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1.
PeerJ ; 9: e12578, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34966587

RESUMO

BACKGROUND: αB-Crystallin (CRYAB) is differentially expressed in various tumors. However, the correlation between CRYAB and immune cell infiltration in colorectal cancer (CRC) remains unclear. MATERIALS & METHODS: Kaplan-Meier survival curves in The Cancer Genome Atlas (TCGA) were used to evaluate the relationship between CRYAB expression and both overall survival and progression-free survival. The relationships between CRYAB expression and infiltrating immune cells and their corresponding gene marker sets were examined using the TIMER database. RESULTS: The expression of CRYAB was lower in CRC tumor tissues than in normal tissues (P < 0.05). High CRYAB gene expression and high levels of CRYAB gene methylation were correlated with high-grade malignant tumors and more advanced tumor, nodes and metastasis (TNM) cancer stages. In addition, in colorectal cancer, there was a positive correlation between CRYAB expression and immune infiltrating cells including neutrophils, macrophages, CD8 + T cells, and CD4 + T cells, as well as immune-related genes including CD2, CD3D, and CD3E. Methylation sites such as cg13084335, cg15545878, cg13210534, and cg15318568 were positively correlated with low expression of CRYAB. CONCLUSION: Because CRYAB likely plays an important role in immune cell infiltration, it may be a potential tumor-suppressor gene in CRC and a potential novel therapeutic target and predictive biomarker for colorectal cancer (CRC).

2.
Turk J Gastroenterol ; 32(2): 148-154, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33960938

RESUMO

BACKGROUND: Patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), have fever, dry cough, dyspnea, and fatigue. The disease has now become a global pandemic. The purpose of this study was to explore the relationship between COVID-19 and gastrointestinal (GI) symptoms. METHODS: We collected and analyzed data on patients with laboratory-confirmed COVID-19 by high-throughput sequencing or reverse transcription-polymerase chain reaction. We reviewed electronic medical records of 405 hospitalized COVID-19 patients in the Third Hospital of Wuhan. RESULTS: Among the 405 confirmed patients, 210 had no GI symptoms, 195 had GI symptoms, and the first symptom of 155 patients was GI. The prevalence of vascular and digestive diseases in the group with GI symptoms was significantly higher than in the group without GI symptoms. In patients with GI symptoms, the proportion with fever, cough, dysphoria, chest tightness, poor appetite, chest pain, and pharyngeal pain was significantly higher than in those without GI symptoms. There was no significant difference in imaging between the 2 groups. In patients with GI symptoms, the proportion with increased procalcitonin (PCT) level and decreased lymphocyte count was significantly higher than in those without GI symptoms. CONCLUSION: COVID-19 patients with GI symptoms had significantly more vascular and digestive system diseases and were more likely to have clinical manifestations of fever, cough, poor appetite, chest tightness, chest pain, insomnia, and pharyngeal pain. There were more patients with diarrhea, nausea, and vomiting. Patients with GI symptoms were more likely to have increased PCT and decreased lymphocyte count.


Assuntos
COVID-19/complicações , Gastroenteropatias/epidemiologia , Gastroenteropatias/virologia , SARS-CoV-2 , Adulto , Idoso , COVID-19/sangue , COVID-19/virologia , China/epidemiologia , Diarreia/sangue , Diarreia/epidemiologia , Diarreia/virologia , Feminino , Humanos , Contagem de Linfócitos , Masculino , Pessoa de Meia-Idade , Náusea/sangue , Náusea/epidemiologia , Náusea/virologia , Pró-Calcitonina/sangue , Vômito/sangue , Vômito/epidemiologia , Vômito/virologia
3.
Technol Cancer Res Treat ; 19: 1533033820945801, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32924881

RESUMO

BACKGROUND: Pancreatic cancer is an aggressive type of cancer with poor prognosis, short survival rate, and high mortality. Drug resistance is a major cause of treatment failure in the disease. MiR-331-3p has been reported to play an important role in several cancers. We previously showed that miR-331-3p is upregulated in pancreatic cancer and promotes pancreatic cancer cell proliferation and epithelial-to-mesenchymal transition-mediated metastasis by targeting ST7L. However, it is uncertain whether miR-331-3p is involved in drug resistance. METHODS: We investigated the relationship between miR-331-3p and pancreatic cancer drug resistance. As part of this, microRNA mimics or inhibitors were transfected into pancreatic cancer cells. Quantitative polymerase chain reaction was used to detect miR-331-3p expression, and flow cytometry was used to detect cell apoptosis. The Cell Counting Kit-8 assay was used to measure the IC50 values of gemcitabine in pancreatic cancer cells. The expression of multidrug resistance protein 1, multidrug resistance-related protein 1, breast cancer resistance protein, ß-Catenin, c-Myc, Cyclin D1, Bcl-2, and Caspase-3 was evaluated by Western blotting. RESULTS: We confirmed that miR-331-3p is upregulated in gemcitabine-treated pancreatic cancer cells and plasma from chemotherapy patients. We also confirmed that miR-331-3p inhibition decreased drug resistance by regulating cell apoptosis and multidrug resistance protein 1, multidrug resistance-related protein 1, and breast cancer resistance protein expression in pancreatic cancer cells, whereas miR-331-3p overexpression had the opposite effect. We further demonstrated that miR-331-3p effects in drug resistance were partially reversed by ST7L overexpression. In addition, overexpression of miR-331-3p activated Wnt/ß-catenin signaling in pancreatic cancer cells, and ST7L overexpression restored activation of Wnt/ß-catenin signaling. CONCLUSIONS: Taken together, our data demonstrate that miR-331-3p contributes to drug resistance by activating Wnt/ß-catenin signaling via ST7L in pancreatic cancer cells. These data provide a theoretical basis for new targeted therapies in the future.


