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1. The establishment of gene expression profiling-guided clinical precision treatment for patients with endometrial carcinoma | |||
ZHOU Jingyi,Yin Fufen,LI Xiaoping,YAO Yuanyang,CHEN Yonghua,GAO Baorong,YANG Yuan,YANG Yingchao,LI Mingzhu,ZHAO Lijun,WANG Zhiqi,SHEN Danhua,WEI Lihui,WANG JianLiu | |||
Clinical Medicine 08 May 2017 | |||
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Abstract:Endometrial carcinoma (EC) is a common gynaecologic cancer. Most EC patients, especially those with early stage endometrioid endometrial adenocarcinoma (EEC), will have a good prognosis. Studies showed that similar staging and histology results in early stage EC patients had completely different prognoses postoperatively. EC is a highly heterogeneous disease, and different genetic alterations may exist in the same histological phenotype of carcinoma, indicating that some flaws exist in the current therapy strategy based on the clinical pathological classification and Bokhman's classification. It's necessary to establish new molecular type of the EC. 492 EC-related genes from the NCBI database were selected, and oligoprobes were then designed with the UniGene Database and the Human Reference Sequence (RefSeq) Database. An EC-related, 492-gene microarray was constructed with the oligoprobes. A hierarchical cluster algorithm was used to sort tumour samples according to gene expression patterns. Significance analysis of microarrays (SAM) was used to select the different expressed genes. Genes' expression were tested by immunohistochemistry assay. Results showed that the UPSC samples exhibited distinct gene expression profiles compared to those of EEC and 46 genes that could highly discriminate UPSC from EEC. 21 genes were selected and defined as EC prognosis-related genes and some of the genes. Our data suggests seeking new molecular type of the EC different from the traditional clinical pathological classification and Bokhman's classification, will help in the accurate prognosis and practice of precise therapy of EC.????? | |||
TO cite this article:ZHOU Jingyi,Yin Fufen,LI Xiaoping, et al. The establishment of gene expression profiling-guided clinical precision treatment for patients with endometrial carcinoma[OL].[ 8 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4729555 |
2. Research Fund for the Doctoral Program of Higher Education of China | |||
YIN Fufen, YANG Yuan,ZHOU Jingyi,ZHAO Lijun,GAO Baorong,WAN Xiaoping,WANG Jianli | |||
Clinical Medicine 26 April 2017 | |||
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Abstract: Previously, our study found that dual-specificity phosphatase 1 (DUSP1) overexpressed in early stage, progesterone receptor (PR) expressed endometrioid adenocarcinoma. However, the function of DUSP1in endometrioid adenocarcinomaprogression and the relationship between DUSP1and medroxyprogesterone are still unclear. The expression of DUSP1 was measured by immunohistochemical analysis and the data was analyzed by χ2 test. The effect of DUSP1 on endometrioid adenocarcinoma cells proliferation was analyzed by CCK8 and colony formation assay. The effect of DUSP1 on cell migration was analyzed by transwell assay. Medroxyprogesterone was used to induce DUSP1 expression in endometrioid adenocarcinoma cell, which was measured by western blot. Results showed DUSP1 expression was deficient in advanced FIGO-stage and high-grade endometrioid adenocarcinoma. DUSP1 expression was substantially higher in endometrioid adenocarcinomacell line Ishikawa than that in RL952, Hec1A and Hec1B cell lines. DUSP1 knocking down promoted proliferation, migration, and activated MAPK/Erk pathway in Ishikawa cells. Medroxyprogesterone up-regulated DUSP1 expression and inhibited MAPK/Erk pathway in Ishikawa cell. Our data suggests DUSP1 deficiency promotes endometrioid adenocarcinomaprogression via activating MAPK/Erk pathway, which could be reversed by medroxyprogesterone. DUSP1 is a possible medroxyprogesterone treatment target in endometrioid adenocarcinoma. | |||
TO cite this article:YIN Fufen, YANG Yuan,ZHOU Jingyi,ZHAO Lijun, et al. Research Fund for the Doctoral Program of Higher Education of China[OL].[26 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4729591 |
3. Effects of rearing as small litters on ovarian morphology and function at puberty and in adulthood in the rat | |||
Xueqing Wu,Xiaofeng Li,Weiting Xia,Bilu Ye,Kevin T O'Bryne | |||
Clinical Medicine 05 June 2016 | |||
