC and BCL2 Co-expression B Cell Lymphomas.

Diffuse large B-cell lymphoma (DLBCL) is the most frequent lymphoma in adults, and is characterized as clinically and biologically heterogeneous lymphomas with diverse response to therapy and variation in clinical behavior. It's well-established that c-MYC and BCL2 play important roles in normal B-cell differentiation and tumorigenesis. B cell lymphoma with dual expression of c-MYC and BCL2 (double-expressor lymphoma, DEL) accounts for approximately one-third of DLBCL cases. DEL patients have poor outcomes after chemoimmunotherapy or autologous stem-cell transplantation. Lack of a genetic mouse tool for DEL hinders us from understanding the lymphogenesis mechanism and developing therapeutic strategies. Here, we investigated whether ectopic expression of c-MYC and BCL2 in different stages of B cells could lead to lymphoma and generate a mouse model for DEL. We observed that Co-expression of c-MYC and BCL2 in germinal center (GC) B cells, or pan-B cells could induce B cell lymphomas. The tumor-bearing mice have enlarged lymphoid organs, and B cells massively infiltrate into non-lymphoid organs including lung, liver and kidney. The tumor-bearing mice also manifested significantly shorter lifespan than the controls. In addition, adoptive transfer of Co-expression B cells leads to B cell lymphoma and host mice death. This model will provide us a tool to further explore the pathogenesis and treatment approaches for DEL.

Unexpectedly high stability and surface reconstruction of PdAuAg nanoparticles for formate oxidation electrocatalysis.

High-performance Pd-based nanocatalysts for alkaline methanol and formate fuel cells have stimulated widespread attention. Hence, a series of ternary Pd-Au-Ag nanoalloys have been synthesized on carbon nanotubes, which demonstrate promising activity and unexpectedly high stability for the formate oxidation reaction (FOR) in alkaline medium. The ternary Pd3Au3Ag1 nanoalloy catalyst showed an initial mass activity of 4.51 A mgPd-1 and a retained mass activity of 1.32 A mgPd-1 after chronoamperometric measurement for 3600 s, which are superior to the best values for all FOR catalysts reported so far. The Pd3Au3Ag1 catalyst also showed a good specific activity of 4.32 mA cm-2 for the methanol oxidation reaction. Furthermore, surface reconstruction of the Pd3Au3Ag1 nanoalloy was observed during FOR, where the activity of Pd3Au3Ag1 catalysts increased up to 33% and the cycling durability retained 55% after cyclic voltammetry with the upper potential of 1.7 V. The FOR enhancement is attributed to the formation of mixed oxidation-state Ag sites and the increase in the Pd surface coverage, and provides a new prospect for the design of ternary nanoalloy electrocatalysts for various fuel oxidation reactions.