Assuntos
Resistencia a Medicamentos Antineoplásicos/genética , Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/metabolismo , Proteínas Supressoras de Tumor/metabolismo , Via de Sinalização Wnt , Linhagem Celular Tumoral , Proliferação de Células/genética , Humanos , Neoplasias Pancreáticas/tratamento farmacológico , Neoplasias Pancreáticas/patologia , Interferência de RNA
4.
J Int Med Res ; 48(8): 300060520949039, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32865077

RESUMO

OBJECTIVE: This study was performed to investigate the clinical characteristics of patients with coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). METHODS: We analyzed the electronic medical records of 405 hospitalized patients with laboratory-confirmed COVID-19 in the Third Hospital of Wuhan. RESULTS: The patients' median age was 56 years, 54.1% were female, 11.4% had a history of smoking, and 10.6% had a history of drinking. All cases of COVID-19 were community-acquired. Fever (76.8%) and cough (53.3%) were the most common clinical manifestations, and circulatory system diseases were the most common comorbidities. Gastrointestinal symptoms were present in 61.2% of the patients, and 2.9% of the patients were asymptomatic. Computed tomography showed ground-glass opacities in most patients (72.6%) and consolidation in 30.9%. Lymphopenia (72.3%) and hypoproteinemia (71.6%) were observed in most patients. About 20% of patients had abnormal liver function. Patients with severe disease had significantly more prominent laboratory abnormalities, including an abnormal lymphocyte count and abnormal C-reactive protein, procalcitonin, alanine aminotransferase, aspartate aminotransferase, D-dimer, and albumin levels. CONCLUSION: SARS-CoV-2 causes a variety of severe respiratory illnesses similar to those caused by SARS-CoV-1. Older age, chronic comorbidities, and laboratory abnormalities are associated with disease severity.


Assuntos
Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/patologia , Gastroenteropatias/diagnóstico , Pneumonia Viral/diagnóstico , Pneumonia Viral/patologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Envelhecimento/fisiologia , Alanina Transaminase/sangue , Aspartato Aminotransferases/sangue , Betacoronavirus , Proteína C-Reativa/análise , COVID-19 , China , Infecções Comunitárias Adquiridas/diagnóstico , Infecções Comunitárias Adquiridas/patologia , Infecções Comunitárias Adquiridas/virologia , Comorbidade , Infecções por Coronavirus/transmissão , Feminino , Gastroenteropatias/patologia , Gastroenteropatias/virologia , Humanos , Contagem de Linfócitos , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/transmissão , Estudos Retrospectivos , SARS-CoV-2 , Índice de Gravidade de Doença , Adulto Jovem
5.
Cancer Manag Res ; 12: 1483-1492, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32161500

RESUMO

BACKGROUND: Pancreatic cancer (PC) is a highly invasive tumor with a poor prognosis, short overall survival rate and few chemotherapeutic choices. Despite the importance of finding ways to treat pancreatic cancer, the mechanisms of tumor progression have not been fully elucidated. microRNA-455-3p (miR-455-3p) has been reported to play an important role in several cancers, but its function in pancreatic cancer remains unclear. METHODS: To investigate the biological functions, miRNAs mimics or inhibitors were transfected into pancreatic cancer cells. Flow cytometry was used to detect cell apoptosis. Wound healing and Transwell assays were employed to observe cell invasion and migration abilities. The expression of Bcl-2, Bax, caspase-3, E-cadherin, N-cadherin, Snail, ß-Catenin, c-Myc and Cyclin D1 were evaluated by qPCR and Western blot. RESULTS: We confirmed that inhibition of miR-455-3p decreases cell apoptosis and increases cell migration, invasion and EMT of pancreatic cancer, whereas forced overexpression of miR-455-3p has the opposite effect. Furthermore, we demonstrated that the tumor suppression effects of miR-455-3p were partially reversed by TAZ overexpression. In addition, miR-455-3p led to inactivation of Wnt/ß-catenin signaling in pancreatic cancer cells, and TAZ overexpression restored the inhibition of Wnt/ß-catenin signaling. CONCLUSION: Taken together, our data demonstrated that miR-455-3p functions as an important tumor suppressor that suppresses the Wnt/ß-catenin signaling pathway via TAZ to inhibit tumor progression in pancreatic cancer. We conclude that the miR-455-3p/TAZ/Wnt axis may be a potential therapeutic target for pancreatic cancer.

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