RESUMO
Torenia violacea (Azaola) Pennell 1943 as a traditional Chinese medicine plant, has been used to treat multiple diseases. In this study, we sequenced, assembled, and characterized the complete plastome of T. violacea. The plastome (OQ167784) exhibited a typical quadripartite structure, with a total length of 154,007 bp, comprising a pair of inverted repeats (IRs; 24,809 bp) separated by a large single-copy (LSC) region (85,559 bp) and a small single-copy (SSC) region (18,830 bp). Through genome annotation, we identified 133 genes, including 87 protein-coding genes, eight rRNA genes, and 38 tRNA genes. Phylogenetic analysis revealed a close relationship between T. violacea and T. fournieri. The research results provide basic genetic resources for the development of species identification and investigation of phylogenetic relationships in the Torenia genus.
RESUMO
As evidenced by the behavior of loss-of-function mutants of PTEN in the context of a gain-of-function mutation of AKT1, the PTEN-AKT1 signaling pathway plays a critical role in human cancers. In this study, we demonstrated that a deficiency in PTEN or activation of AKT1 potentiated the expression of platelet-derived growth factor receptor α (PDGFRα) based on studies on Pten-/- mouse embryonic fibroblasts, human cancer cell lines, the hepatic tissues of Pten conditional knockout mice, and human cancer tissues. Loss of PTEN enhanced PDGFRα expression via activation of the AKT1-CREB signaling cascade. CREB transactivated PDGFRα expression by direct binding of the promoter of the PDGFRα gene. Depletion of PDGFRα attenuated the tumorigenicity of Pten-null cells in nude mice. Moreover, the PI3K-AKT signaling pathway has been shown to positively correlate with PDGFRα expression in multiple cancers. Augmented PDGFRα was associated with poor survival of cancer patients. Lastly, combination treatment with the AKT inhibitor MK-2206 and the PDGFR inhibitor CP-673451 displayed synergistic anti-tumor effects. Therefore, activation of the AKT1-CREB-PDGFRα signaling pathway contributes to the tumor growth induced by PTEN deficiency and should be targeted for cancer treatment.
