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1.
Med Sci Monit ; 29: e939464, 2023 01 11.
Artículo en Inglés | MEDLINE | ID: mdl-36628645

RESUMEN

This publication has been retracted by the Editor due to the identification of non-original figure images and manuscript content that raise concerns regarding the credibility and originality of the study and the manuscript. Reference: Jiang, He Li, Heping Xiang, Ming Gao, Chunlin Yin, Haiping Wang, Yuansong Sun, Maoming Xiong. Long Chain Non-Coding RNA (lncRNA) HOTAIR Knockdown Increases miR-454-3p to Suppress Gastric Cancer Growth by Targeting STAT3/Cyclin D1. Med Sci Monit, 2019; 25: 1537-1548. DOI: 10.12659/MSM.913087.

2.
Molecules ; 27(12)2022 Jun 17.
Artículo en Inglés | MEDLINE | ID: mdl-35745003

RESUMEN

Acute pancreatitis (AP) is a pancreatic inflammatory disease that varies greatly in course and severity. To further the understanding of the pathology of AP, we carried out data-independent acquisition-based proteomic analyses using proteins extracted from the plasma of patients with severe acute pancreatitis (SAP) (experimental group) and healthy volunteers (control group). Compared to the control group, there were 35 differentially expressed proteins (DEPs) in the plasma of patients with SAP. Of those, the expression levels for 6 proteins were significantly increased, and 29 proteins were significantly decreased. Moreover, six candidate biomarkers-VWF, ORM2, CD5L, CAT, IGLV3-10, and LTF-were matched as candidate biomarkers of the disease severity of AP. The area under the receiver operating characteristic of 0.903 (95% CI: 0.839, 0.967) indicated that this combination of these six candidate biomarkers had a good prediction accuracy for predicting the severity of AP. Our study provides specific DEPs that may be useful in the diagnosis and prognosis of SAP, which suggests new theoretical bases for the occurrence and development of SAP and offers potential novel treatment strategies for SAP.


Asunto(s)
Pancreatitis , Enfermedad Aguda , Biomarcadores , Proteínas Sanguíneas , Humanos , Pancreatitis/diagnóstico , Proteómica , Curva ROC , Índice de Severidad de la Enfermedad
3.
Med Sci Monit ; 25: 1537-1548, 2019 Feb 27.
Artículo en Inglés | MEDLINE | ID: mdl-30810117

RESUMEN

BACKGROUND Gastric cancer is a common gastrointestinal tumor. The incidence and mortality of gastric cancer are very high. Therefore, it is important to study targeted drugs. Recent studies found long chain non-coding RNA (lncRNAs) and microRNAs (miRNAs) were abnormal in gastric cancer. MATERIAL AND METHODS We collected adjacent normal and cancer tissues of gastric cancer patients and measured HOTAIR, miR-454-3p, STAT3, and Cyclin D1 expression and analyzed the correlation with clinical status. We also measured AGS and SGC7901 cells proliferation rate of different groups by MTT assay, and we evaluated AGS and SGC7901 cell apoptosis and cell cycle by flow cytometry. In addition, we assessed the relative proteins expressions by WB assay. Finally, we explored the correlation between miR-454-3p and STAT3 by use of double luciferase reporter. RESULTS lncRNA HOTAIR was negatively correlated with miR-454-3p expression in gastric cancer tissues. lncRNA HOTAIR knockdown suppressed AGS and SGC7901, which are gastric cancer cell lines that promote cell proliferation by increasing cell apoptosis and keeping the cell cycle in G1 phase. In further mechanism research, we found that the STAT3 and Cyclin D1 proteins expressions were suppressed by lncRNA HOTAIR down-regulation in AGS and SGC7901 cells. CONCLUSIONS Our results suggest that lncRNA HOTAIR knockdown stimulates miR-454-3p expression to inhibit gastric cancer growth by depressing STAT3/Cyclin D1 activity.


Asunto(s)
Ciclina D1/genética , MicroARNs/genética , ARN Largo no Codificante/genética , Factor de Transcripción STAT3/genética , Neoplasias Gástricas/genética , Apoptosis/genética , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Ciclina D1/metabolismo , Técnicas de Silenciamiento del Gen , Genes bcl-1 , Humanos , MicroARNs/metabolismo , ARN Largo no Codificante/metabolismo , Factor de Transcripción STAT3/metabolismo , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patología
4.
Mol Biol Rep ; 40(11): 6371-7, 2013 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-24078094

RESUMEN

A number of case­control studies have been conducted to investigate the association of CDKN1B gene polymorphisms with breast cancer. However, these studies reported conflicting results. The aim of our study was to quantitatively summarize the association of CDKN1B gene polymorphisms with breast cancer. Systemic searches of the PubMed, Excerpta Medica Database, and Chinese Biomedical Literature Database databases were performed, with the last report up to Oct 2012. Odds ratios (ORs) with 95 % confidence intervals (CIs) were used to assess the strength of the association. Seven studies including 6,822 cases and 7,186 controls were involved in this meta-analysis, which was performed for two CDKN1B gene polymorphisms (rs2066827 and rs34330). Significant association was found for rs34330 polymorphism (T versus C: OR = 1.10, 95 % CI = 1.03­1.18, P = 0.003; CT + TT versus CC: OR = 1.38, 95 % CI = 0.98­1.93, P = 0.07; TT versus CC + CT: OR = 1.06, 95 % CI = 0.93­1.21, P = 0.38; TT versus CC: OR = 1.23, 95 % CI = 1.04­1.45, P = 0.02; CT versus CC: OR = 1.42, 95 % CI = 0.97­2.09, P = 0.07), but not for rs2066827 polymorphism (G versus T: OR = 0.99, 95 % CI = 0.91­1.08, P = 0.84; TG + GG versus TT: OR = 0.98, 95 % CI = 0.89­1.08, P = 0.69; GG versus TT + TG: OR = 1.04, 95 % CI = 0.83­1.30, P = 0.75; GG versus TT: OR = 1.03, 95 % CI = 0.82­1.30, P = 0.77; TG versus TT: OR = 0.97, 95 % CI = 0.88­1.08, P = 0.58). This meta-analysis suggests that breast cancer may be associated with CDKN1B gene rs34330 polymorphism, but not rs2066827 polymorphism.


Asunto(s)
Neoplasias de la Mama/genética , Inhibidor p27 de las Quinasas Dependientes de la Ciclina/genética , Predisposición Genética a la Enfermedad , Polimorfismo de Nucleótido Simple , Alelos , Femenino , Genotipo , Humanos , Oportunidad Relativa , Sesgo de Publicación
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