Publications by authors named "Su'e Chang"

17 Publications

  • Page 1 of 1

Vitamin D3 mediates miR-15a-5p inhibition of liver cancer cell proliferation via targeting E2F3.

Oncol Lett 2020 Jul 24;20(1):292-298. Epub 2020 Apr 24.

Department of Gastroenterology, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.

Vitamin D3 has been demonstrated to suppress the development and progression of liver cancer, but the mechanism is unclear. The effects of vitamin D3 and microRNA (miR)-15a-5p on liver cancer cells were investigated in the present study using MTT and colony formation assays, flow cytometry, western blotting and reverse transcription-quantitative PCR. A dual-luciferase reporter assay was performed to determine whether E2F transcription factor 3 (E2F3) was a target of miR-15a-5p. The effects of silencing the E2F3 gene expression in liver cancer cells were investigated using a small interfering RNA. Vitamin D3 suppressed liver cancer cell proliferation, induced apoptosis and increased miR-15a-5p expression. Treatment with the miR-15a-5p mimics significantly suppressed liver cancer cell proliferation compared with that of the controls. Bioinformatics analysis and a dual-luciferase reporter assay demonstrated that E2F3 was a target of miR-15a-5p and that silencing E2F3 inhibited liver cancer cell proliferation. Therefore, Vitamin D3 suppressed cell proliferation by miR-15a-5p-mediated silencing of E2F3 gene expression. These findings suggested a role for vitamin D3 and E2F3 targeting as potential novel liver cancer therapies.
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http://dx.doi.org/10.3892/ol.2020.11572DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285896PMC
July 2020

Transplantation of sh-miR-199a-5p-Modified Olfactory Ensheathing Cells Promotes the Functional Recovery in Rats with Contusive Spinal Cord Injury.

Cell Transplant 2020 Jan-Dec;29:963689720916173

Department of Orthopaedics, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.

MicroRNAs (miRNAs) function as gene expression switches, and participate in diverse pathophysiological processes of spinal cord injury (SCI). Olfactory ensheathing cells (OECs) can alleviate pathological injury and facilitate functional recovery after SCI. However, the mechanisms by which OECs restore function are not well understood. This study aims to determine whether silencing miR-199a-5p would enhance the beneficial effects of the OECs. In this study, we measured miR-199a-5p levels in rat spinal cords with and without injury, with and without OEC transplants. Then, we transfected OECs with the sh-miR-199a-5p lentiviral vector to reduce miR-199a-5p expression and determined the effects of these OECs in SCI rats by Basso-Beattie-Bresnahan (BBB) locomotor scores, diffusion tensor imaging (DTI), and histological methods. We used western blotting to measure protein levels of Slit1, Robo2, and srGAP2. Finally, we used the dual-luciferase reporter assay to assess the relationship between miR-199-5p and Slit1, Robo2, and srGAP2 expression. We found that SCI significantly increased miR-199a-5p levels ( < 0.05), and OEC transplants significantly reduced miR-199a-5p expression ( < 0.05). Knockdown of miR-199a-5p in OECs had a better therapeutic effect on SCI rats, indicated by higher BBB scores and fractional anisotropy values on DTI, as well as histological findings. Reducing miR-199a-5p levels in transplanted OECs markedly increased spinal cord protein levels of Slit1, Robo2, and srGAP2. Our results demonstrated that transplantation of sh-miR-199a-5p-modified OECs promoted functional recovery in SCI rats, suggesting that miR-199a-5p knockdown was more beneficial to the therapeutic effects of OEC transplants. These findings provided new insights into miRNAs-mediated therapeutic mechanisms of OECs, which helps us to develop therapeutic strategies based on miRNAs and optimize cell therapy for SCI.
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http://dx.doi.org/10.1177/0963689720916173DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7586279PMC
June 2021

EGR1 interacts with DNMT3L to inhibit the transcription of miR-195 and plays an anti-apoptotic role in the development of gastric cancer.

J Cell Mol Med 2019 11 12;23(11):7372-7381. Epub 2019 Sep 12.

Department of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'anJiaotong University Health Science Center, Xi'an Jiaotong University, Xi'an, China.

