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1. Mechanisms of RhoGDI2 Mediated Lung Cancer Epithelial-Mesenchymal Transition Suppression | |||
Niu Huiyan,Wu Baogang,Jiang Hongfang,Li Hui,Zhang Yi,Peng Yang,He Ping | |||
Clinical Medicine 12 December 2014 | |||
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Abstract:The aim of this study was to evaluate the function of RhoGDI2 in lung cancer epithelial-mesenchymal transition (EMT) process and to illustrate the underlying mechanisms that will lead to improvement of lung cancer treatment. Methods: The RhoGDI2 knock-down and overexpressing A549 cell lines were first constructed. The influence of RhoGDI2 on cytoskeleton in A549 cells was studied using two approaches: G-LISA-based Rac1 activity measurement and immunostaining-based F-actin distribution. The expression levels of key EMT genes were analyzed using real time quantitative polymerase chain reaction (RT-qPCR), western blot and immunostaining in untreated and RhoGDI2 knock-down or overexpressing A549 cells in both in vivo and in vitro experimental settings. Results: Our study showed that the activity of Rac1, a key gene that is crucial for the initiation and metastasis of human lung adenocarcinoma, causing the redistribution of F-actin with partial loss of cell-cell adhesions and stress fibers, was significantly suppressed by RhoGDI2. RhoGDI2 promoted the expression of EMT marker gene E-cadherin and repressed EMT promoting genes Slug, Snail, α-SMA in both A549 cells and lung and liver organs derived from the mouse models. Knocking-down RhoGDI2 induced abnormal morphology for lung organs. Conclusion: These findings indicate that RhoGDI2 repressed the activity of Rac1 and may be involved in the rearrangement of cytoskeleton in lung cancer cells. RhoGDI2 suppresses the metastasis of lung cancer mediated through EMT by regulating the expression of key genes such as E-cadherin, Slug, Snail and α-SMA in both in vivo and in vitro models. | |||
TO cite this article:Niu Huiyan,Wu Baogang,Jiang Hongfang, et al. Mechanisms of RhoGDI2 Mediated Lung Cancer Epithelial-Mesenchymal Transition Suppression[OL].[12 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4622828 |
2. Expression of different POT1 variant is Associated with Telomere Length and radiosensitivity in Colon and Gastric Adenocarcinoma cells in vitro | |||
Lei Han,Tian Muyou,Zhong Yahua,Zhou Fuxiang,Xie Conghua,Zhou Yunfeng,Liao Zhengkai | |||
Clinical Medicine 01 March 2014 | |||
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Abstract:Protection of telomeres 1 (POT1) is a telomere-binding protein, which binds to the single-stranded DNA extensions of telomeres and regulates telomere length. Different POT1 mRNA variants were examined and compared with telomere length and radiosensitivity in Colon and Gastric Adenocarcinoma cells. POT1 production and telomere lengths were assessed in 10 human cancer cell lines by Real-time quantitative RT-PCR, respectively. POT1 mRNA levels, which were relatively stable, were significantly correlated with telomere length in gastric cancer cells and colon cancer groups excluding the HT29 with low telomerase activity (P<0.01). Meanwhile, POT1 v5 indexes were correlated with radiosensitivity in both colon cancer cells or gastric cancer cells (P<0.05). Pot1 might be a good marker for the examination of cell-specific telomere length and radiosensitivity. In this report, we identi?ed a key role for POT1 in the maintenance of telomeric single-stranded tails as well as DNA damage protective functions. | |||
TO cite this article:Lei Han,Tian Muyou,Zhong Yahua, et al. Expression of different POT1 variant is Associated with Telomere Length and radiosensitivity in Colon and Gastric Adenocarcinoma cells in vitro[OL].[ 1 March 2014] http://en.paper.edu.cn/en_releasepaper/content/4587832 |
3. miR-126 Functions as a Tumor Suppressor in Osteosarcoma by Targeting Sox2 | |||
YANG Chenglin,HOU Chunyin,ZHANG Hepeng,WANG Dewei,MA Yan,ZHANG Yunqi,XU Xiaoyan,BI Zhenggang,GENG Shuo | |||
Clinical Medicine 14 December 2013 | |||
