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| There are 37 papers published in subject: > since this site started. | |||
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| 1. LAPTM4B Expression Predicts Chemoresistance and Poor Clinical Outcomes in Patients with Local Advanced Cervical Cancer Treated with Neoadjuvant Chemotherapy Prior to Radical Hysterectomy | |||
| Fanling Meng,Pan shang,Hongtao Song,Ge Lou | |||
| Clinical Medicine 07 June 2016 | |||
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| Abstract:Objectives: LAPTM4B (lysosomal protein transmembrane-4 beta) plays a critical role in tumor progression and chemoresistance. The aim of this study was to evaluate the significance of LAPTM4B expression to predict response to platinum-based neoadjuvant chemotherapy and survival of patients with locally advanced cervical cancer (LACC) who subsequently underwent radical hysterectomy. Materials and methods: Biopsy specimens of cervical cancer before neoadjuvant chemotherapy were obtained from 116 patients who subsequently underwent radical hysterectomy. The expression of LAPTM4B protein was analyzed by immunohistochemistry. Findings were evaluated in relation to LAPTM4B expression and chemotherapy resistance. Survival analyses were performed by the Kaplan-Meier curves and a Cox regression model to determine overall survival (OS) and disease-free survival (DFS). Results: Our result showed that LAPTM4B was highly expressed in 73.3% of LACC sections. Expression of LAPTM4B was significantly associated with poor clinical response (P=0.012). Moreover, high expression of LAPTM4B was significantly associated with poor OS and DFS compared with the low expression group (both P<0.05). Multivariate analysis revealed that LAPTM4B expression was an independent prognostic factor for OS (P<0.05). Conclusions: In conclusion, elevated LAPTM4B expression in patients with locally advanced cervical cancer contributes to chemoresistance and predicts poor prognosis. | |||
| TO cite this article:Fanling Meng,Pan shang,Hongtao Song, et al. LAPTM4B Expression Predicts Chemoresistance and Poor Clinical Outcomes in Patients with Local Advanced Cervical Cancer Treated with Neoadjuvant Chemotherapy Prior to Radical Hysterectomy[OL].[ 7 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4693514 | |||
| 2. Over-expression of LAPTM4B-35 and VEGF is related to poor prognosis in local advanced cervical carcinoma | |||
| Fanling Meng,Pan Shang,Hongtao Song,Ge Lou | |||
| Clinical Medicine 04 June 2016 | |||
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| Abstract:Objectives: Patients with locally advanced cervical cancer (LACC) are difficult to treat. The purpose of this study is to investigate lysosome-associated protein transmembrane 4?-35 (LAPTM4B-35) and vascular endothelial growth factor (VEGF) expression in LACC and evaluate their clinicopathological and prognostic significance. Methods: The expression of LAPTM4B-35 and VEGF proteins was analyzed by immunohistochemistry in 119 LACC and 40 normal cervical specimens. Results: LAPTM4B-35 and VEGF were expressed in 73.9% and 75.6% of cervical cancer, respectively, which are higher than the normal cervical tissues. LAPTM4B-35 expression was positively correlated with the expression of VEGF. The expression of LAPTM4B-35 and VEGF was significantly correlated with FIGO stage, Histological grade and lymph node metastasis (P<0.05). Kaplan-Meier analysis showed that LACC patients with high expression of LAPTM4B-35 and VEGF exhibited poor overall survival (OS) and disease-free survival (DFS) (P<0.05). Conclusions: We demonstrate that LAPTM4B-35 correlates with VEGF and is a poor prognostic factor in local advanced cervical cancer. | |||
| TO cite this article:Fanling Meng,Pan Shang,Hongtao Song, et al. Over-expression of LAPTM4B-35 and VEGF is related to poor prognosis in local advanced cervical carcinoma[OL].[ 4 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4693517 | |||
| 3. Differentially expressed miRNA in hepatocellular carcinoma cells under hypoxic conditions is linked to transcription and phosphorylation | |||
| SUN Haixiang,TANG Weiguo,HU Bo | |||
Clinical Medicine 16 May 2016