EGR1 regulates the expression of its downstream target genes and may exert different biological effects in different tumours. We found that the expression of EGR1 was increased in gastric cancer (GC), and silencing the expression of EGR1 promoted the apoptosis of GC cells. Moreover, overexpression of EGR1 repressed the apoptosis of GC cells. Bioinformatics analysis showed that EGR1 had binding sites at the upstream promoter region of miR-195; ChIP assays were applied to determine EGR1 occupancy of the miR-195 promoter. The RT-PCR results showed that EGR1 suppressed the expression of miR-195. The mechanism by which EGR1 acts as a transcriptional repressor is still unclear. Bioinformatics analysis showed that EGR1 may interact with DNMT3L. We confirmed that EGR1 and DNMT3L formed a complex, and EGR1 was an important player in the transcriptional control of miR-195. Overexpression of miR-195 inhibited proliferation and promoted apoptosis in GC cells. We found a well-matched miR-195 binding site at the AKT3 3'-UTR. Double luciferase reporter assays showed that AKT3 was a target of miR-195, and silencing AKT3 repressed cell proliferation and promoted apoptosis. Our results indicated EGR1 may interact with DNMT3L to inhibit the miR-195-AKT3 axis and regulate the GC cell apoptosis.
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http://dx.doi.org/10.1111/jcmm.14597DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6815817PMC
November 2019

MicroRNA-1297 inhibits proliferation and promotes apoptosis in gastric cancer cells by downregulating CDC6 expression.

Anticancer Drugs 2019 09;30(8):803-811

Department of Cell Biology and Genetics/Key Laboratory of Environment and Genes Related to Diseases, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center.

Gastric cancer (GC), one of the most common malignant tumors and the second most common leading cause of cancer-related death worldwide, is a biologically heterogeneous disease accompanied by various genetic and epigenetic alterations. However, the molecular mechanisms underlying this disease are complex and not completely understood. Increasing studies have shown that aberrant microRNA (miRNA) expression is associated with GC tumorigenesis and growth. MiR-1297 has been confirmed to be a cancer suppressor in diverse tumors in humans. However, to date, the function and mechanism of miR-1297 in GC have not been determined. Here, we found that the expression of miR-1297 was significantly reduced in GC tissues or GC cell lines compared with paracarcinoma normal tissue or normal cell lines. Exogenic overexpression of miR-1297 in GC cell lines can inhibit cell proliferation and colony formation and induce apoptosis, and inhibition of miR-1297 in GC cell lines can promote cell proliferation and colony formation, and reduce apoptosis in vitro. We further confirmed that miR-1297 acted as a tumor suppressor through targeting cell division control protein 6 (CDC6) in GC. Moreover, the inverse relationship between miR-1297 and CDC6 was verified in GC cell lines. Our results indicated that miR-1297 is a potent tumor suppressor in GC, and its antiproliferative and gene-regulatory effects are, in part, mediated through its downstream target gene, CDC6. These findings implied that miR-1297 might be used as a novel therapeutic target of GC.
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http://dx.doi.org/10.1097/CAD.0000000000000776DOI Listing
September 2019

miR-99b-3p is induced by vitamin D3 and contributes to its antiproliferative effects in gastric cancer cells by targeting HoxD3.

Biol Chem 2019 Jul 9. Epub 2019 Jul 9.

Department of Cell Biology and Genetics, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, No. 76, Yanta West Road, Xi'an, Shaanxi 710061, China.

Vitamin D3 is known to have anticancer actions by affecting tumorigenesis including the cell cycle and cell apoptosis in gastric cancer (GC) cells; the genes including microRNAs (miRNAs) regulated by vitamin D3 signaling remain discovered. miR-99b-3p, the tumor suppressor gene, is not only decreased in GC tissues, but is also induced by vitamin D3 through the vitamin D receptor (VDR) binding on the promoter domain of miR-99b. Further study indicates that miR-99b-3p inhibits cell viability and induces cell arrest in the S-phase in GC cells, the direct target gene of miR-99b-3p is verified to be HoxD3, which is also overexpressed in GC cell lines. Overall, our results show that miR-99b-3p mediates the antiproliferative of vitamin D3 in GC cells and might hold promise for prognosis and therapeutic strategies for GC treatment.
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http://dx.doi.org/10.1515/hsz-2019-0102DOI Listing
July 2019

MECP2 promotes the growth of gastric cancer cells by suppressing miR-338-mediated antiproliferative effect.

Oncotarget 2016 Jun;7(23):34845-59

Department of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, P. R. China.

