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miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway Scopus
期刊论文 | 2018 | Pathology Research and Practice
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Abstract :

© 2018 Background: Previous studies indicated that miR-218 was deregulated in gastric cancer patients and correlated with tumor invasion and prognosis. The aim of this study was to clarify the effect of miR-218 on the malignant behavior of gastric cancer and its role in regulating Bmi-1/Akt signaling pathway. Materials and methods: We used miR-218 mimic to transfect gastric cancer cell lines AGS and SGC-7901, and the overexpression efficiency was validated using qRT-PCR assay. MTT assay and Transwell chamber system were performed to detect the effect of miR-218 on cell proliferation, invasion and migration on gastric cancer. Western blot and qRT-PCR assay was used to test the role of miR-218 in regulating Bmi-1/Akt signaling pathway. Results: As shown in our research, ectopic expression of miR-218 in gastric cancer cells inhibits the proliferation, invasion and migration of gastric cancer cells. In addition, miR-218 re-expression inhibits the expression of Bmi-1 and its downstream target p-Akt473, as well as MMPs and EMT process. Conclusions: miR-218 inhibits the proliferation, invasion and migration of gastric cancer cells through modulating EMT process and the expression of MMPs via Bmi-1/Akt signaling pathway.

Keyword :

Akt Bmi-1 EMT Gastric cancer miR-218 MMPs

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GB/T 7714 Wu, Yongxing , Tian, Sijia , Chen, Yijun et al. miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway [J]. | Pathology Research and Practice , 2018 .
MLA Wu, Yongxing et al. "miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway" . | Pathology Research and Practice (2018) .
APA Wu, Yongxing , Tian, Sijia , Chen, Yijun , Ji, Meiju , Qu, Yiping , Hou, Peng . miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway . | Pathology Research and Practice , 2018 .
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Long telomere length predicts poor clinical outcome in esophageal cancer patients SCIE PubMed Scopus
期刊论文 | 2017 , 213 (2) , 113-118 | PATHOLOGY RESEARCH AND PRACTICE | IF: 1.466
WoS CC Cited Count: 4
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Abstract :

Background: Abnormal telomere length is widely reported in various human cancers, and it is considered to be an important hallmark of cancer. However, there is remarkably little consensus on the value of telomere length in the prognostic evaluation of esophageal cancers. Here, we attempted to determine the association of variable telomere length with clinical outcome of esophageal cancer patients. Materials and methods: Using real-time quantitative PCR, we examined relative telomere lengths (RTL) in a cohort of esophageal cancer and normal esophageal tissues, and statistically investigated the association between RTL and clinical outcomes of esophageal cancer patients. Results: The majority of esophageal cancers in this study had longer RTLs as compared to adjacent non tumor tissues. Enhanced tumor RTL was associated with smoking habit, poor differentiation, advanced tumor stage, lymph node metastasis and cancer related death. In particular, a close relationship between longer RTL and poor survival was fully demonstrated by using cox regression and Kaplan-Maier survival curves. Conclusions: We found frequent telomere elongation in esophageal cancer tissues, and demonstrated longer RTL may be an independent poor prognostic factor for esophageal cancer patients. (C) 2016 Elsevier GmbH. All rights reserved.

Keyword :

Clinical outcome Esophageal cancer Relative telomere length Biomarker

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GB/T 7714 Lv, Yanyan , Zhang, Yong , Li, Xinru et al. Long telomere length predicts poor clinical outcome in esophageal cancer patients [J]. | PATHOLOGY RESEARCH AND PRACTICE , 2017 , 213 (2) : 113-118 .
MLA Lv, Yanyan et al. "Long telomere length predicts poor clinical outcome in esophageal cancer patients" . | PATHOLOGY RESEARCH AND PRACTICE 213 . 2 (2017) : 113-118 .
APA Lv, Yanyan , Zhang, Yong , Li, Xinru , Ren, Xiaojuan , Wang, Meichen , Tian, Sijia et al. Long telomere length predicts poor clinical outcome in esophageal cancer patients . | PATHOLOGY RESEARCH AND PRACTICE , 2017 , 213 (2) , 113-118 .
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TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas SCIE PubMed Scopus
期刊论文 | 2016 , 7 (8) , 8712-8725 | ONCOTARGET | IF: 5.168
WoS CC Cited Count: 24
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Abstract :

