Time filter

Source Type

Xiaohong Z.,Maternal and Child Health Hospital of Hainan Province | Lichun F.,Maternal and Child Health Hospital of Hainan Province | Na X.,Hainan Medical University | Kejian Z.,Hainan Province Peoples Hospital | And 2 more authors.
Tumor Biology | Year: 2016

MicroRNAs (miRNAs) play an important role in the tumorigenesis of ovarian cancer. Previously, we have reported the dysregulation of miR-203 in the ovarian cancer tissues. However, the biological functions and molecular mechanisms of miR-203 in ovarian cancer remain unknown. Here, we showed that the expression of miR-203 was increased in ovarian cancer tissues compared with the adjacent non-cancerous tissues and the transcription of miR-203 was inhibited by P53. Forced expression of miR-203 in ovarian cancer promoted cell growth and migration, while depletion of miR-203 inhibited the growth and migration of ovarian cancer cells. In addition, miR-203 promoted the metastasis of ovarian cancer cells in vivo and shorted the survival of the nude mice. Mechanically, miR-203 targeted the 3′-UTR of pyruvate dehydrogenase B (PDHB) and increased the consumption of glucose and the production of lactate. Overexpression of PDHB abolished the oncogenic effects of miR-203 on the growth of ovarian cancer cells. Together, our data suggested the oncogenic roles of miR-203 in ovarian cancer by promoting glycolysis, and miR-203 might be a therapeutic target for ovarian cancer. © 2016 International Society of Oncology and BioMarkers (ISOBM)


PubMed | Hainan Province Hospital, Hainan Medical University, Maternal and Child Health Hospital of Hainan Province and Hainan Province Peoples Hospital
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

MicroRNAs (miRNAs) play an important role in the tumorigenesis of ovarian cancer. Previously, we have reported the dysregulation of miR-203 in the ovarian cancer tissues. However, the biological functions and molecular mechanisms of miR-203 in ovarian cancer remain unknown. Here, we showed that the expression of miR-203 was increased in ovarian cancer tissues compared with the adjacent non-cancerous tissues and the transcription of miR-203 was inhibited by P53. Forced expression of miR-203 in ovarian cancer promoted cell growth and migration, while depletion of miR-203 inhibited the growth and migration of ovarian cancer cells. In addition, miR-203 promoted the metastasis of ovarian cancer cells in vivo and shorted the survival of the nude mice. Mechanically, miR-203 targeted the 3-UTR of pyruvate dehydrogenase B (PDHB) and increased the consumption of glucose and the production of lactate. Overexpression of PDHB abolished the oncogenic effects of miR-203 on the growth of ovarian cancer cells. Together, our data suggested the oncogenic roles of miR-203 in ovarian cancer by promoting glycolysis, and miR-203 might be a therapeutic target for ovarian cancer.


Wang S.,Maternal and Child Health Hospital of Hainan Province | Zhao X.,Maternal and Child Health Hospital of Hainan Province | Wang J.,Maternal and Child Health Hospital of Hainan Province | Wen Y.,Maternal and Child Health Hospital of Hainan Province | And 5 more authors.
Medical Oncology | Year: 2013

MicroRNA-203 (miR-203), possessing tumor suppressive or promotive activities, has been found to be downregulated or upregulated in different cancer types. The purpose of this study was to investigate whether the increased expression of miR-203 can be used as a noninvasive diagnostic and prognostic biomarker in epithelial ovarian cancer (EOC). Real-time quantitative PCR was performed to detect the expression levels of miR-203 in EOC tissues. The expression levels of miR-203 were significantly higher in EOC tissues compared to adjacent noncancerous tissues (p < 0.001). High expression of miR-203 was observed in 65.38 % (102/156) of EOC. In addition, high miR-203 expression was found to be closely correlated with advanced FIGO stage (p < 0.001), higher histological grade (p = 0.02), lymph node involvement (p < 0.001), and positive recurrence (p < 0.001). Moreover, high miR-203 expression was correlated with shorter overall survival (p < 0.001) and shorter progression-free survival (p < 0.001) of EOC patients. Furthermore, multivariate analysis showed that the status of miR-203 expression was an independent predictor for both overall survival and progression-free survival in EOC. These findings provide the convincing evidence for the first time that the upregulation of miR-203 may serve as a novel molecular marker to predict the aggressive tumor progression and unfavorable prognosis of EOC patients. © Springer Science+Business Media New York 2013.