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Abstract:Rearing rats in small litters leads to obesity and reproductive dysfunction. We investigated the effects of rearing female rats in small litters on various reproductive parameters during puberty and into adulthood, and the possible involvement of local ovarian sympathetic nervous activity. The litter size was adjusted on postnatal day one to four pups for the small litter and 12 pups per dam for the normal litter. Vaginal opening was recorded, and oestrous cyclicity was monitored daily immediately post puberty for 14 days and again at 8-9 weeks of age. At the time of puberty and 10 weeks of age, the ovaries were collected. The thickness of the theca interna of the largest antral follicles was measured. Ovarian sympathetic nerve activity was assessed immunohistochemically by measuring levels of ovarian nerve growth factor receptor (p75NGFR) and tyrosine hydroxylase (TH). In rats reared in small litters, there was a significant advancement of puberty and disruption of oestrous cyclicity immediately post puberty. The thickness of the theca interna increased and the expression profiles of ovarian p75NGFR and TH increased in small litter rats at puberty, but this did not persist into adulthood. These data suggest that rearing rats in small litters leads to irregular reproductive cycles, which might involve increased local ovarian sympathetic nerve activity. | |||
TO cite this article:Xueqing Wu,Xiaofeng Li,Weiting Xia, et al. Effects of rearing as small litters on ovarian morphology and function at puberty and in adulthood in the rat[OL].[ 5 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4696709 |
4. Effects of LIV1 expression on the proliferation of epithelial ovarian cancer cells to cisplatin | |||
MA Xiaoli,DUAN Hua | |||
Clinical Medicine 16 December 2014 | |||
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Abstract:Drug resistance to cisplatin is the primary cause of death in patients with epithelial ovarian cancer. The aim of this study was to investigate the effect of LIV1 expression on sensitivity of epithelial ovarian cancer cells SKOV3 to cisplatin. We tested the induction of LIV1 in epithelial ovarian cancer cells SKOV3 after cisplatin treatment by real-time PCR and western blot. We investigated the effect of LIV1 expression on sensitivity of epithelial ovarian cancer cells SKOV3 to cisplatin by MTT assay. Finally, we analyzed the mechanism of LIV1 in ovarian cancer cells SKOV3 by western blot. The level of LIV1 mRNA and protein was significantly upregulated after cisplatin treatment. The proliferation rate of ovarian cancer cells SKOV3 transfected with AS-LIV1(PCEP4 carrying antisense LIV1 cDNA) were obviously higher than control detected by MTT assays. Using Western Blot, we demostrated that the inhibition of cisplatin-induced apoptosis by knockdown of LIV1 might be associated with decreased endogenous levels of Bcl-2.The data presented in this report may contribute to understanding the molecular mechanisms of drug resistance to cisplatin, LIV1 may be a potential molecular target. | |||
TO cite this article:MA Xiaoli,DUAN Hua. Effects of LIV1 expression on the proliferation of epithelial ovarian cancer cells to cisplatin[OL].[16 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4624058 |
5. Human Epididymis Protein4 inhibits proliferation of human ovarian cancer cells via the MAPK and PI3K/AKT pathways | |||
Kong Xiuli,Chang Xiaohong,Ye Xue,Ma Ruiqiong,Cheng Hongyan,Cui Heng | |||
Clinical Medicine 20 December 2013 | |||
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Abstract:Objectives: Human epididymis protein 4 (HE4) is a promising novel biomarker for the detection of epithelial ovarian cancer (EOC). The role of HE4 in EOC tumorigenesis is unclear. This study investigated the cellular and molecular mechanisms of HE4 in ovarian cancer cell proliferation. Methods: We generated HE4-overexpressing SKOV3 cells and silenced HE4 gene expression in SKOV3.ip1 cells. We used the Cell Counting Kit-8 assay to evaluate cell proliferation and western blotting to analyze the expression of proliferation- and apoptosis-associated proteins such as Bax, Bcl-2, and caspase 3. Results: Overexpression of HE4 in SKOV3, an ovarian carcinoma cell line, inhibited cell proliferation. In contrast, HE4 silencing in SKOV3.ip1 cells promoted cell proliferation; however, conditioned medium containing HE4 and human recombinant HE4 protein (hrHE4) had no effect on proliferation in SKOV3 or SKOV3.ip1 cells. HE4 inhibited MEK, ERK1/2, and AKT phosphorylation, but promoted JNK1/2/3 and c-JUN phosphorylation; however, p38 phosphorylation was impaired in HE4-overexpressing and silenced cells. HE4 had no effect on EGFR phosphorylation or on the apoptosis-associated proteins Bax, Bcl-2, and caspase 3. Conclusions: HE4 might play a protective role in the progression of EOC by inhibiting cell proliferation. Antiproliferative activity was mediated by intracellular HE4, and not the secreted protein. HE4 might inhibit cell proliferation by regulating MAPK and PI3K/AKT signal transduction in vitro.?? | |||
TO cite this article:Kong Xiuli,Chang Xiaohong,Ye Xue, et al. Human Epididymis Protein4 inhibits proliferation of human ovarian cancer cells via the MAPK and PI3K/AKT pathways[OL].[20 December 2013] http://en.paper.edu.cn/en_releasepaper/content/4577103 |
6. Discrepant clinicopathologic characteristics and HE4 performance in type I and type II epithelial ovarian cancer | |||