Increasing evidences have implicated somatic gain-of-function mutations at the telomerase reverse transcriptase (TERT) promoter as one of the major mechanisms that promote transcriptional activation of TERT and subsequently maintain telomere length in human cancers including glioma. To investigate the prognostic value of these mutations and telomere length, individually and their coexistence, in gliomas, we analyzed two somatic mutations C228T and C250T in the TERT promoter, relative telomere length (RTL), IDH1 mutation and MGMT methylation in 389 glioma patients, and explored their associations with patient characteristics and clinical outcomes. Our data showed that C228T and C250T mutations were found in 17.0% (66 of 389) and 11.8% (46 of 389) of gliomas, respectively, and these two mutations were mutually exclusive in this cancer. Moreover, they were significantly associated with WHO grade. We also found that the RTL was significant longer in gliomas than in meningiomas and normal brain tissues (Median, 0.89 vs. 0.44 and 0.50; P < 0.001), and demonstrated that the RTL was strongly correlated with tumor recurrence. Importantly, TERT promoter mutations or long RTL caused a significantly poorer survival than TERT wild-type or short RTL. Coexisting TERT promoter mutations and long RTL were more commonly associated with poor patient survival than they were individually. Notably, the patients with TERT promoter mutations particularly C228T or long RTL were resistant to radiotherapy. Collectively, TERT promoter mutations and long RTL are not only prognostic factors for poor clinical outcomes, but also the predictors of radiotherapy resistance in gliomas.

Keyword :

TERT promoter mutations poor survival radiotherapy resistance glioma relative telomere length

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GB/T 7714 Gao, Ke , Li, Gang , Qu, Yiping et al. TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas [J]. | ONCOTARGET , 2016 , 7 (8) : 8712-8725 .
MLA Gao, Ke et al. "TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas" . | ONCOTARGET 7 . 8 (2016) : 8712-8725 .
APA Gao, Ke , Li, Gang , Qu, Yiping , Wang, Maode , Cui, Bo , Ji, Meiju et al. TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas . | ONCOTARGET , 2016 , 7 (8) , 8712-8725 .
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Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study SCIE PubMed Scopus
期刊论文 | 2016 , 46 (6) , 542-547 | XENOBIOTICA | IF: 1.932
WoS CC Cited Count: 1
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Abstract :

1. CYP1A2 is a highly polymorphic gene and CYP1A2 enzyme results in broad inter-individual variability in response to certain pharmacotherapies, while little is known about the genetic variation of CYP1A2 in Uyghur Chinese population. The aim of the present study was to screen Uyghur volunteers for CYP1A2 genetic polymorphisms. 2. We used DNA sequencing to investigate promoter, exons, introns, and 3' UTR of the CYP1A2 gene in 96 unrelated healthy Uyghur individuals. We also used SIFT (Sorting Intolerant From Tolerant) and PolyPhen-2 (Polymorphism Phenotyping v2) to predict the protein function of the novel non-synonymous mutation in CYP1A2 coding regions. 3. We identified 20 different CYP1A2 polymorphisms in the Uyghur Chinese population, including two novel variants (119A > G and 2410G > A). Variant 119A > G was predicted to be probably damaging on protein function by PolyPhen-2, by contrast, 2410G > A was identified as benign. The allele frequencies of CYP1A2*1A, *1B, *1F, *1G, *1J, *1M, *4, and *9 were 23.4%, 53.1%, 3.7%, 2.6%, 2.6%, 13.5%, 0.5%, and 0.5%, respectively. The frequency of *1F, a putative high inducibility allele, was higher in our sample population compared with that in the Caucasian population (p < 0.05). The most common genotype combinations were *1A/*1B (46.9%) and *1B/*1M (27.1%). 4. Our results provide basic information on CYP1A2 polymorphisms in Uyghur individuals and suggest that the enzymatic activities of CYP1A2 may differ among the diverse ethnic populations of the world.