Zhao X.,Maternal and Child Health Hospital of Hainan Province | Zhou Y.,The Third Peoples Hospital Of Huaian | Nie M.,Maternal and Child Health Hospital of Hainan Province | Xian S.,Maternal and Child Health Hospital of Hainan Province | And 6 more authors.
Tumor Biology | Year: 2015

Epithelial ovarian cancer is one of the most common and aggressive diseases among the female reproductive organ malignancies, and the molecular mechanism underlying this disease remains largely unknown. EMSY, a binding partner of BRCA2, has been reported to be amplified in ovarian cancer. However, the expression pattern and biological functions of EMSY in the progression of ovarian cancer are not fully understood. In this study, it was found that the expression of EMSY was significantly elevated in ovarian cancer samples compared to their adjacent normal tissues. Moreover, overexpression of EMSY promoted the growth and migration of ovarian cancer cells, while knocking down the expression of EMSY inhibited the growth, migration, and tumorigenesis of ovarian cancer cells in vitro and in vivo. Mechanistically, EMSY was found to interact with beta-catenin and activate beta-catenin/TCF signaling. Our study demonstrated that EMSY played an oncogenic role in the progression of ovarian cancer cells and EMSY might be a promising target for the treatment. © 2014, International Society of Oncology and BioMarkers (ISOBM).


PubMed | Maternal and Child Health Hospital of Hainan Province
Type: Journal Article | Journal: Medical oncology (Northwood, London, England) | Year: 2013

MicroRNA-203 (miR-203), possessing tumor suppressive or promotive activities, has been found to be downregulated or upregulated in different cancer types. The purpose of this study was to investigate whether the increased expression of miR-203 can be used as a noninvasive diagnostic and prognostic biomarker in epithelial ovarian cancer (EOC). Real-time quantitative PCR was performed to detect the expression levels of miR-203 in EOC tissues. The expression levels of miR-203 were significantly higher in EOC tissues compared to adjacent non-cancerous tissues (p<0.001). High expression of miR-203 was observed in 65.38% (102/156) of EOC. In addition, high miR-203 expression was found to be closely correlated with advanced FIGO stage (p<0.001), higher histological grade (p=0.02), lymph node involvement (p<0.001), and positive recurrence (p<0.001). Moreover, high miR-203 expression was correlated with shorter overall survival (p<0.001) and shorter progression-free survival (p<0.001) of EOC patients. Furthermore, multivariate analysis showed that the status of miR-203 expression was an independent predictor for both overall survival and progression-free survival in EOC. These findings provide the convincing evidence for the first time that the upregulation of miR-203 may serve as a novel molecular marker to predict the aggressive tumor progression and unfavorable prognosis of EOC patients.


PubMed | Maternal and Child Health Hospital of Hainan Province
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2015

Epithelial ovarian cancer is one of the most common and aggressive diseases among the female reproductive organ malignancies, and the molecular mechanism underlying this disease remains largely unknown. EMSY, a binding partner of BRCA2, has been reported to be amplified in ovarian cancer. However, the expression pattern and biological functions of EMSY in the progression of ovarian cancer are not fully understood. In this study, it was found that the expression of EMSY was significantly elevated in ovarian cancer samples compared to their adjacent normal tissues. Moreover, overexpression of EMSY promoted the growth and migration of ovarian cancer cells, while knocking down the expression of EMSY inhibited the growth, migration, and tumorigenesis of ovarian cancer cells in vitro and in vivo. Mechanistically, EMSY was found to interact with beta-catenin and activate beta-catenin/TCF signaling. Our study demonstrated that EMSY played an oncogenic role in the progression of ovarian cancer cells and EMSY might be a promising target for the treatment.

Loading Maternal and Child Health Hospital of Hainan Province collaborators
Loading Maternal and Child Health Hospital of Hainan Province collaborators