Bo Di,Jiang Jinghong,Chang Xiaohong,Ye Xue,Cheng Hongyan,Cui Heng | |||
Clinical Medicine 20 December 2013 | |||
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Abstract:Backgroud Recent studies demonstrated that epithelial ovarian cancer (EOC) has been several different diseases and the two-tier system divided it to type I and type II EOC. HE4 has been a complementary biomarker for diagnosis of epithelial ovarian cancer (EOC). This study aimed to evaluate the difference of clinicopathologic characteristics and HE 4 expression in these two type EOC. Methods This retrospective study included 127 EOC patients. Data on patient demographics, cancer stages, grades, histology, operation procedures performed, residual disease, adjuvant chemotherapy, recurrence, and survival were collected. 134 ovarian carcinoma tissue specimens and 40 matching borderline ovarian tumor specimens were picked from the archive of pathologic department. Immunohistochemistry was applied to assess HE4 expression in EOC and borderline ovarian tumor tissue specimens. Results Of the 127 patients, there were 42 type I EOC(7 low grade serous carcinomas, 8 mucinous carcinomas, 12 endometriod carcinomas and 15 clear cell carcinomas) and 85 type II EOC( 83 high grade serous carcinomas and 2 malignant mixed mesodermal tumors). The median followed-up time was 18.3 months. There were statistic difference between the two type EOC in terms of menopausal state, FIGO stage and pathologic differentiation, but not in residual tumor and chemotherapy relieveation. In type I EOC, the median follow-up time was 31 months (4-72m) and the median progression-free survival was 72 months (95%CI:40.34-103.66).There were 15(35.7%) relapsed or progressive patients. In type II EOC, the median follow-up time was 17 months(0-60m) and the median progression-free survival was 27 months (95%CI:17.83-36.17). There were 47(55.3%) relapsed or progressive patients. There had significant statistic difference between the two type EOC in terms of progression-free survival (p<0.001). Among the 44 type I specimens, 25 were positive expression of HE4 (56.8%), in contract, the positive expression specimens in type II was 78 (86.7%). There was significant difference between type I and type II EOC in expression of HE4. Also, there had significant difference between high-grade serous carcinoma and borderline serous tumor, but no difference between low-grade serous carcinoma and borderline serous tumor or other EOC and its corresponding borderline tumor. Conclusion The different clinic-pathologic characteristics between type I and type II EOC make the two-tier system of EOC reasonable and reliable. HE4 would be a powerful biomarker to distinguish type II EOC from borderline tumor but it is less useful in type I EOC. Type I EOC would be generated from its corresponding borderline tumor. | |||
TO cite this article:Bo Di,Jiang Jinghong,Chang Xiaohong, et al. Discrepant clinicopathologic characteristics and HE4 performance in type I and type II epithelial ovarian cancer[OL].[20 December 2013] http://en.paper.edu.cn/en_releasepaper/content/4577100 |
7. Laparoscopic surgery for ectopic pregnancy within caesarean scar | |||
JIANG Sheng,ZHAO Shaojie | |||
Clinical Medicine 13 November 2013 | |||
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Abstract:Background: Ectopic pregnancy in a previous caesarean section scar is rarely reported. And it is very difficult to manage it. There have been only 12 cases were successfully managed under laparoscopy to date. Cases: Two females were admitted to our hospital and were suspected suffering from ectopic pregnancy in a previous caesarean section scar under the impression of Doppler ultrasound. Conservative regimen was first applied to one patient but failed to demonstrate enough efficacy. The β-HCG of the other patient was extremely high so conservative treatment was not considered. Then laparoscopic surgery was performed for the two patients and not only confirmed the diagnosis but also removed the ectopic gestational products successfully. The operation under laparoscopy was very smoothly. Total operation time was 80 minutes, blood loss was only about 100ml and blood transfusion was not necessary. Conclusion: It seems that for a skilled surgeon, laparoscopy may be a sound and reasonable technique to diagnose and resect ectopic pregnancy within a caesarean scar. | |||
TO cite this article:JIANG Sheng,ZHAO Shaojie. Laparoscopic surgery for ectopic pregnancy within caesarean scar[J]. |
8. Estrogen promotes the growth of decidual stromal cells through estrogen receptor beta-mediated IL-24 down-regulation in human early pregnancy | |||
Li Mingqing,Shao Jun,Meng Yuhan,Li Dajin | |||
Clinical Medicine 11 July 2013 | |||
