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1.
Cell Mol Biol (Noisy-le-grand) ; 70(5): 214-219, 2024 May 27.
Artículo en Inglés | MEDLINE | ID: mdl-38814210

RESUMEN

This study explored the role of circular RNA circ_0006168 in the progression of hepatocellular carcinoma (HCC) and its interaction with microRNA-125b. The expression of circ_0006168 was examined in 42 pairs of HCC tumor and adjacent tissue specimens using quantitative polymerase chain reaction (qPCR). Elevated circ_0006168 expression in HCC tissues was significantly associated with advanced pathological staging and lower overall survival rates. Lentivirus-mediated circ_0006168 knockdown in HCC cell lines (Hep3B and Huh7) demonstrated a notable reduction in cell proliferation and an increase in apoptosis. MicroRNA-125b expression exhibited a marked reduction in HCC tissues, negatively correlating with circ_0006168 levels. Luciferase reporting assays indicated that circ_0006168 was a direct target of microRNA-125b. Additionally, cell recovery experiments suggested a reciprocal regulation between circ_0006168 and microRNA-125b, contributing to the accelerated malignant progression of HCC. The study underscored the significantly increased expression of circ_0006168 in both HCC tissues and cell lines, highlighting its association with advanced pathological stages and poor prognosis in HCC patients. Furthermore, circ_0006168 appeared to play a pivotal role in elevating the proliferation rate of HCC cells through its modulation of microRNA-125b. These findings contribute to a deeper understanding of the molecular mechanisms underlying HCC development and may offer potential therapeutic targets for intervention.


Asunto(s)
Apoptosis , Carcinoma Hepatocelular , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Neoplasias Hepáticas , MicroARNs , ARN Circular , Humanos , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patología , Carcinoma Hepatocelular/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patología , ARN Circular/genética , ARN Circular/metabolismo , Proliferación Celular/genética , Línea Celular Tumoral , Masculino , Femenino , Persona de Mediana Edad , Apoptosis/genética , Pronóstico , Secuencia de Bases , Progresión de la Enfermedad
2.
J Int Med Res ; 51(9): 3000605231191580, 2023 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-37737100

RESUMEN

OBJECTIVE: The most common site of metastasis in patients with colon cancer is the liver. This study aimed to identify patients with colon cancer at high risk of developing liver metastasis and to explore their prognosis. METHODS: The clinical characteristics, treatment methods and survival outcomes of patients diagnosed with colon cancer from 2010 to 2015 were identified from the Surveillance, Epidemiology and End Results (SEER) database. Patients were divided into two groups according to the presence of liver metastasis, and multivariate logistic and Cox regression models were used to identify risk and prognostic factors. RESULTS: A total of 60,018 patients with colon cancer were selected from the SEER database. The incidence of liver metastasis was 9.2%. African American ethnicity, poor differentiation, higher tumor stage, higher lymph node ratio, and lung metastases were common factors associated with both liver metastasis risk and prognosis. CONCLUSIONS: Metastasectomy might improve survival among patients with colon cancer with resectable liver metastasis lesions and no other organ involvement.


Asunto(s)
Neoplasias del Colon , Neoplasias Hepáticas , Humanos , Población Negra/estadística & datos numéricos , Neoplasias del Colon/epidemiología , Neoplasias del Colon/mortalidad , Neoplasias del Colon/patología , Neoplasias del Colon/terapia , Neoplasias Hepáticas/epidemiología , Neoplasias Hepáticas/mortalidad , Neoplasias Hepáticas/secundario , Neoplasias Hepáticas/terapia , Pronóstico , Factores de Riesgo , Programa de VERF/estadística & datos numéricos , Estados Unidos/epidemiología
3.
World J Clin Cases ; 11(36): 8527-8534, 2023 Dec 26.
Artículo en Inglés | MEDLINE | ID: mdl-38188201

RESUMEN

BACKGROUND: Castleman disease (CD) was first reported in 1954. It is a rare non-malignant lymphoproliferative disease with unclear etiology. As the clinical manifestations of CD are different, there are difficulties in its diagnosis and treatment. Therefore, for patients with CD, it is important to establish the diagnosis in order to choose the appropriate treatment. CASE SUMMARY: In this report, three patients with intraperitoneal CD treated at our center from January 2018 to June 2023 were reviewed, and the clinical and paraclinical examinations, diagnosis, and treatment were analyzed, and all three patients were diagnosed with CD by routine histopathological and immunohistochemical examinations. CONCLUSION: CD is a complex and rare disease. Because there are no special clinical symptoms and laboratory abnormalities, the diagnosis often depends on routine pathological and immunohistochemical findings.

