Phenylisotertronic acids from the TCM endophytic fungus Phyllosticta sp.

Four new phenylisotertronic acids (1a/1b, 2a, and 3a) were isolated from a TCM endophytic fungal strain Phyllosticta sp. J13-2-12Y obtained from the leaves of Acorus tatarinowii, along with two known ones (2b and 3b). Compounds 1-3 all existed as mixtures of enantiomers, and their corresponding optically pure enantiomers were successfully isolated by chiral HPLC. The structures of isolated compounds were determined by comprehensive spectroscopic analyses and X-ray diffraction. Their absolute configurations were determined by ECD experiments and quantum chemical calculations. In addition, the antimicrobial activities and the cytotoxicities of these three pairs of optically pure enantiomers (1a/1b, 2a/2b, and 3a/3b) had been evaluated.

Phyllomeroterpenoids A-C, Multi-biosynthetic Pathway Derived Meroterpenoids from the TCM Endophytic Fungus Phyllosticta sp. and their Antimicrobial Activities.

Phyllomeroterpenoids A-C (1-3), multi-biosynthetic pathway derived meroterpenoids from amino acid/pentose phosphate/terpenoid pathways, were isolated from the TCM endophytic fungus Phyllosticta sp. J13-2-12Y, together with six biosynthetically related compounds (4-9). All structures were determined by extensive spectroscopic analysis, chemical derivatization, and ECD experiments. A plausible biosynthetic pathway of 1-3 was proposed. In addition, the antimicrobial activities of all isolated compounds were evaluated against Staphylococcus aureus 209P (bacterium) and Candida albicans FIM709 (fungus).

XIAP 3'-untranslated region as a ceRNA promotes FSCN1 function in inducing the progression of breast cancer by binding endogenous miR-29a-5p.

The non-coding 3'-untranslated region (UTR) of genes play an important role in the regulation of microRNA (miRNA) functions, since it can bind and inactivate multiple miRNAs. Herein, we report that ectopic expression of XIAP 3'UTR increased human breast cancer cells proliferation, colony formation, migration, invasion and xenograft tumor growth and suppressed tumor cell death. To investigate this process, we further correlated the genome-wide transcriptional profiling with the gene expression alterations after transfecting XIAP 3'UTR in MCF-7 cells. We identified a robust, genome-wide mechanism of cell migration, motility and epithelial to mesenchymal transition by which mediated by a previously described cellular component movement factor FSCN1. Expression of XIAP and FSCN1 were up-regulated synergistically after transfecting XIAP 3'UTR in vitro and in vivo. Interactions between XIAP and FSCN1 appear to be a key determinant of these processes. Co-transfection with Dicer siRNA reversed the XIAP 3'UTR-mediated oncogenicity, suggesting the miRNAs might be involved in that process. Furthermore, we demonstrated that one miRNA, miR-29a-5p, can bind to both the XIAP and FSCN1 3'UTRs and play an important role in that interactions. We showed that the 3'UTR of XIAP was able to antagonize miR-29a-5p, and resulted in the increased translation of XIAP and FSCN1. Thus, our findings reveal important new insights into how XIAP 3'UTR works, suggesting that the non-coding XIAP 3'UTR serves as a competitor for miRNA binding and subsequently inactivates miRNA functions, by which XIAP 3'UTR frees the target mRNAs from being repressed.