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Abstract: Osteosarcoma (OS) is the most common malignant bone tumor in children and young adults, the early symptoms and signs of which are non-specific. The discovery of microRNAs (miRNAs) provides a new avenue for the early diagnosis and treatment of OS. MiR-126 has been reported to be highly expressed in vascularized tissues, and is recently widely studied in cancers. Herein, we explored the expression and significance of miR-126 in OS. Using TaqMan RT-PCR analysis, we analyzed the expression of miR-126 in 32 paired OS tumor tissues and 4 OS cell lines and found that miR-126 was consistently under-expressed in OS tissues and cell lines compared with normal bone tissues and normal osteoblast cells (NHOst), respectively. As miR-126 is significantly decreased in OS tissues and cell lines, we sought to compensate for its loss through exogenous transfection into MG-63 cells with a miR-126 mimic. Ectopic expression of miR-126 inhibited cell proliferation, migration and invasion, and induced apoptosis of MG-63 cells. Moreover, bioinformatic prediction suggested that the sex-determining region Y-box 2 (Sox2) is a target gene of miR-126. Using mRNA and protein expression analysis, luciferase assays and rescue assays, we demonstrate that restored expression of Sox2 dampened miR-126-mediated suppression of tumor progression, which suggests the important role of miR-126/Sox2 interaction in tumor progression. Taken together, our data indicate that miR-126 functions as a tumor suppressor in OS, which exerts its activity by suppressing the expression of Sox2. | |||
TO cite this article:YANG Chenglin,HOU Chunyin,ZHANG Hepeng, et al. miR-126 Functions as a Tumor Suppressor in Osteosarcoma by Targeting Sox2[OL].[14 December 2013] http://en.paper.edu.cn/en_releasepaper/content/4575255 |
4. miR-21 regulates the radiation resistance of glioblastoma cells by inhibiting its target gene PDCD4 and hMSH2 | |||
CHAO Tengfei,XIONG Huihua,LIU Wei,CHEN Yang,ZHANG Jiaxuan | |||
Clinical Medicine 17 September 2013 | |||
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Abstract:The purpose of this study was to investigate the molecular mechanism by which miR-21 and its target genes mediate radiation resistance of glioblastoma cells. Real-time PCR was employed to de-tect miR-21 expression in normal brain tissues, glioblastoma tissues and glioblastoma cell lines (A172, T98G and U87MG). T98G cells were transfected with anti-miR-21 oligonucleotides, or plasmids con-taining PDCD4 or hMSH2 (PDCD4-pcDNA3 and hMSH2-pcDNA3). The survival curve was obtained to investigate the sensitivity of T98G cells to radiation. Cell apoptosis was measured by using the Cas-pase-3/7 kit and cell cycle by flow cytometry. Western blotting was performed to detect the expression of hMSH2 and PDCD4 in miR-21-inhibiting T98G cells. The results showed that miR-21 expression in glioblastoma cells and tissues was conversely associated with the radiation sensitivity. Over-expression of miR-21 resulted in radiation resistance, while knockdown of miR-21 led to higher sensitivity of glioblastma cells to radiation. After miR-21 knockdown, the apoptosis of T98Gcells was significantly increased and the G2phase arrest was more significant. Inaddition, miR-21 knockdown increased the expression of endogenous PDCD4 and hMSH2, which contributed to the apoptosis and G2arrest of T98G cells. The findings suggested that miR-21 may mediate the resistance of glioblastoma cells against radiation via its target genes PDCD4 and hMSH2. MiR-21 and its target genes may be used as potential molecular targets for clinical radiotherapy sensitization in the future. | |||
TO cite this article:CHAO Tengfei,XIONG Huihua,LIU Wei, et al. miR-21 regulates the radiation resistance of glioblastoma cells by inhibiting its target gene PDCD4 and hMSH2[OL].[17 September 2013] http://en.paper.edu.cn/en_releasepaper/content/4560409 |
5. Combination of antiangiogeneses effectively inhibits cancer growth and metastasis in a xenograft model | |||
HOU Li | |||
Clinical Medicine 07 April 2013 | |||
