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1.
Cancer Biol Ther ; 25(1): 2315651, 2024 12 31.
Artigo em Inglês | MEDLINE | ID: mdl-38390840

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/metabolismo
2.
BMC Complement Med Ther ; 23(1): 239, 2023 Jul 17.
Artigo em Inglês | MEDLINE | ID: mdl-37461034

RESUMO

INTRODUCTION: Colon cancer remains one of the most prevalent cancers worldwide. Unfortunately, there are no recognized and effective therapeutic strategies to prevent tumor recurrence after radical resection and chemotherapy, and the disease-free survival (DFS) in patients with stage IIIB or IIIC disease remains unsatisfactory. Xian-Lian-Jie-Du optimization decoction (XLJDOD) is a Chinese herbal medicine (CHM) empirical prescription, which has been validated experimentally and clinically that could inhibit the progression of colorectal cancer and ameliorate the symptoms. The purpose of this study is to evaluate the efficacy and safety of XLJDOD in prevention of recurrence of colon cancer. METHODS: This study is a multi-center, double-blind, randomized, placebo-controlled trial conducted at 13 hospitals of China. Following the completion of surgery and adjuvant 5- fluorouracil-based chemotherapy, a total of 730 subjects with stage IIIB or IIIC colon cancer will be randomized in a 1:1 ratio to an intervention group (n = 365; XLJDOD compound granule) and a control group (n = 365; Placebo). Patients will receive 6-month treatments and be followed up with 3 monthly assessments for 2 years. The primary outcome is 2-year DFS rate and the secondary outcomes are 1, 2-year relapse rate (RR), overall survival (OS) and quality of life (QoL). Safety outcomes such as adverse events will be also assessed. A small number of subgroup analysis will be carried out to explore the heterogeneity of effects of XLJDOD. DISCUSSION: The outcomes from this randomized controlled trial will provide objective evidences to evaluate XLJDOD's role as an adjuvant treatment in colon cancer. TRIAL REGISTRATION: www. CLINICALTRIALS: gov , identifier: NCT05709249. Registered on 31 Jan 2023.


Assuntos
Neoplasias do Colo , Qualidade de Vida , Humanos , Resultado do Tratamento , Neoplasias do Colo/tratamento farmacológico , Intervalo Livre de Doença , Método Duplo-Cego , Ensaios Clínicos Controlados Aleatórios como Assunto , Estudos Multicêntricos como Assunto
3.
Artigo em Chinês | MEDLINE | ID: mdl-34628823

RESUMO

Laryngeal carcinoma is one of the most common malignant tumors in the area of head and neck, and the main pathological type is laryngeal squamous cell carcinoma. Due to the fact that the disease usually have no overt clinical symptoms at the early stage and easy to relapse, it has a poor prognosis and low five-year survival rate. microRNA is a class of endogenous, non-coding RNA with a length of 19-25 nucleotides. microRNAs, mainly regulate the expression of target genes at the post-transcriptional level after complementing and pairing with the 3'-UTR area of the target gene. Studies have shown that the abnormal expression of microRNA is closely related to the occurrence, development, metastasis and prognosis of various cancers including laryngeal carcinoma. In this article, the research progress of microRNA in laryngeal squamous cell carcinoma is reviewed.


Assuntos
Carcinoma de Células Escamosas , Neoplasias de Cabeça e Pescoço , MicroRNAs , Carcinoma de Células Escamosas/genética , Humanos , MicroRNAs/genética , Recidiva Local de Neoplasia , Carcinoma de Células Escamosas de Cabeça e Pescoço/genética
4.
Microbiol Res ; 186-187: 44-51, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27242142

RESUMO

Enterococcus faecalis (E. faecalis) is one of the major causes of biofilm infections. Berberine hydrochloride (BBH) has diverse pharmacological effects; however, the effects and mechanisms of BBH on E. faecalis biofilm formation and dispersion have not been reported. In this study, 99 clinical isolates from the urine samples of patients with urinary tract infections (UTIs) were collected and identified. Ten strains of E. faecalis with biofilm formation ability were studied. BBH inhibited E. faecalis biofilm formation and promoted the biofilm dispersion of E. faecalis. In addition, sortase A and esp expression levels were elevated during early E. faecalis biofilm development, whereas BBH significantly reduced their expression levels. The results of this study indicated that BBH effectively prevents biofilm formation and promotes biofilm dispersion in E. faecalis, most likely by inhibiting the expressions of sortase A and esp.