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| Abstract:Hypoxia is a critical aspect of tumor biology and has been associated with poor prognosis and resistance to traditional therapy. In this study, we screened for differentially expressed genes and microRNAs (miRNAs) inhepatocellular carcinoma(HCC) cell line Huh7 under hypoxic conditions. Based on microarray data, we identified11,508 mRNAs and 58 miRNAs showing at least a 1.5-fold change in expressionunder hypoxic conditions. Gene ontology (GO) and pathway analysis showed that the differentially expressed genes were mainly involved in cell cycle regulation, cell division, transcription, and G-protein coupled receptor signaling pathways.By usingthe TargetScan and miRanda software packageswith the miRNA-mRNA negative expression network, differentially expressed miRNA targets were predicted. GO analysis showed that the primary function of these miRNAswas to regulatetranscription and phosphorylation.The miRNA-mRNA networksfor both transcription and phosphorylation were further analyzed. Network analysis showed that the key miRNAsin these networkswere miR-19a, miR-34a, miR-29a, mir-196a, miR-25 and miR-1207, whose potential gene targets include DNA-binding proteins, zinc finger proteins, and transcription factors. Some protein kinases, such as MAPK1, MAP3K4, and CDK18, were also shown to be presentin the network,demonstrating the importance of miRNAs in protein phosphorylation. These findings provide evidence that miRNAs play an important role in transcription and phosphorylation in the hypoxic response of HCC cells. | |||
| TO cite this article:SUN Haixiang,TANG Weiguo,HU Bo. Differentially expressed miRNA in hepatocellular carcinoma cells under hypoxic conditions is linked to transcription and phosphorylation[OL].[16 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4688662 | |||
| 4. Optimizing the treatment of bevacizumab in metastatic breast cancer: a meta-analysis of published randomized trials | |||
| Yin Wenjin,Yin Kai,Wang Yaohui,Lu Jinsong | |||
| Clinical Medicine 10 May 2016 | |||
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| Abstract: Background: Angiogenesis contributes to the progression of breast cancer and vascular endothelial growth factor (VEGF) plays an essential role in neovascularization. Bevacizumab, as a humanized recombinant monoclonal antibody,specifically targets the VEGF receptors. Manifold data have demonstrated that the addition of bevacizumab to chemotherapy improved progression-free survival (PFS), while none of the trials revealed its significant survival benefit. Furthermore, it still remains suspended how to maximize the benefits of bevacizumab and minimize its risks in the metastatic setting. Objectives: We sought to conduct a meta-analysis to assess the benefits of bevacizumab with chemotherapy as well as to identify the best partner of bevacizumab in the treatment of metastatic breast cancer patients.? Methods: Computerized and manual searches were performed to identify randomized clinical trials comparing salvage chemotherapy with or without bevacizumab in metastatic breast cancer patients. Hazard ratios (HR) and risk ratios (RR) with their 95% confidence intervals (CIs) were used to estimate the association between the addition of bevacizumab to salvage chemotherapy and various survival outcomes. The fixed effects or random-effects model was used to combine data. Primary outcomes were objective response rate (ORR), PFS and overall survival (OS). Results: With five trials identified, this analysis included 3,544 eligible patients. The addition of bevacizumab to salvage chemotherapy resulted in a statistically significant improvement in PFS (HR = 0.73, 95% CI=0.64-0.83, P<0.001) and ORR (RR = 1.464, 95% CI=1.324-1.618, P<0.001) rather than OS (HR = 0.92, 95%CI=0.82-1.04, P=0.191) when compared with chemotherapy alone. Subgroup analysis further verified that PFS advantages were merely discerned for taxanes/anthracyclines and first-line chemotherapy. Conclusion: This meta-analysis reveals that the addition of bevacizumab to chemotherapy yielded PFS benefit in patients with metastatic breast cancer. Bevacizumab treatment might be recommended in combination with taxanes/anthracyclines and for first-line treatment in the metastatic setting. | |||
| TO cite this article:Yin Wenjin,Yin Kai,Wang Yaohui, et al. Optimizing the treatment of bevacizumab in metastatic breast cancer: a meta-analysis of published randomized trials[OL].[10 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4688737 | |||