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Abstract:Angiogenesis is a cooperative process that includes endothelial growth and sprouting and interaction with the surrounding matrix. The combined use of endothelial growth inhibitor and matrix blocker expected to inhibit the angiogenesis. Antiangiogenesis is one of strategies for treating cancer. Fumagillin is an inhibitor of type 2 methionine aminopeptidase and Cyclo (Arg-Gly-Asp-D-Phe-Val), an integrin ?v?3 antagonist can block blood vessel formation. In this study, male SCID mice were injected with colon cancer cells in the subcutis and then treated with Fumagillin and Cyclo. The tumor weight, microvessel density (MVD), and number of pulmonary metastatic foci were examined. Inhibitary effect of endothelial cell growth and tube formation was examined by human umbilical endothelial cells (HUVECs), which reflect the in vivo angiogenesis. The combination of Fumagillin and Cyclo-treated mice showed the greatest effect on the tumor mass reduction, lesser number of the pulmonary metastases, and lower MVD-CD105 levels than control animals. In vitro proliferation and tube formation of HUVEC was also decreased best by the combination of both. In conclusion, The combination of Fumagillin and Cyclo at their low doses, one tenth to one hundredth was found to suppress best colorectal cancer growth and metastasis by suppressing angiogenesis. | |||
TO cite this article:HOU Li. Combination of antiangiogeneses effectively inhibits cancer growth and metastasis in a xenograft model[OL].[ 7 April 2013] http://en.paper.edu.cn/en_releasepaper/content/4535053 |
6. Combined Operation Modality vs. Imatinib Mesylate Alone for Patients with Recurrent or Metastatic Gastrointestinal Stromal Tumors: the Randomized COMVIA Trial | |||
DU Chunyan,ZHOU Ye,SONG Chun,WANG Yongpeng,JIE Zhigang,LIANG Xiaobo,HE Yulong,CAO Hui,YAN Zhongshu,SHI Yingqiang | |||
Clinical Medicine 22 January 2013 | |||
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Abstract:Objectives:Gastrointestinal Stromal Tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. For advanced GIST patients who are responding to imatinib mesylate, the role of surgery has not been formally demonstrated. Therefore, this multicenter, randomized, controlled trial was designed to assess whether surgeries to treat residual disease for patients with recurrent/metastatic GISTs responding to imatinib mesylate (IM) improves progression free survival (PFS) compared with IM treatment alone. Methods: Between 3 and 12 months after starting molecular-targeted therapy with IM for recurrent/metastatic GISTs, eligible patients were randomized to two arms: Arm A (surgery for residual disease) and Arm B (IM treatment alone). In Arm A (19 pts), surgery was performed to remove residual macroscopic lesions as completely as possible, and IM treatment continued after surgery. In Arm B (22 pts), IM was given alone at a dose of 400mg per day until disease progression. The primary endpoint was PFS, measured from the date IM starts. This study is registered in the ChiCTR registry with the ID number ChiCTR-TRC-00000244. Results: This randomized trial was closed early due to poor accrual. Only 41 patients were enrolled as opposed to 210 planned. After a median follow-up of 23 months (ranging from 15-34 months), the 2-year PFS was 88.4% in the surgery arm and 57.7% in the IM-alone arm (P=0.089). A trend towards survival benefit is observed in the surgery arm; however, it did not result in a statistically significant improvement in PFS. The most likely reason was the limited number of eligible patients, which was well below expectation. Conclusions: Surgeries to treat residual disease for patients with recurrent/metastatic GISTs responding to IM showed a trend to prolonging 2-year PFS compared with IM treatment alone, but no statistically significant conclusion is drawn from the study. | |||
TO cite this article:DU Chunyan,ZHOU Ye,SONG Chun, et al. Combined Operation Modality vs. Imatinib Mesylate Alone for Patients with Recurrent or Metastatic Gastrointestinal Stromal Tumors: the Randomized COMVIA Trial[OL].[22 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4514217 |
7. Livin expression is an independent factor in rectal cancer patients with or without preoperative radiotherapy | |||
DING Zhenyu,ZHAN Hong,BIRGIT Olsson,Gunnar Adell,SUN Xiaofeng | |||
Clinical Medicine 23 December 2012 | |||