The methyl-CpG-binding protein 2 (MECP2), a transcriptional suppressor, is involved in gene regulation by binding to methylated promoters. We found that MECP2 is overexpressed in gastric cancer (GC), and that Mecp2 knockdown affects the growth of GC cells both in vitro and in vivo. MECP2 can directly bind to the methylated-CpG island of miR-338 promoter and suppress the expression of two mature microRNAs, namely, miR-338-3p and miR-338-5p. Furthermore, miR-338-5p can suppress GC cell growth by targeting BMI1 (B lymphoma Mo-MLV insertion region 1 homolog). We additionally found that decreased miR-338-5p expression in GC tissues, relative to normal tissues, was significantly negatively correlated with increased BMI1 expression. Silencing MECP2 can indirectly lead to reduced expression of P-REX2, which has been identified as the miR-338-3p target, as well as BMI1 and increasing expression of P16 or P21 both in vitro and in vivo. Altogether, our results indicate that MECP2 promote the proliferation of GC cells via miR-338 (miR-338-3p and miR-338-5p)-mediated antitumor and gene regulatory effect.
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http://dx.doi.org/10.18632/oncotarget.9197DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5085194PMC
June 2016

MicroRNA-214 suppresses the proliferation of human hepatocellular carcinoma cells by targeting E2F3.

Oncol Lett 2015 Dec 25;10(6):3779-3784. Epub 2015 Sep 25.

Department of Genetics and Molecular Biology, Xi'an Jiaotong University, College of Medicine, Xi'an, Shaanxi 710061, P.R. China; Cardiovascular Research Center, Xi'an Jiaotong University, College of Medicine, Xi'an, Shaanxi 710061, P.R. China; Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education, Xi'an, Shaanxi 710061, P.R. China.

MicroRNAs (miRNAs) are important gene regulators that participate in tumorigenesis. Previous studies have implicated that miR-214 is a tumor suppressor that is capable of inhibiting human hepatocellular carcinoma (HCC) cell growth. However, the mechanism by which miR-214 suppresses tumor development remains unknown. In the present study, miR-214 was observed to suppress tumor proliferation by directly targeting E2F transcription factor 3 (E2F3) in HCC cells. Colony formation, cell cycle and proliferation assays were employed to study the tumor suppressor role of miR-214 in cell proliferation. In addition, western blotting and dual-luciferase reporter assays were used to evaluate whether E2F3 was a target of miR-214. The results of these analyses revealed that E2F3 was a novel target of miR-214. Furthermore, enhanced expression of miR-214 or silencing of E2F3 inhibited the proliferation of HCC SMMC-7721 cells. These findings suggest that miR-214 suppresses HCC growth by targeting E2F3, and may provide a novel approach for the treatment of human HCC.
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http://dx.doi.org/10.3892/ol.2015.3745DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4665883PMC
December 2015

MicroRNA-302b Enhances the Sensitivity of Hepatocellular Carcinoma Cell Lines to 5-FU via Targeting Mcl-1 and DPYD.

Int J Mol Sci 2015 Oct 6;16(10):23668-82. Epub 2015 Oct 6.

Department of Genetics and Molecular Biology, Xi'an Jiaotong University College of Medicine, Xi'an 710061, China.

MiR-302b is a member of miR-302-367 cluster. The miR-302-367 cluster played important roles in maintaining pluripotency in human embryonic stem cells (hESCs) and has been proved to be capable of suppressing cell growth in several types of cancer cell lines including Hepatocellular Carcinoma (HCC) Cell lines. However, the role that miR-302b plays in the 5-Fluorouracil (5-FU) sensitivity of HCC has not been known. This study showed that miR-302b could enhance the sensitivity to 5-FU in HCC cell lines and verified its two putative targeted genes responsible for its 5-FU sensitivity.
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http://dx.doi.org/10.3390/ijms161023668DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632720PMC
October 2015

miRNA-99b-3p functions as a potential tumor suppressor by targeting glycogen synthase kinase-3β in oral squamous cell carcinoma Tca-8113 cells.

Int J Oncol 2015 Oct 27;47(4):1528-36. Epub 2015 Aug 27.

Department of Genetics and Molecular Biology, Key Laboratory of Environment and Genes Related to Diseases, College of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.