| 5. Single-nucleotide polymorphism in microRNA-binding site of SULF1 target gene as a protective factor against the susceptibility to breast cancer: a case-control study | |||
| Yin Wenjin,Zhou Qiong,Jiang Yiwei,Wang Yaohui,Lu Jinsong | |||
| Clinical Medicine 10 May 2016 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Purpose: Numerous clinical studies have suggested that chemopreventive drugs for breast cancer such as tamoxifen and exemestane can effectively reduce the incidence of estrogen receptor (ER)-positive breast cancer. However, it remains unclear how to identify those who are susceptible to ER-positive breast cancer. Accordingly, there is a great demand for a probe into the predisposing factors so as to provide precise chemoprevention. Recent evidence has indicated that ER expression can be regulated by microRNAs (miRNAs), such as miR-206, in breast cancer. We assumed that single-nucleotide polymorphisms (SNPs) in the miR-206-binding sites of the target genes may be associated with breast cancer susceptibility with different ER statuses. Methods: We genotyped the SNPs that reside in and around the miR-206-binding sites of two target genes - heparan sulfatase 1 (SULF1) and RPTOR-independent companion of mammalian target of rapamycin Complex 2 (RICTOR) - which were related to the progression or metastasis of breast cancer cells in 710 breast cancer patients and 294 controls by the matrix-assisted laser desorption ionization-time of flight mass spectrometry method. Modified odds ratios (ORs) with their 95% confidence intervals (CIs) were calculated by a multivariate logistic regression analysis to evaluate the potential association between the SNPs and breast cancer susceptibility. Results: For rs3802278, which is located in the 3'-untranslated region (3'-UTR) of SULF1, the frequency of the AA genotype was less in breast cancer patients than that in the controls as compared to that of the GG+GA genotype not only for ER-positive breast cancer patients (adjusted OR=0.663, P=0.032) but also for hormone receptor-positive breast cancer patients (adjusted OR=0.610, P=0.018). Besides, the frequency of the AA genotype was less than that of the GG genotype between the ER-positive breast cancer patients and the controls (adjusted OR=0.791, P=0.038). For rs66916453, which is located in the 3'-UTR of RICTOR, no significant difference was observed between the case and the control group for the genotypes or alleles (P>0.05). Conclusion: The SNPs in the miRNA-binding sites within the 3'-UTR of SULF1 may serve as protective factors against the susceptibility to breast cancer, especially to ER-positive breast cancer in the Chinese population. These SNPs are promising candidate biomarkers to predict the susceptibility of breast cancer and guide the administration of targeted preventive endocrine therapy. | |||
| TO cite this article:Yin Wenjin,Zhou Qiong,Jiang Yiwei, et al. Single-nucleotide polymorphism in microRNA-binding site of SULF1 target gene as a protective factor against the susceptibility to breast cancer: a case-control study[OL].[10 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4688734 | |||
| 6. High expression of c-Fos promotes radioresistance and predicts poor prognosis in malignant glioma | |||
| LIU Zhigang,WANG Hui | |||
Clinical Medicine 29 December 2015
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| Abstract:c-Fos is a major component of activator protein (AP)-1 complex, which has been implicated in cell differentiation, proliferation, angiogenesis, invasion and metastasis. In this study, we investigated the role of c-Fos gene in glioma radiosensitivity and figured out the involved molecular mechanisms. Following downregulation of c-Fos gene by lenti-virus in glioma cell lines, we analyzed the radiosensitivity, DNA damage repair capacity, and cell cycle distribution of c-Fos. At last, we explored its prognostic value in 41 malignant glioma patients by immunohistochemistry. Our results showed that c-Fos inhibition could sensitize glioma cells to radiation by increasing radiation induced DNA double strand breaks(DSBs), disturbing the DNA damage repair process, promoting G2 cell cycle arrest and apoptosis. c-Fos protein overexpression correlated with poor prognosis in glioma patients who received standard treatment. Our findings provide new insights into the mechanism of radioresistance in malignant glioma. Therefore, c-Fos may hopefully become a novel therapeutic target for malignant glioma patients. | |||