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Abstract:Purpose To investigate the expression significance of Livin in relation to radiotherapy (RT), clinicopathological, and biologicalprognostic factors of rectal cancer patients. Methods We included 144 primary rectal cancer patients who participated in a Swedish clinical trial of preoperative radiotherapy. Tissue microarray samples from the excised primary rectal cancers, and the adjacent andor distant normal mucosa and lymph node metastases were immunostained with Livin antibody. Survival probability was computed by the Kaplan-Meier method and Cox regression model. The proliferation of colon cancer cell lines SW620 and RKO was assayed after Livin knock-down. Results The expression of Livin was significantly increased from adjacent (P=0.051) or distant (P=0.028) normal mucosa to primary tumors. The frequency of Livin-positive expression in primary cancers was decreased with preoperative RT (from 97% to 83%, P=0.004). The expression of Livin was associated with lower frequency of stage I and higher frequency of stage II, III or IV cases (P=0.044), and related to poor differentiation of cancers (P=0.033). The positivenegative expression of Livin was associated with advancedearlier TNM stage and worsegood differentiedation of tumors (after you change the result re-write this part). The survival rate of the patients with Livin-positive tumors tended to be lower than that those with Livin-negative tumors (P=0.091). In multivariate analyses, Livin expression predictated poor survival (odds ratio=5.09, 95%CI: 1.01-25.64, P=0.048) independent on TNM stage, local and distant recurrence, grade of differentiation, gender, and age. In the current study, the median overall survival was similar between patients with (129 months) or withourt (114 months) preoperative RT (P=252). In the in vitro study, SW620 and RKO cells with Livin knock-down exhibited significant decrease in proliferation compared scramble siRNA treated controls after RT. Conclusions The expression of Livin was related to the higher frequency of advanced stage of cancer. Livin expression was independently related to survival in rectal cancer patients. The preoperative RT had no influence on the survival. Our data implicated Livin as a useful prognostic factor for rectal cancer patients and possibly served as a potential therapeutic target. Livin positive expression was related to the more advanced stage of cancer. Livin expression was independently related to survival in rectal cancer patients. Our data implicated Livin was a useful prognostic factor for rectal cancer patients and possibly served as a potential therapeutic target. | |||
TO cite this article:DING Zhenyu,ZHAN Hong,BIRGIT Olsson, et al. Livin expression is an independent factor in rectal cancer patients with or without preoperative radiotherapy[OL].[23 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4504253 |
8. Increased expression of tyrosine phosphatase SHP-2(PTPN11) in Helicobacter pylori-infected gastric cancer | |||
JIANG Jing,KONG Fei,JING Meishan,CAO Xueyuan | |||
Clinical Medicine 21 December 2012 | |||
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Abstract:AIM To explore the alteration of Tyrosine phosphatase SHP-2 (PTPN11) protein expression in gastric cancer and to assess its prognostic values. METHODS Three hundred and five consecutive cases of gastric cancer were enrolled in the study. SHP-2 expression was carried out in 305 gastric cancer specimen, of which 83 had paired adjacent normal gastric mucus samples using a tissue microarray immunohistochemistry method. Correlations were analyzed between expression levels of SHP-2 protein and tumor parameters or clinical outcomes. Serum anti- Helicobacter pylori (H.pylori) IgG was detected by enzyme-linked immunosorbent assay (ELISA) method. Cox proportional hazards model was used to evaluate prognostic values by compassion of the expression levels of SHP-2 and disease-specific survivals in patients. RESULTS SHP-2 staining was mainly found diffuse in the cytoplasm and the weak staining was also observed in the nucleus in gastric mucosa cells. 32.5% of normal epithelial specimen and 62.6% of gastric cancer specimen were identified to stain with SHP-2 antibody positively (P < 0.001). Though SHP-2 staining intensities were observed stronger in the H.pylori (+) group compared to the H.pylori (-) group, however, no statistically significant difference was found in the expression levels of SHP-2 between H.pylori (+) and H.pylori (-) gastric cancer (P=0.40). The SHP-2 expression in gastric cancer was not significantly associated with cancer stages, lymph node metastases, and distant metastasis of the tumors (P=0.34, P=0.17, P=0.52). Multivariate analysis demonstrated no correlation between SHP-2 expression and disease free survival (P=0.86). CONCLUSION Increased expression of SHP-2 protein in gastric cancer specimen suggesting the aberrant upregulation of SHP-2 protein might play an important role in the gastric carcinogenesis. | |||