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Abstract:Interleukin-24 (IL-24) is a novel tumor suppressor gene, which has suppressor activity in a broad spectrum of human cancer cells.The present study aimed to elucidate the biological function of IL-24 and its receptors (IL-20R1, IL-20R2 and IL-22R1) in decidual stromal cells (DSCs) at human maternal-fetal interface. The DSCs behaviors in vitro were verified by viability (MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and apoptosis assay, respectively. Additionally, the effects of pregnancy-associated hormones on IL-24 and the effect of IL-24 on the correspondent functional molecules were investigated by ELISA, in-cell western and flow cytometry, respectively. Here we found that DSCs expressed IL-24 and its receptors, and IL-24 obviously suppressed the viability and stimulated the apoptosis in DSCs. On the contrary, both anti-IL-24 and IL-22R1 neutralizing antibodies markedly promoted growth and reduced the apoptosis. Estrogen but not progesterone could significantly decrease IL-24 but not its receptors, and these effects could be abolished by the antagonist of estrogen receptor beta (ERb). IL-24 significantly restricted the stimulatory effect of estrogen on the viability, anti-apoptosis, anti-apoptosis gene Bcl-2 and proliferation relative gene Ki-67 in DSCs. Our study has demonstrated that IL-24/IL-20R2/IL-22R1 axis is involved in the regulation of estrogen/ERb signaling on the growth of DSCsthrough up-regulating the expression of Bcl-2 and Ki67, which suggests that estrogen plays an important role in DSC growth of the early pregnancy through down-regulating IL-24. | |||
TO cite this article:Li Mingqing,Shao Jun,Meng Yuhan, et al. Estrogen promotes the growth of decidual stromal cells through estrogen receptor beta-mediated IL-24 down-regulation in human early pregnancy[J]. |
9. The synergistic regulation of the NODAL gene by transcription factors Smad2 and Cited2 during cardiac development | |||
SUN Lei,LI Hui | |||
Clinical Medicine 06 March 2013 | |||
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Abstract:The Nodal signaling pathway has been demonstrated to play a critical role during mammalian cardiac development. As recent tests that have been conducted on gene-targeted mice indicate, its expression is frequently altered where cardiac defects are present. However, the function and the molecular mechanism of Nodal pathway in VSD genesis have not been clarified. In this report, we had revealed decreased NODAL gene expression in patients with supracristal ventricular septal defect, membranous ventricular septal defect, and atrioventricular canal defect compared with the controls. Meanwhile, we found the low expression of CITED2 was associated with low-expression of NODAL gene in VSD tissue. Further study showed Smad2 and Cited2 existed in the same transcriptional complex to regulate the NODAL gene expression by luciferase reporter and co-immunoprecipitation assays. The data presented in this report may contribute to understanding the molecular mechanisms of NODAL regulation, which may be a potential molecular target for halting the onset of VSDs.) | |||
TO cite this article:SUN Lei,LI Hui. The synergistic regulation of the NODAL gene by transcription factors Smad2 and Cited2 during cardiac development[OL].[ 6 March 2013] http://en.paper.edu.cn/en_releasepaper/content/4524413 |
10. Functional analysis of two novel mutations in TWIST1 protein motifs found in ventricular septal defect patients | |||
DENG Xiaopeng,WANG Binbin,WANG Jing,PAN Hong,CHENG Zhi,CHENG Longfei,ZHAO Lixi,LI Hui,MA Xu | |||
Clinical Medicine 04 March 2013 | |||
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Abstract:Aims: To investigate the possible genetic effect of sequence variations in TWIST1 on the pathogenesis of ventricular septal defect in humans. Methods: We examined the coding region of TWIST1 in a cohort of 196 Chinese people with non-syndromic ventricular septal defect patients and 200 healthy individuals as the controls.Results: We identified two novel potential disease-associated mutations, NM_000474.3:c.247G>A (p.Gly83Ser) and NM_000474.3:c.283A>G (p. Ser95Gly). Both of them were identified for the first time and were not observed in the 200 controls without congenital heart disease. Using a dual-luciferase reporter assay, we showed that both of the mutations significantly down-regulated the repressive effect of TWIST1 on the E-cadherin promoter. Furthermore, a mammalian two-hybrid assay showed that both of the mutations significantly affected the interaction between TWIST1 and KAT2B. Conclusions: New mutations in the transcription factor TWIST1 that affect protein function were identified in 1.0% (2/196) of Chinese patients with ventricular septal defect. Our data show, for the first time, that TWIST1 has a potential causative effect on the development of ventricular septal defect. | |||
TO cite this article:DENG Xiaopeng,WANG Binbin,WANG Jing, et al. Functional analysis of two novel mutations in TWIST1 protein motifs found in ventricular septal defect patients[OL].[ 4 March 2013] http://en.paper.edu.cn/en_releasepaper/content/4526423 |
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