4.
Genes Dis ; 8(4): 521-530, 2021 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-34179314

RESUMEN

Colorectal carcinoma (CRC) is one of the most common cancers, and is associated with a poor clinical outcome. The key genes and potential prognostic markers in colorectal carcinoma remain to be identified and explored for clinical application. DNA expression/methylation profiles were downloaded from the Gene Expression Omnibus (GEO) database to identify differentially expressed/methylated genes (DEGs and DEMs). A total of 255 genes and 372 genes were identified as being up-regulated and down-regulated, respectively, in GSE113513, GSE81558, and GSE89076. There were a total of 3350 hypermethylated genes and 443 hypomethylated genes identified in GSE48684. Twenty genes were found to be hypermethylated as well as down-regulated, and a functional enrichment analysis revealed that these genes were mainly involved in cancer-related pathways. Among these 20 genes, GPM6A, HAND2 and C2orf40 were related to poor outcomes in cancer patients based on a survival analysis. Concurrent decreases of GPM6A, HAND2 and C2orf40 protein expression were observed in highly-differentiated colorectal carcinoma tissues, and higher expression levels were found in undifferentiated or minimally-differentiated colorectal carcinoma tissues. In conclusion, 20 genes were found to be downregulated and hypermethylated in CRC, among which GPM6A, HAND2 and C2orf40 were explored for their potential prognostic value.

5.
Int J Nanomedicine ; 15: 9859-9873, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-33324055

RESUMEN

BACKGROUND: Circular RNAs (circRNAs) play an important role in the tumorigenesis of pancreatic cancer. However, the expression profiles and roles of circRNAs in pancreatic cancer remain largely unknown. METHODS: To identify differentially expressed circRNAs (DEcircRNAs) between pancreatic cancer and matched normal tissues, bioinformatics analysis was performed. Hsa_circ_0000069 was identified by 0.bioinformatics analysis. In addition, the level of hsa_circ_0000069 in pancreatic cancer tissues and cell lines, and pancreatic cancer cell-derived exosomes were assessed using RT-qPCR assay. RESULTS: The expression of hsa_circ_0000069 was markedly upregulated in pancreatic cancer tissues and cell lines. SCL/TAL1 interrupting locus (STIL) is the parent gene for hsa_circ_0000069, and its high expression was related to poor overall survival in patients with pancreatic cancer. In addition, downregulation of hsa_circ_0000069 markedly suppressed STIL expression, induced the apoptosis and cell cycle arrest, and inhibited the proliferation, migration and invasion in pancreatic cancer cells. Moreover, hsa_circ_0000069 knockdown inhibited the growth of xenograft pancreatic cancer tumors in vivo. Furthermore, human pancreatic duct epithelial cells (HPDE) are capable of internalizing SW1990 cell-derived exosomes, allowing the transfer of hsa_circ_0000069. Significantly, SW1990 cell-derived exosomes promoted the proliferation, migration and cell cycle progression of HPDE cells, whereas exosomes with downregulated hsa_circ_0000069 suppressed the proliferation, migration and cell cycle progression of HPDE cells, by suppressing STIL expression. CONCLUSION: Our results suggest that hsa_circ_0000069 knockdown could inhibit pancreatic cancer tumorigenesis and exosomes with downregulated hsa_circ_0000069 could suppress HPDE cell malignant transformation. Collectively, hsa_circ_0000069 might be a therapeutic target for the treatment of pancreatic cancer.


Asunto(s)
Carcinogénesis/genética , Transformación Celular Neoplásica/genética , Exosomas/genética , Técnicas de Silenciamiento del Gen , Péptidos y Proteínas de Señalización Intracelular/genética , Neoplasias Pancreáticas/patología , ARN Circular/genética , Apoptosis/genética , Puntos de Control del Ciclo Celular/genética , Línea Celular Tumoral , Proliferación Celular/genética , Regulación Neoplásica de la Expresión Génica/genética , Humanos , Neoplasias Pancreáticas/genética , ARN Circular/deficiencia
6.
Anticancer Agents Med Chem ; 20(12): 1447-1458, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32384038

RESUMEN

BACKGROUND: Pancreatic Ductal Adenocarcinoma (PDAC) is the most common form of pancreatic cancer and leading causes of pancreatic cancer death because of most PDAC patients with advanced unresectable disease at that time, which is remarkably resistant to all forms of chemotherapy and radiotherapy. OBJECTIVE: PDAC increases the social and patient's family burden. However, the PDAC pathogenesis is not identified. We are trying to uncover the underlying mechanism in the future. METHODS: In our research, the drug-resistant cell line was successfully induced in the vitro by progressive concentrations of Afatinib, which we named it as BxPC3-AR. RESULTS: It has been observed that the effect of autophagy was on the resistance of BxPC3-AR to Afatinib. CONCLUSION: It has been confirmed that autophagy plays a certain role in BxPC3-AR resistance to Afatinib. Our findings provide a new perspective on the role of autophagy in pancreatic ductal adenocarcinoma.


Asunto(s)
Afatinib/farmacología , Antineoplásicos/farmacología , Carcinoma Ductal Pancreático/tratamiento farmacológico , Neoplasias Pancreáticas/tratamiento farmacológico , Afatinib/química , Animales , Antineoplásicos/química , Carcinoma Ductal Pancreático/patología , Movimiento Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Ensayos de Selección de Medicamentos Antitumorales , Humanos , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Estructura Molecular , Neoplasias Experimentales/tratamiento farmacológico , Neoplasias Experimentales/patología , Neoplasias Pancreáticas/patología , Relación Estructura-Actividad , Células Tumorales Cultivadas
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