TO cite this article:JIANG Jing,KONG Fei,JING Meishan, et al. Increased expression of tyrosine phosphatase SHP-2(PTPN11) in Helicobacter pylori-infected gastric cancer[OL].[21 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4505643 |
9. The mechanism of the blood-brain tumor barrier permeability increase induced by minoxidil sulfate in a rat brain tumor model | |||
Gu Yan-ting,Xue Yi-xue,Wang Yan-feng,ShangGuan QianRu,Lian Yan | |||
Clinical Medicine 13 December 2012 | |||
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Abstract:Adenosine 5'-triphosphate-sensitive potassium channel (KATP channel) activator, minoxidil sulfate (MS), can selectively increase the permeability of the blood-tumor barrier (BTB); however, the mechanism by which this occurs is still under investigation. Using a rat brain glioma (C6) model, we examined the expression levels of occludin and claudin-5 at different time points after intracarotid infusion of MS (30 μg/kg/min) by western blotting. The protein expression levels of occludin and claudin-5 showed no changes after 1 hour and began to decrease significantly after 2 hours of MS infusion, accompanied by tight junction (TJ) opening. The reactive oxygen species (ROS) scavenger, N-2-mercaptopropionyl glycine (MPG), significantly attenuated the MS-induced BTB permeability increases. In the in vitro co-culture of brain microvascular endothelial cells (BMECs) with C6 glioma cells, MS induced a time-dependent increase in ROS production which reached its maximum peak at 2 hours post incubation (100 μmol/ml), as determined by DHE fluorescence measurements. Taken together, all of these results suggested that MS might increase BTB permeability in a time-dependent manner by down-regulating TJ protein expression and this effect could be reversed by the ROS scavenger, MPG. | |||
TO cite this article:Gu Yan-ting,Xue Yi-xue,Wang Yan-feng, et al. The mechanism of the blood-brain tumor barrier permeability increase induced by minoxidil sulfate in a rat brain tumor model[OL].[13 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4503754 |
10. Sema4C determines aggressiveness of human cervical cancers by the AKT pathway | |||
WU Mingfu,YANG Jie,LI Nin,LIU Lijiang | |||
Clinical Medicine 08 May 2012 | |||
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Abstract:Increasing evidences indicated that Semaphorins involved in tumorigenesis and tumor development. In our previous observations, a trans-membrane protein Sema4C has been identified as a novel molecular target in human breast cancer and Sema4C abnormal expression in the lymphatic endothelial cells of human cervical cancers provided another new molecular machenism for lymphatic metastasis of cervical cancer. However, the role and function of Sema4C in human cervical cancers are stiil unkown. In this study, we first detected the relationship between Sema4C expression and malignant behaviors in four different human cervical cancer cells, and then further investigated the effect of specific silencing Sema4C on malignant phenotype and its molecular mechanism in different tumor cell lines was. We observed the universal high expression of Sema4C in cervical cancer cell lines, but Sema4C expression was the strongest in Caski cells. Sema4C siRNA significantly inhibited the capabilities of invasion and proliferation of Caski cells. Furthermore, decreased phosphorylation levels of AKTThr-308 but no obvious alteration of the expression of total AKT and phosphorylation of AKTSer-473 were showed after effective silencing of Sema4C. These findings above showed that Sema4C promotes malignant behaviors of cervical cancer cells via altered phosphorylation levels of AKTThr-308, suggesting that Sema4C may be a novel therapeutic target for the treatment of cervical cancer. | |||
TO cite this article:WU Mingfu,YANG Jie,LI Nin, et al. Sema4C determines aggressiveness of human cervical cancers by the AKT pathway[OL].[ 8 May 2012] http://en.paper.edu.cn/en_releasepaper/content/4477457 |
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