Dysregulation of microRNAs (miRNAs) has been associated with carcinogenesis in oral squamous cell carcinoma (OSCC). In the present study, we investigated the expression and function of miR-99b-3p in human OSCC. We found that the expression levels of miR-99b-3p decreased in 21 clinical OSCC samples (84%). Furthermore, ectopic expression of miR-99b-3p inhibited OSCC cell proliferation by downregulating glycogen synthase kinase-3β (GSK3β), an miR-99b-3p' target gene, at the mRNA and protein levels, both in vitro and in vivo. Moreover, the silencing of GSK3β recapitulated the cellular and molecular effects in a similar manner to the overexpression of miR-99b-3p, which included inhibition of OSCC cell proliferation and suppression of p65 (RelA) and G1 regulators (cyclin D1, CDK4 and CDK6) in vitro. Our data suggest that miR-99b-3p functions as a tumor suppressor in OSCC via GSK3β downregulation.
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http://dx.doi.org/10.3892/ijo.2015.3135DOI Listing
October 2015

miR-302b suppresses cell invasion and metastasis by directly targeting AKT2 in human hepatocellular carcinoma cells.

Tumour Biol 2016 Jan 8;37(1):847-55. Epub 2015 Aug 8.

Department of Genetics and Molecular Biology, Xi'an Jiaotong University Health Science Center, Xi'an, China.

MicroRNAs (miRNAs) have been shown to play essential roles in regulating the activity of human hepatocellular carcinoma (HCC) cells, thereby contributing to the suppression of invasion and metastasis. In this study, using gain and loss of function assays, we demonstrated that miR-302b was frequently down-regulated in clinical HCC specimens, as compared with 15 corresponding adjacent normal tissues. Overexpression of miR-302b suppressed HCC cell invasion and metastasis. Regulation of NF-κB and matrix metalloproteinase (MMP)-2 expression by miR-302b was mediated via AKT2 in SMMC-7721 cells. Silencing AKT2 produced effects similar to those of miR-302b overexpression, which included inhibiting SMMC-7721 cell invasion and metastasis and dereasing NF-κB and MMP-2 expression. Furthermore, overexpression of AKT2 attenuated the effects of miR-302b overexpression. Taken together, our findings indicate that miR-302b inhibits SMMC-7721 cell invasion and metastasis by targeting AKT2, suggesting that miR-302b might represent a potential therapeutic target for HCC intervention.
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http://dx.doi.org/10.1007/s13277-015-3330-5DOI Listing
January 2016

miR-15b-5p induces endoplasmic reticulum stress and apoptosis in human hepatocellular carcinoma, both in vitro and in vivo, by suppressing Rab1A.

Oncotarget 2015 Jun;6(18):16227-38

Department of Genetics and Molecular Biology, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi, China.

In human hepatocellular carcinoma (HCC), aberrant expression of miRNAs correlates with tumor cell proliferation, apoptosis, invasion, and migration by targeting downstream proteins. miR-15b levels are reported increased in HCC tissues; however, they negatively correlate to HCC recurrence. Our aim was to understand the reason for this phenomenon. We used the reverse transcription-polymerase chain reaction (RT-PCR) to measure miR-15b-5p expression in both HCC tissues and HCC cell lines. Our results were consistent with the report. Using bioinformatics and luciferase reporter assays, we identified Rab1A as a novel and direct target of miR-15b-5p. Inhibiting the function of Rab1A with shRab1A also inhibited the growth of HCC cells and induced endoplasmic reticulum stress (ERS) and apoptosis. Similarly, suppressing Rab1A by overexpression of miR-15b-5p also inhibited cell growth and induced ERS and apoptosis. Moreover, re-expression of Rab1A rescued the miR-15b-5p-induced ERS, apoptosis, and growth inhibition in HCC cells. In vivo assays were further performed to testify them. Taken together, our data suggest that miR-15b-5p induces ERS, apoptosis, and growth inhibition by targeting and suppressing Rab1A, acting as a tumor suppressor gene in HCC. This finding suggests a novel relation among Rabs, miRNAs, and apoptosis.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599266PMC
http://dx.doi.org/10.18632/oncotarget.3970DOI Listing
June 2015

miR-145 mediates the antiproliferative and gene regulatory effects of vitamin D3 by directly targeting E2F3 in gastric cancer cells.

Oncotarget 2015 Apr;6(10):7675-85

Department of Genetics and Molecular Biology/Key Laboratory of Environment and Genes Related to Diseases, College of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi, P. R. China.