| TO cite this article:LIU Zhigang,WANG Hui. High expression of c-Fos promotes radioresistance and predicts poor prognosis in malignant glioma[OL].[29 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4673825 | |||
| 7. OLA1 regulates epithelial-mesenchymal transition through the modulation of GSK-3β-Snail-E-cadherin signaling | |||
| ZHANG Jiawei,BAI Li,CHENG Huarong,SHI Zhengzheng | |||
| Clinical Medicine 15 December 2015 | |||
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| Abstract:OLA1 is a member of the Obg family of P-loop NTPases with a putative GTPase-like molecular switch function. In this study the role of OLA1 in the regulation of epithelial-mesenchymal transition (EMT) was characterized in human lung cells and carcinomas. RNAi-mediated silencing of OLA1 rendered both A549 (lung adenocarcinoma-derived) and Beas-2B (noncancerous) cells resistant to transforming growth factor (TGF)-β1-induced transition to mesenchymal morphology accompanied, at molecular level, by reduced loss of epithelial marker E-cadherin and largely demolished Snail, the transcriptional repressor of E-cadherin. Because degradation of Snail is mediated by its phosphorylation by GSK-3, OLA1's effect on GSK-3 was further investigated. OLA1 was found to interact with GSK-3 and be involved in the phosphorylation (Ser9)-mediated GSK-3 deactivation. The protein-protein interaction required the presence of the OLA1 TGS domain, indicating TGS' novel function. These results suggest that OLA1 plays an important role in EMT, especially in lung epithelial cells and tumors, through regulating GSK-3β activity, Snail stability, and expression of E-cadherin. | |||
| TO cite this article:ZHANG Jiawei,BAI Li,CHENG Huarong, et al. OLA1 regulates epithelial-mesenchymal transition through the modulation of GSK-3β-Snail-E-cadherin signaling[OL].[15 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4669464 | |||
| 8. Epigenetic silencing of protocadherin 10 in colorectal cancer | |||
| ZHANG Jiawei,ZHONG Xian,SHEN Hong,ZHENG Shu | |||
| Clinical Medicine 15 December 2015 | |||
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| Abstract:Colorectal cancer (CRC) is one of the leading malignant tumors in the world and known as a multi-step process resulting from the accumulation of both genetic and epigenetic alterations of the genome. Although the molecular mechanisms of its pathogenesis remain unclear, inactivation of tumor-suppressor genes (TSGs) through promoter methylation plays an important role in the development of CRC. Aberrant methylation is the most well-defined hallmark in CRC. Recently, epigenetic silencing of protocadherin 10 (PCDH10) was found, as a frequent and early event, in CRC. PCDH10 has been identified as an important tumor suppressor gene (TSG) with key roles of colorectal carcinogenesis, invasion and metastasis. The advantages of gene methylation as a target for detection and diagnosis in tumor tissues and body fluids have led to discovering non-invasive screening methods for CRC. This article aims mainly to review the epigenetic alteration of PCDH10 and the possibility of a non-invasive biomarker for CRC. | |||
| TO cite this article:ZHANG Jiawei,ZHONG Xian,SHEN Hong, et al. Epigenetic silencing of protocadherin 10 in colorectal cancer[OL].[15 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4669482 | |||
| 9. CDX-2 as a marker in identification of CTCs in patients with metastatic colorectal cancer | |||
| Hu Huali,Fenglei Yu,Li,Wang | |||
Clinical Medicine 25 November 2015
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| Abstract:Purpose:Current CTC technologies in patients with colorectal cancer, such as Cellsearch, flow cytometry and RT-PCR, are all epithelial marker-depent method. While a number of researches have found that EMT was present in CTC, which undermined their authority in CTC detection and therefore hampered their wider application clinically. We aimed at exploring another approach to detect CTC circuvmenting the phenomenon of EMT and test its effectiveness in patients with metastatic colorectal cancer. Methods: Colorectal cell lines SW480, lung adenocarcinoma cell lines A549, and human skin cell lines Hacat were used to eastablish expeimental model in vitro. Peripheral blood from 14 patients with metastatic colorectal