Crystal structure of hexa-methyl 4,4',4'',4''',4'''',4'''''-[(1,3,5,2λ5,4λ5,6λ5-tri-aza-triphosphinine-2,2,4,4,6,6-hexa-yl)hexa-kis-(-oxy)]hexa-benzoate.

The title compound, C48H42N3O18P3, achieved in a two-step synthesis, comprises a cyclo-triphosphazene core and six 4-meth-oxy-carbonyl-phen-oxy groups. Each P atom is attached to two substituents located up and down with respect to the plane of the phosphazene ring, the central P3N3 ring having a twist-boat conformation. The three O/P/O planes and five of the six benzene rings are nearly perpendicular to the mean plane through the phosphazene ring [dihedral angles = 82.98 (8)-88.92 (8)°], while the remaining benzene ring forms a dihedral angle of 25.72 (7)°. The crystal packing is stabilized by van der Waals inter-actions only.

Regulation of cancerous progression and epithelial-mesenchymal transition by miR-34c-3p via modulation of MAP3K2 signaling in triple-negative breast cancer cells.

Emerging but limited data have evidenced an essential involvement of microRNAs (miRNAs) in the development and progression of triple negative breast cancer (TNBC), which empowers these small regulators as an innovative therapeutic approach, especially for this unique tumor subgroup still lacking an efficient and specific therapeutic target. Herein, we reported the down-regulation of miR-34c-3p level in TNBC tissues, and its expression was closely associated with estrogen receptor alpha (ERα), but not other receptors, in well-characterized breast cancer (BCa) cells. Functionally, ectopic expression of miR-34c-3p inhibited migration, invasion and epithelial-mesenchymal transition (EMT) in TNBC cells. From a mechanistic standpoint, bioinformatics coupled with luciferase and gain-of-function, loss-of-function assays showed that miR-34c-3p may regulate TNBC progression by directly targeting the 3'-untranslated region (UTR) of mitogen-activated protein kinase kinase kinase 2 (MAP3K2). Consistently, MAP3K2 overexpression could effectively rescue miR-34c-3p mimics-induced suppression of cell invasion and EMT. In light of these findings, miR-34c-3p may function as a tumor suppressor in regulating of TNBC invasiveness and EMT through negatively modulating MAP3K2 pathway. Future endeavor in this field may help to identify a novel biomarker to predict prognosis and response to therapy in TNBC.

Effects of T20N Site-directed Mutation on GTPase Activities of OsRacD from Oryza sativa / 中国生物工程杂志

OsRacD belonging to rice Rho family of the small GTP binding proteins,is a pivotal gene involved in rice photoperiod fertility conversion of photoperiod sensitive genic male sterile rice,which influences rice fertility via controlling the pollen tube growth.T20N site-directed mutation was introduced into its highly conserved G1 motif by PCR-mediated method to mimic its GDP-binding state based on the sequences alignment and conserved domains analysis.The prokaryotic expression vector of OsRacD and T20N-OsRacD were constructed,and the His6 tag fused proteins were expressed and purified from E.coli.After identified by Western blot,the GTP hydrolysis activities were detected.The results showed that the GTPase activities of T20N-OsRacD were significantly reduced comparing with that of OsRacD,suggested that OsRacD and T20N-OsRacD have different biochemical characteristics.

Identification of the Genetic Interaction Between OsMY1 and OsRacD from Oryza sativa.L / 中国生物工程杂志

OsRacD is a critical molecular switch involved in photoperiod fertility conversion of photoperiod sensitive genic male sterile rice.Taking OsRacD as bait,a new rice myosin heavy chain partial cDNA was isolated from the rice panicle by yeast two-hybrid,and designated OsMY1.The interaction between OsMY1 and OsRacD had been testified by yeast two-hybrid and pull down assay,it showed that OsMY1 could bind with OsRacD,suggested that OsMY1 maybe the target of OsRacD.The important evidence for further study on the functional relationship between OsMY1 and OsRacD in vivo are also provided.