Keyword :

CYP1A2 Uyghur populations ethnic groups genetic polymorphism

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GB/T 7714 Geng, Tingting , Zhang, Xi Yang , Wang, Li et al. Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study [J]. | XENOBIOTICA , 2016 , 46 (6) : 542-547 .
MLA Geng, Tingting et al. "Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study" . | XENOBIOTICA 46 . 6 (2016) : 542-547 .
APA Geng, Tingting , Zhang, Xi Yang , Wang, Li , Wang, Huijuan , Shi, Xugang , Kang, Longli et al. Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study . | XENOBIOTICA , 2016 , 46 (6) , 542-547 .
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Hypermethylation in gastric cancer SCIE PubMed Scopus
期刊论文 | 2015 , 448 , 124-132 | CLINICA CHIMICA ACTA | IF: 2.799
WoS CC Cited Count: 10
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Abstract :

Although gastric cancer (GC) is highly prevalent in China and is a leading cause of cancer-related death, major advances in early diagnostic and effective therapeutic strategies have not been made. GC patients are usually diagnosed at an advanced stage and the prognosis is still poor. Over the years, many efforts have been done on exploring the pathology of GC. In particular, genome-wide analysis tools have been widely used in the detection of genetic and epigenetic alterations in GC. For example, many tumor suppressor genes have been found to be aberrantly hypermethylated in GCs, and some even in gastric precancerous lesions, suggesting a role of this molecular event in early gastric tumorigenesis. In addition, accumulating evidences have demonstrated that some hypermethylated genes can be used as potential biomarkers for detection and diagnosis of GC in biopsy specimens and non-invasive body fluids. These exciting advances provide unprecedented opportunities for the development of molecular-based novel diagnostic, prognostic, and therapeutic strategies for GC. Here, we reviewed recent findings on the promoter hypermethylation of tumor suppressor genes in GC and aimed to provide better understanding of the contribution of this epigenetic event to gastric tumorigenesis. (C) 2015 Elsevier B.V. All rights reserved.

Keyword :

Clinical utility Gastric cancer Epigenetics Biomarkers Gene methylation

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GB/T 7714 Li, Yujun , Liang, Junrong , Hou, Peng . Hypermethylation in gastric cancer [J]. | CLINICA CHIMICA ACTA , 2015 , 448 : 124-132 .
MLA Li, Yujun et al. "Hypermethylation in gastric cancer" . | CLINICA CHIMICA ACTA 448 (2015) : 124-132 .
APA Li, Yujun , Liang, Junrong , Hou, Peng . Hypermethylation in gastric cancer . | CLINICA CHIMICA ACTA , 2015 , 448 , 124-132 .
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Frequent amplification of PTP1B is associated with poor survival of gastric cancer patients SCIE PubMed
期刊论文 | 2015 , 14 (5) , 732-743 | CELL CYCLE | IF: 3.952
WoS CC Cited Count: 5
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The protein tyrosine phosphatase 1B (PTP1B), a non-transmembrane protein tyrosine phosphatase, has been implicated in gastric pathogenesis. Several lines of recent evidences have shown that PTP1B is highly amplified in breast and prostate cancers. The aim of this study was to investigate PTP1B amplification in gastric cancer and its association with poor prognosis of gastric cancer patients, and further determine the role of PTP1B in gastric tumorigenesis. Our data demonstrated that PTP1B was significantly up-regulated in gastric cancer tissues as compared with matched normal gastric tissues by using quantitative RT-PCR (qRT-PCR) assay. In addition, copy number analysis showed that PTP1B was amplified in 68/131 (51.9%) gastric cancer cases, whereas no amplification was found in the control subjects. Notably, PTP1B amplification was positively associated with its protein expression, and was significantly related to poor survival of gastric cancer patients. Knocking down PTP1B expression in gastric cancer cells significantly inhibited cell proliferation, colony formation, migration and invasion, and induced cell cycle arrested and apoptosis. Mechanically, PTP1B promotes gastric cancer cell proliferation, survival and invasiveness through modulating Src-related signaling pathways, such as Src/Ras/MAPK and Src/phosphatidylinositol-3-kinase (PI3K)/Akt pathways. Collectively, our data demonstrated frequent overexpression and amplification PTP1B in gastric cancer, and further determined the oncogenic role of PTP1B in gastric carcinogenesis. Importantly, PTP1B amplification predicts poor survival of gastric cancer patients.