cancer were obtained and filtered though a filter with 8 um pore membrane to isolate CTC. Blood samples from 14 healthy voluteers were used as negative control. Immunofluorescence and in situ immunocytochemistry following Pap stain was proceed to directed at AE3/Vimentin and CDX-2 respectivelly. Results: In cell experiments, we verified that CDX-2 could be used as marker in differential diagnosis between SW480 cells and A549 cells or Hacat cells, while pan cytokeratin could not. In clinical detection, we found it effective in CTC isolation using ISET. Immunocytochemistry results showed that all the CHNCs-MF were postive for CDX-2 while part of CTCs were postive for pan-cytokeratin. Meanwhile, we found one CTC expressing vimentin only in a patients with metastatic colorectal cancer and a number of circulating cells without morphologically malignant feartures showing postive expression of pan-cytokeratin in peripheral blood of a healthy voluteer. Conclusion: We found a way to detect CTCs circumventing EMT in patients with metastatic colorectal cancer for the first time. Both the ISET and the CDX-2 marker are regardless of the EMT in the CTCs detection,showing advantage compared with current detection technology depending on epithelial marker. This method could be a promising way to detect CTCs in patients with colorectal cancer. | |||
| TO cite this article:Hu Huali,Fenglei Yu,Li,Wang. CDX-2 as a marker in identification of CTCs in patients with metastatic colorectal cancer[OL].[25 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4665344 | |||
| 10. Mir-200b Regulates Epithelial-Mesenchymal Transition of Chemotherapy-resistant Breast Cancer Cell by Targeting FN1 | |||
| Yang Xing,Hu Qian,Lin Xiao,Dinglin Xiaoxiao,Yao Herui | |||
| Clinical Medicine 12 October 2015
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| Abstract:Background：Chemotherapy, being as one of the three cornerstones in breast cancer treatment, is playing an important role in controlling the disease. However, growing evidences indicate that after several regimens, chemotherapy does not effectively alleviate disease for patients with advanced breast cancer. Different studies had indicated that the tumor cells underwent epithelial-mesenchymal transition (EMT). In recent years, there have been literature studies confirmed that miRNAs play a regulatory role in chemotherapy resistance and chemotherapy-induced EMT. However the underlying mechanisms is not clear. Methods：To address this question, we constructed drug-resistant breast cancer cell lines, and then observed if breast cancer resistant cell lines EMT displayed. Changes in cell morphology are observed under the microscope. We also detected the expressions of EMT markers E-cadherin, Vimentin, N-cadherin by qRT-PCR, western blotting, and the invasion and migration ability of tumor cells by modified chamber assay. Results：Compared with the parental cells, there were 16 miRNA expression increased and 20 downregulated miRNA in resistant cell lines, demonstrated by miRNA microarray. Of which miR-200b is the most obvious. Elavated miR-200b level in drug-resistant cells could reverse features of parental cells, and inhibit invasion and migration ability, but increase sensitivity to doxorubicin. Knockdown miR-200b in parental cells can promote transition to mesenchymal features, increase the invasion and migration ability, induce resistance to doxorubicin. Luciferase experiments showed that miR-200b target was FN1.Upregulated miR-200b inhibit FN1 expression and luciferase activity. Compared with the parental cell line, FN1 was significantly elevated in MCF-7/Adr. Knockdowning FN1 reverse mesenchyal features, decrease cell migration and invasion capacity, and improve drug sensitivity to doxorubicin. Conclusion: Our data suggest that FN1 is the target of mir-200b, which gets the regulation role of the chemotherapeutic resistance to doxorubicin in breast cancer cells. Therefore miR-200b may serve as an effective tumor inhibitor, play a role in the future to pave the way for targeted cancer therapy. | |||
| TO cite this article:Yang Xing,Hu Qian,Lin Xiao, et al. Mir-200b Regulates Epithelial-Mesenchymal Transition of Chemotherapy-resistant Breast Cancer Cell by Targeting FN1[OL].[12 October 2015] http://en.paper.edu.cn/en_releasepaper/content/4654569 | |||
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