Huizhou Municipal Central Hospital of Guangdong Province

Huizhou, China

Huizhou Municipal Central Hospital of Guangdong Province

Huizhou, China
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Huang W.,Huizhou Municipal Central Hospital of Guangdong Province | Li J.,Huizhou Municipal Central Hospital of Guangdong Province | Guo X.,Huizhou Municipal Central Hospital of Guangdong Province | Zhao Y.,University of Missouri | Yuan X.,Huizhou Municipal Central Hospital of Guangdong Province
Biomedicine and Pharmacotherapy | Year: 2016

Hepatocellular carcinoma (HCC) is a highly aggressive solid malignancy throughout the world. Dysregulation of miRNAs play essential roles in HCC progression via aberrant regulation of cell proliferation, apoptosis, as well as metastasis. miR-663a is a poorly investigated miRNA. Whether miR-663a regulates HCC development remains unknown. The aim of the study was to explore the role of miR-663a in HCC development. To determine the expression level of miR-663a in HCC, we analyzed the data from GSE21362 and TCGA. The results showed that miR-663a was significantly down-regulated in HCC tissue compared with adjacent non-tumor tissue. Gain of function and loss of function assays revealed that miR-663a distinctly inhibited cell proliferation, migration and invasion. Mechanistic investigations demonstrated that miR-663a modulated cell functions through targeting and suppressing high mobility group A2 (HMGA2). In addition, overexpression of HMGA2 remarkably attenuated the tumor repressive effect of miR-663a. Taken together, miR-663a inhibits HCC cell proliferation and motility by targeting HMGA2. © 2016.


Weizhen H.,Huizhou Municipal Central Hospital of Guangdong Province | Tian Y.,Huizhou Municipal Central Hospital of Guangdong Province | Shaoting D.,Huizhou Municipal Central Hospital of Guangdong Province | Cha Y.,Huizhou Municipal Central Hospital of Guangdong Province | And 3 more authors.
Oncology Reports | Year: 2017

Accumulating evidence has revealed that aberrantly expressed long non-coding transcripts are involved in the development and progression of colorectal cancer (CRC). Small nucleolar RNA host gene 3 (SNHG3) is a newly identified lncRNA, and little is known about its clinical significance and biological functions in the development of CRC. In the present study, we found that the expression of SNHG3 was significantly upregulated in CRC, and upregulation of SNHG3 predicted poor prognosis for patients with CRC as determined through analysis of the data obtained from TCGA database. Gain-of function and loss-of function assays revealed that SNHG3 markedly promoted cellular proliferation of CRC cells. Gene Set Enrichment Analysis (GSEA) suggested that high expression of SNHG3 was positively associated with c-Myc and its targets genes. Furthermore, ectopic overexpression of SNHG3 increased the expression of c-Myc and its target genes, whereas inhibition of SNHG3 had opposite effect on the expression of c-Myc and its targets. Mechanistic investigations demonstrated that SNHG3 functioned as a competing endogenous RNA (ceRNA) to 'sponge' miR-182-5p, thus leading to the release of c-Myc from miR-182-5p and modulating the expression of c-Myc. In conclusion, SNHG3 promoted CRC progression via sponging miR-182-5p and upregulating c-Myc and its target genes.


Xiong H.-L.,Huizhou Municipal Central Hospital of Guangdong Province | Zhou S.-W.,Huizhou Municipal Central Hospital of Guangdong Province | Sun A.-H.,Huizhou Municipal Central Hospital of Guangdong Province | He Y.,Huizhou Municipal Central Hospital of Guangdong Province | And 2 more authors.
Molecular Medicine Reports | Year: 2015

MicroRNAs (miRNAs) are a group of small non-coding RNA molecules, which serve an important function in the development of multidrug resistance in cancer through the post-transcriptional regulation of gene expression and RNA silencing. In the present study, the functional effects of miR-197 were analyzed in chemo-resistant gastric cancer cells. Low expression levels of miR-197 were observed in the fluorouracil (5-FU)-resistant gastric cell line SGC7901/5-FU when compared with those in the parental gastric cell line SGC7901. Overexpression of miR-197 in SGC7901/5-FU cells was identified to partially restore 5-FU sensitivity. miRNA target prediction algorithms suggested that mitogen-activated protein kinase 1 (MAPK1) is a candidate target gene for miR-197. A luciferase reporter assay confirmed that miR-197 led to silencing of the MAPK1 gene by recognizing and then specifically binding to the predicted site of the MAPK1 mRNA 3'untranslated region. When miR-197 was overexpressed in SGC7901 cells, the protein levels of MAPK1 were downregulated. Furthermore, MAPK1 knockdown significantly increased the growth inhibition rate of the SGC7901/5-FU cells compared with those in the control group. These results indicated that miR-197 may influence the sensitivity of 5-FU treatment in a gastric cancer cell line by targeting MAPK1.


PubMed | Huizhou Municipal Central Hospital of Guangdong Province and University of Missouri
Type: | Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie | Year: 2016

Hepatocellular carcinoma (HCC) is a highly aggressive solid malignancy throughout the world. Dysregulation of miRNAs play essential roles in HCC progression via aberrant regulation of cell proliferation, apoptosis, as well as metastasis. miR-663a is a poorly investigated miRNA. Whether miR-663a regulates HCC development remains unknown. The aim of the study was to explore the role of miR-663a in HCC development. To determine the expression level of miR-663a in HCC, we analyzed the data from GSE21362 and TCGA. The results showed that miR-663a was significantly down-regulated in HCC tissue compared with adjacent non-tumor tissue. Gain of function and loss of function assays revealed that miR-663a distinctly inhibited cell proliferation, migration and invasion. Mechanistic investigations demonstrated that miR-663a modulated cell functions through targeting and suppressing high mobility group A2 (HMGA2). In addition, overexpression of HMGA2 remarkably attenuated the tumor repressive effect of miR-663a. Taken together, miR-663a inhibits HCC cell proliferation and motility by targeting HMGA2.

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