VitaminD3 signaling is involved in inhibiting the development and progression of gastric cancer (GC), while the active vitamin D metabolite 1-alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3)-mediated gene regulatory mechanisms in GC remain unclear. We found that miR-145 is induced by 1,25(OH)2D3 in a dose- and vitamin D receptor (VDR)-dependent manner in GC cells. Inhibition of miR-145 reverses the antiproliferative effect of 1,25(OH)2D3. Furthermore, miR-145 expression was lower in tumors compared with matched normal samples and correlated with increased the E2F3 transcription factor protein staining. Overexpression of miR-145 inhibited colony formation, cell viability and induced cell arrest in S-phase in GC cells by targeting E2F3 and CDK6. miR-145 inhibition consistently abrogates the 1,25(OH)2D3-mediated suppression of E2F3, CDK6, CDK2 and CCNA2 genes. Altogether, our results indicate that miR-145 mediates the antiproliferative and gene regulatory effects of vitamin D3 in GC cells and might hold promise for prognosis and therapeutic strategies for GC treatment.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480708PMC
http://dx.doi.org/10.18632/oncotarget.3048DOI Listing
April 2015

MicroRNA-195 acts as a tumor suppressor by directly targeting Wnt3a in HepG2 hepatocellular carcinoma cells.

Mol Med Rep 2014 Nov 28;10(5):2643-8. Epub 2014 Aug 28.

Department of Genetics and Molecular Biology, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, P.R. China.

MicroRNAs (miRNAs) are a class of small, non‑coding, endogenous RNAs that are important in tumor cell biological processes as they regulate gene expression. miR-195 has been demonstrated to be a tumor repressor in numerous types of human cancer. However, the mechanism by which miR‑195 suppresses tumor development remains to be elucidated. The aim of this study was to investigate the effect of miR-195 on the biological functions of HepG2 hepatocellular carcinoma (HCC) cells and identify the association between miR-195 and Wnt3a in HCC. miR-195 mRNA expression levels in HCC tissues and cell lines were measured by reverse transcription polymerase chain reaction analysis. miR-195 function was measured with cell proliferation, cell cycle and apoptosis assays following transfection with miR‑195 and anti‑miR‑195 sequences, and the respective controls. Luciferase reporter assay was used to determine whether Wnt3a was a target of miR-195. In addition, Wnt3a expression levels were determined in HCC cells using western blot analysis. The miR-195 expression levels were found to be reduced in HCC tissues and cell lines. miR-195 overexpression resulted in a reduction in cell proliferation. In addition, the overexpression of miR-195 in HCC cells induced G1 phase cell cycle arrest and promoted apoptosis. Furthermore, Wnt3a was demonstrated to be directly targeted by miR-195. These findings suggest that miR-195 is key in regulating cell proliferation, cell cycle and apoptosis through targeting Wnt3a. In addition, overexpression of miR-195 may be a potential therapeutic strategy in the treatment of HCC.
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http://dx.doi.org/10.3892/mmr.2014.2526DOI Listing
November 2014

IGF-1R, a target of let-7b, mediates crosstalk between IRS-2/Akt and MAPK pathways to promote proliferation of oral squamous cell carcinoma.

Oncotarget 2014 May;5(9):2562-74

Department of Oral Maxillofacial Surgery, Stomatology Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi, P. R. China.

Insulin-like growth factor (IGF) signaling is involved in oral squamous cell carcinoma (OSCC), but IGF-1 receptor (IGF-1R)-mediated intricate regulatory networks among molecular interactions and signalling path ways in OSCC remain unclear. Here, we found that overexpression of IGF-1R and insulin receptor substrate-2 (IRS-2) was negatively associated with histological differentiation. IGF signaling stimulated OSCC cell growth. Conversely, overexpression of let-7b inhibited proliferation and colony formation and triggered S/G2 cell cycle arrest by targeting IGF-1R and IRS-2 through the Akt pathway. Also, the inverse relationship between expression of let-7b and IGF-1R/IRS-2 was confirmed in OSCC tumor xenografts and clinical specimens. Furthermore, by activating ERK1/2, IGF-1R transcriptionally upregulated IRS-2. Our results indicate that let-7b/IGF-1R-mediated crosstalk between IRS-2/Akt and MAPK is involved in OSCC and is a potential therapeutic target for therapy.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058027PMC
http://dx.doi.org/10.18632/oncotarget.1812DOI Listing
May 2014

[Construction of pcDNA3-HERG-G572R expression vector and establishment of a cell line stably expressing HKE-HERG-G572R].