Assuntos
Antibacterianos/farmacologia , Berberina/farmacologia , Biofilmes/efeitos dos fármacos , Enterococcus faecalis/efeitos dos fármacos , Aminoaciltransferases/antagonistas & inibidores , Aminoaciltransferases/biossíntese , Proteínas de Bactérias/antagonistas & inibidores , Proteínas de Bactérias/biossíntese , Cisteína Endopeptidases/biossíntese , Enterococcus faecalis/isolamento & purificação , Enterococcus faecalis/fisiologia , Expressão Gênica/efeitos dos fármacos , Humanos , Proteínas de Membrana/antagonistas & inibidores , Proteínas de Membrana/biossíntese , Infecções Urinárias/microbiologia , Urina/microbiologia
5.
J Biochem Mol Toxicol ; 28(4): 181-9, 2014 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-24488958

RESUMO

Cigarette smoking is known to have negative effects on tissue repair and healing. The aim of this study is to investigate the effects of nicotine in human umbilical cord mesenchymal stem cells (MSCs). After nicotine treatment, MSCs became pyknotic, vacuoles appeared in the cytoplasm and nucleus, and the nuclear boundary became fuzzy as observed using atomic force microscopy. Cell proliferation was inhibited in a dose-dependent manner (P < 0.05 for all concentrations). The proportion of apoptotic MSCs was significantly increased in a dose-dependent manner. The mitochondrial membrane potential was significantly decreased (P < 0.05). Nicotine-treated MSCs had a significantly higher G0/G1 ratio (P < 0.05). Peptide mass fingerprinting identified 27 proteins that were differentially expressed between MSCs with and without nicotine treatment. These nicotine exerted toxic effects on MSCs are likely related, at least in part, to the altered expression of multiple proteins that are essential to the health and proliferation of these cells.


Assuntos
Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Células-Tronco Mesenquimais/fisiologia , Nicotina/toxicidade , Apoptose/efeitos dos fármacos , Forma Celular/efeitos dos fármacos , Células Cultivadas , Regulação para Baixo/efeitos dos fármacos , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Células-Tronco Mesenquimais/efeitos dos fármacos , Proteoma/metabolismo , Cordão Umbilical/citologia
6.
BMC Cell Biol ; 12: 32, 2011 Aug 09.
Artigo em Inglês | MEDLINE | ID: mdl-21827650

RESUMO

BACKGROUND: The therapeutic efficacy of human mesenchymal stem cells (hMSCs) for the treatment of hypoxic-ischemic diseases is closely related to level of hypoxia in the damaged tissues. To elucidate the potential therapeutic applications and limitations of hMSCs derived from human umbilical cords, the effects of hypoxia on the morphology and proliferation of hMSCs were analyzed. RESULTS: After treatment with DFO and CoCl2, hMSCs were elongated, and adjacent cells were no longer in close contact. In addition, vacuole-like structures were observed within the cytoplasm; the rough endoplasmic reticulum expanded, and expanded ridges were observed in mitochondria. In addition, DFO and CoCl2 treatments for 48 h significantly inhibited hMSCs proliferation in a concentration-dependent manner (P < 0.05). This treatment also increased the number of cells in G0/G1 phase and decreased those in G2/S/M phase. CONCLUSIONS: The hypoxia-mimetic agents, DFO and CoCl2, alter umbilical cord-derived hMSCs morphology and inhibit their proliferation through influencing the cell cycle.


Assuntos
Compostos Aza/farmacologia , Proliferação de Células , Cobalto/farmacologia , Células-Tronco Mesenquimais/efeitos dos fármacos , Cordão Umbilical/citologia , Diferenciação Celular , Hipóxia Celular , Células Cultivadas , Citometria de Fluxo , Humanos , Células-Tronco Mesenquimais/citologia , Células-Tronco Mesenquimais/metabolismo , Cordão Umbilical/metabolismo
7.
Zhonghua Xue Ye Xue Za Zhi ; 32(11): 739-43, 2011 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-22339908

RESUMO

OBJECTIVE: To analyze the differential proteomics in human umbilical cord mesenchymal stem cells (MSC) induced by chemical hypoxia-mimetic agent cobalt chloride (CoCl(2)) by two-dimensional gel electrophoresis (2-DE) and mass-spectrometry. METHODS: 2-DE was performed to separate proteins from treated and untreated human umbilical cord MSC with CoCl(2). 2-DE images were analyzed by ImageMaster 2D Platinum software 6.0. The differential expressed proteins was identified by MALDI-TOF-MS. The differential proteins were classified based on their functions. RESULTS: 2-DE reference patterns of CoCl(2) treated human umbilical cord MSC were established. A total of twenty-six differential proteins were identified, of them eleven proteins were up-regulated and fifteen down-regulated. Their biological functions involved in carbohydrate metabolism, protein metabolism and modification, lipid metabolism, coenzyme and prosthetic group metabolism, cell cycle, immunity and defense, cell structure and motility, signal transduction, protein targeting and localization, neuronal activities, muscle contraction, etc. Peroxiredoxin1 (Prdx) was down-regulated, whereas alpha-enolase (ENO1) and vesicle amine transport protein 1 homolog (VAT1) up-regulated. CONCLUSION: The effects of hypoxia on human umbilical cord MSC were participated by multiple proteins and involved in multiple functional pathways.


Assuntos
Cobalto/farmacologia , Células-Tronco Mesenquimais/efeitos dos fármacos , Células-Tronco Mesenquimais/metabolismo , Proteoma/análise , Humanos , Proteômica , Cordão Umbilical/citologia , Cordão Umbilical/efeitos dos fármacos
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