RESUMO
In this study, a series of enantioenriched sp3-Ge/B bimetallic modules were successfully synthesized via an enantioselective copper-catalyzed hydroboration of carbagermatrane (Ge)-containing alkenes. Orthogonal cross-coupling selectivity under different Pd-catalyzed conditions was achieved in an enantiospecific manner. Notably, the chiral secondary Ge exhibited a remarkable transmetallation ability prior to primary or secondary Bpin. The effectiveness of this Ge/B bimetallic strategy was further demonstrated through the development of new functional small molecules with Aggregation-Induced Emission (AIE) and Circularly Polarized Luminescence (CPL) performance. This represents the first successful example of synthesis of enantioenriched alkylgermanium reagents that permit enantiospecific cross-coupling reactions.
RESUMO
Metabolic reprogramming plays a critical role in hepatocarcinogenesis. However, the mechanisms regulating metabolic reprogramming in primary liver cancer (PLC) are unknown. Differentially expressed miRNAs between PLC and normal tissues were identified using bioinformatic analysis. RT-qPCR was used to determine miR-10b-5p and SCL38A2 expression levels. IHC, WB, and TUNEL assays were used to assess the proliferation and apoptosis of the tissues. The proliferation, migration, invasion, and apoptosis of PLC cells were determined using the CCK-8 assay, Transwell assay, and flow cytometry. The interaction between miR-10b-5p and SLC38A2 was determined using dual-luciferase reporter assay. A PLC xenograft model in BALB/c nude mice was established, and tumorigenicity and SLC38A2 expression were estimated. Finally, liquid chromatography - mass spectrometry (LC-MS) untargeted metabolomics was used to analyze the metabolic profiles of xenograft PLC tissues in nude mice. miR-10b-5p was a key molecule in the regulation of PLC. Compared with para-carcinoma tissues, miR-10b-5p expression was increased in tumor tissues. miR-10b-5p facilitated proliferation, migration, and invasion of PLC cells. Mechanistically, miR-10b-5p targeted SLC38A2 to promote PLC tumor growth. Additionally, miR-10b-5p altered the metabolic features of PLC in vivo. Overexpression of miR-10b-5p resulted in remarkably higher amounts of lumichrome, folic acid, octanoylcarnitine, and Beta-Nicotinamide adenine dinucleotide, but lower levels of 2-methylpropanal, glycyl-leucine, and 2-hydroxycaproic acid. miR-10b-5p facilitates the metabolic reprogramming of PLC by targeting SLC38A2, which ultimately boosts the proliferation, migration, and invasion of PLC cells. Therefore, miR-10b-5p and SLC38A2 are potential targets for PLC diagnosis and treatment.
Assuntos
Neoplasias Hepáticas , MicroRNAs , Animais , Camundongos , Humanos , Camundongos Nus , Linhagem Celular Tumoral , MicroRNAs/genética , MicroRNAs/metabolismo , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Carcinogênese , Proliferação de Células , Movimento Celular/genética , Regulação Neoplásica da Expressão Gênica , Apoptose , Sistema A de Transporte de Aminoácidos/metabolismoRESUMO
OBJECTIVES: This study aimed to investigate role of Numb in the epithelial mesenchymal transition (EMT) of breast cancer. METHODS: Numb and ß-catenin were inhibited in MCF-7 cells using sh-RNA and overexpressed in T47D cells by pcDNA3.0-Numb, pcDNA3.0-ß-catenin. Cell proliferation, invasion and migration were evaluated using MTT and Transwell assay, respectively. ß-catenin, Lin28, and EMT related markers were determined using qRT-PCR and Western Blotting. RESULTS: Knockdown of Numb significantly promoted the proliferation, invasion and migration of MCF-7 cells, further increased the expression of ß-catenin, Lin28, Snail-1, and N-cadherin, as well as decreased E-cadherin. In T47D cells transfected with pcDNA3.0-Numb, the results were quite the reverse. CONCLUSIONS: Knockdown of Numb could promote the EMT of breast cancer cells via ß-cateni/Lin28 signaling pathway.
Assuntos
Neoplasias da Mama/metabolismo , Proteínas de Membrana/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Proteínas de Ligação a RNA/metabolismo , beta Catenina/metabolismo , Neoplasias da Mama/genética , Neoplasias da Mama/patologia , Caderinas/genética , Caderinas/metabolismo , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Transição Epitelial-Mesenquimal/genética , Feminino , Humanos , Células MCF-7 , Proteínas de Membrana/genética , Proteínas do Tecido Nervoso/genética , Interferência de RNA , Proteínas de Ligação a RNA/genética , Transdução de Sinais/genética , beta Catenina/genéticaRESUMO
OBJECTIVE: To treat superficial hemangioma in children according to the local blood flow. METHODS: A total of 98 children with superficial hemangiomas admitted to our hospital from January 2005 to June 2009, and their clinical data were analyzed. RESULTS: According to the local blood flow velocity, 98 children were treated with injections or injection plus surgical treatment, respectively. Ninety-four children (95.9%) were cured. CONCLUSION: Injection therapy is effective for children with superficial hemangioma, but we should arrange individualized treatment according to the local blood flow in children.
