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1.
J Ovarian Res ; 15(1): 113, 2022 Oct 15.
Artículo en Inglés | MEDLINE | ID: mdl-36243865

RESUMEN

BACKGROUND: Ovarian cancer is a common cause of death among women and a health problem worldwide. Circ_0000144 has been confirmed to be an oncogene involved in cancer progression, such as gastric cancer. However, the role of circ_0000144 in ovarian cancer remains unclear and needs to be elucidated. This retrospective study aimed to investigate the underlying mechanism of circ_0000144 in ovarian cancer. METHODS: Differentially expressed circ_0000144 expression in ovarian cancer and normal tissues was identified by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). In vitro assays were performed to explore the biological functions of circ_0000144 in ovarian cancer cells. An in vivo xenograft model was used to investigate the efficacy of circ_0000144 in the progression of ovarian cancer. RESULTS: Circ_0000144 was significantly upregulated in ovarian cancer cells and tissues. Circ_0000144 overexpression significantly promoted ovarian cancer cell proliferation, migration, and invasion. This study further demonstrated that circ_0000144 downregulated ELK3 levels by sponging miR-610 in ovarian cancer cells. Moreover, circ_0000144 significantly promotes ovarian cancer tumorigenesis in vivo. CONCLUSION: Our data indicate that circ_0000144 could enhance the carcinogenesis of ovarian cancer by specifically targeting miR-610, which may serve as a novel target for the diagnosis and prognosis of ovarian cancer.


Asunto(s)
MicroARNs , Neoplasias Ováricas , Carcinogénesis/genética , Carcinoma Epitelial de Ovario/genética , Línea Celular Tumoral , Proliferación Celular/genética , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , MicroARNs/metabolismo , Neoplasias Ováricas/genética , Proteínas Proto-Oncogénicas c-ets/genética , Proteínas Proto-Oncogénicas c-ets/metabolismo , ARN Circular/genética , Estudios Retrospectivos
2.
J Diabetes Res ; 2021: 4542367, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34869777

RESUMEN

The objective of the study is to analyze the association between early pregnancy body mass index (BMI), gestational weight gain (GWG), and maternal and neonatal outcomes. The retrospective cohort study was conducted at Quanzhou First Hospital Affiliated to Fujian Medical University from January 2018 to May 2021, with 552 women enrolled. Women were divided into the underweight group, normal weight group, overweight group, and obese group according to early pregnancy BMI. Univariate and multivariate logistic regression analyses were performed. The absolute risk of adverse maternal and neonatal outcomes in the early pregnancy BMI group was calculated to further analyze the association between GWG and adverse maternal and neonatal outcomes. Of the 552 women, 390 (70.65%) women had adverse maternal and neonatal outcomes. The result revealed that overweight was associated with increased risk of adverse maternal and neonatal outcomes (odds ratio (OR): 1.643, 95% confidence interval (CI): 1.006-2.684), maternal complications (OR: 1.937, 95% CI: 1.188-3.159), and large for gestational age (LGA) (OR: 1.905, 95% CI: 1.061-3.422). In the obese group, the risk of adverse maternal and neonatal outcomes (OR: 5.760, 95% CI: 1.997-16.786), maternal complications (OR: 3.112, 95% CI: 1.645-5.887), gestational diabetes mellitus (GDM) (OR: 2.943, 95% CI: 1.509-5.741), cesarean section (OR: 1.899, 95% CI: 1.002-3.599), and preterm delivery (OR: 4.752, 95% CI: 1.395-16.185) increased. Besides, there was an association between insufficient GWG and decreased risk of LGA (OR: 0.392, 95% CI: 0.187-0.826) and higher risk of preterm delivery (OR: 2.818, 95% CI: 1.171-6.784). This study demonstrates that BMI and GWG are related to maternal and neonatal outcomes. It is necessary to regularly monitor the weight of pregnant women during pregnancy. And regional guidelines for GWG also need to be explored.


Asunto(s)
Índice de Masa Corporal , Ganancia de Peso Gestacional/fisiología , Resultado del Embarazo/epidemiología , Adulto , China/epidemiología , Estudios de Cohortes , Femenino , Ganancia de Peso Gestacional/etnología , Humanos , Recién Nacido , Embarazo , Estudios Retrospectivos
3.
Oncol Rep ; 44(4): 1343-1354, 2020 10.
Artículo en Inglés | MEDLINE | ID: mdl-32945477

RESUMEN

Increasing research has demonstrated that lncRNAs participate in the development of multiple cancer types. However, the role of TTN­AS1 in endometrial cancer (EC) remains unknown. The present study aimed to explore the function of titin­antisense RNA1 (TTN­AS1) in EC progression and the underlying mechanisms. qRT­PCR was performed to assess the TTN­AS1 expression patterns in EC tissues and cell lines. Loss of function experiments were carried out to estimate the effects of TTN­AS1 on EC cell proliferation, migration and invasion. To reveal the underlying mechanisms, informatics tools were used to predict the targets. Rescue experiments were performed to investigate the TTN­AS1­regulated miR­376a­3p/pumilio homolog 2 (PUM2) axis involved. The results of the present study revealed that TTN­AS1 was highly expressed in both EC tissues and cell lines, and TTN­AS1 knockdown inhibited EC cell proliferation, migration and invasion. With respect to the mechanisms, miR­376a­3p was revealed to be targeted by TTN­AS1, and reversed the effects on EC development induced by TTN­AS1. In addition, PUM2 was positively regulated by TTN­AS1, and miR­376a­3p mediated the regulation between them. Furtherly, in vivo experiments confirmed the results. Collectively, TTN­AS1 enhanced EC cell proliferation and metastasis by targeting the miR­376a­3p/PUM2 axis, which may shed light on EC diagnosis and treatment.


Asunto(s)
Conectina/genética , Neoplasias Endometriales/genética , MicroARNs/genética , ARN Largo no Codificante/genética , Proteínas de Unión al ARN/genética , Apoptosis/genética , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Neoplasias Endometriales/patología , Femenino , Regulación Neoplásica de la Expresión Génica/genética , Humanos
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