Nan Fang Yi Ke Da Xue Xue Bao 2014 Mar;34(3):308-11

Department of Genetics and Molecular Biology, Xi'an Jiaotong University College of Medicine, Xi'an 710061, China. E-mail:

Objective: To construct the pcDNA3-HERG-G572R expression vector and establish a cell line stably expressing HKE-HERG-G572R.

Methods: HERG-G572R mutant fragment was constructed by over-lap extension PCR and validated by DNA sequencing. The HKE-HERG-G572R expression vector was constructed and transfected into HEK293 cells to obtain a cell line stably expressing HKE-HERG-G572R.

Results: The pcDNA3-HERG-G572R expression vector was successfully constructed and the cell line stably expressing HKE-HERG-G572R was established. Real-time PCR and Western blotting revealed a 632-fold HKE-HERG-G572R overexpression in the transfected HEK293 cells as compared with that in control HEK293 cells transfected with pcDNA3 (P<0.01).

Conclusion: The protocol can be used to construct the cell line stably expressing HKE-HERG-G572R to provide a cell model for studying individualized therapy.
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March 2014

Clinicopathological and prognostic significance of p27 expression in oral squamous cell carcinoma: a meta-analysis.

Int J Biol Markers 2013 Dec 17;28(4):e329-35. Epub 2013 Dec 17.

Department of Oral Maxillofacial Surgery, Stomatological Hospital, College of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi - China and Key Laboratory of Environment and Genes Related to Diseases, College of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi - China.

Despite being already known that p27 can regulate cell proliferation, cell motility and apoptosis, the role of p27 expression in oral squamous cell carcinoma (OSCC) remains controversial. The purpose of this study was to comprehensively evaluate, with a meta-analysis, the clinicopathological and prognostic role of p27 expression in OSCC. A meta-analysis of eligible studies was performed to assess the effects of p27 expression on clinicopathological parameters and overall survival (OS) in patients with OSCC, using pooled relative risks with 95% confidence intervals. Heterogeneity and publication bias were also assessed. Fourteen studies involving a total of 1,010 patients met the inclusion criteria. Low p27 expression was significantly associated with advanced TNM stage (p<0.001), worse histology (p=0.025), and lymph node metastasis (p<0.001), but not with tumor size (p=0.181). The pooled RR of 0.743 (p=0.002) suggested that low p27 expression has a poor prognosis in patients with OSCC. A significant heterogeneity among studies was detected for lymph node status (χ(2)=34.60, I(2)=68.2%, p<0.001) and OS (χ(2)=14.86, I(2)=39.4%, p=0.095). We did not detect a significant publication bias in this meta-analysis. Our meta-analysis suggests that p27 expression status might be useful as a predictive biomarker in clinical practice, and might potently predict OS in OSCC patients.
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http://dx.doi.org/10.5301/jbm.5000035DOI Listing
December 2013

Downregulation of miR-145 expression in oral squamous cell carcinomas and its clinical significance.

Onkologie 2013 18;36(4):194-9. Epub 2013 Mar 18.

Department of Oral Maxillofacial Surgery, Stomatological Hospital, College of Medicine, Xi'an, Shaanxi, P.R. China.

Background: MicroRNAs have been reported to play roles as oncogenes or tumor suppressor genes in human cancers. However, the expression levels of miR-145 in oral squamous cell carcinoma (OSCC) are unclear. The purpose of this study was to investigate the status of miR-145 expression in OSCC and determine its clinical significance.

Patients And Methods: We examined miR-145 levels in 62 OSCC tissue samples and cell lines by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). The relationship between miR-145 expression and clinicopathologic factors of OSCC patients was analyzed.

Results: The proportion of miR-145 low expression was 82.26% (51/62) among the 62 OSCC patients, and expression levels of miR-145 in OSCC tissue samples and cell lines were significantly lower than in non-tumor controls. miR-145 expression levels were not significantly associated with age (p = 0.607), sex (p = 0.213), location (p = 0.952), histology (p = 0.603), pT stage (p = 0.305), pTNM stage (p = 0.471), and lymphatic metastasis (p = 1.000).

Conclusion: miR-145 may be involved in the early tumorigenesis of oral squamous cells, and might be a potential biomarker in the early diagnosis of OSCC.
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http://dx.doi.org/10.1159/000349956DOI Listing
September 2013