Keyword :

PTP1B Gastric cancer poor prognosis signaling pathways genomic amplification

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GB/T 7714 Wang, Na , She, Junjun , Liu, Wei et al. Frequent amplification of PTP1B is associated with poor survival of gastric cancer patients [J]. | CELL CYCLE , 2015 , 14 (5) : 732-743 .
MLA Wang, Na et al. "Frequent amplification of PTP1B is associated with poor survival of gastric cancer patients" . | CELL CYCLE 14 . 5 (2015) : 732-743 .
APA Wang, Na , She, Junjun , Liu, Wei , Shi, Jing , Yang, Qi , Shi, Bingyin et al. Frequent amplification of PTP1B is associated with poor survival of gastric cancer patients . | CELL CYCLE , 2015 , 14 (5) , 732-743 .
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A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter EI SCIE
期刊论文 | 2015 , 11 (6) , 1016-1026 | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY | IF: 3.929
WoS CC Cited Count: 1
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5-Methylcytosine (5mC) can be converted to 5-hydroxymethylcytosine (5hmC) in mammalian DNA by the ten-eleven translocation (TET) enzymes. Traditional bisulfite-based DNA methylation analysis techniques have been widely used in the detection of 5mC. However, they can not discriminate 5hmC from 5mC, leading to overestimate 5mC levels. We here introduce a strategy, combination of selective oxidation and bisulfite pyrosequencing (BS-Pyroseq), for quantification of both 5mC and 5hmC at CpG sites within the promoters of CDH1, DAPK, RAR ss and RUNX3 genes in a panel of cell lines and clinical samples. As expected, oxidative bisulfite pyrosequencing (oxBS-Pyroseq) assay decreased overall or site-specific methylation levels of three of these genes in most cell lines as compared with BS-Pyroseq assay. Similarly, decreased overall or site-specific methylation levels of DAPK, RAR ss and RUNX3 genes in laryngeal, gastric and thyroid cancer and their matched normal tissues, respectively, were also found by a comparison between these two techniques, particularly in cancerous tissues. In addition, by using this combined strategy and hydroxymethylcytosine DNA immunoprecipitation (hMeDIP) assay, we demonstrated that TET1 up-regulated DAPK expression through promoter demethylation. Collectively, this strategy is easy to establish and accurately discriminates and quantifies 5mC and 5hmC at CpG sites within selected gene promoters.

Keyword :

5-Methylcytosine (5mC) Gene Promoter Bisulfite Pyrosequencing Selective Oxidation 5-Hydroxymethylcytosine (5hmC)

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GB/T 7714 Qu, Yiping , Yang, Qi , Sui, Fang et al. A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter [J]. | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY , 2015 , 11 (6) : 1016-1026 .
MLA Qu, Yiping et al. "A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter" . | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY 11 . 6 (2015) : 1016-1026 .
APA Qu, Yiping , Yang, Qi , Sui, Fang , Lu, Rong , Dang, Siwen , Ji, Meiju et al. A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter . | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY , 2015 , 11 (6) , 1016-1026 .
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Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway SCIE PubMed
期刊论文 | 2015 , 6 (28) , 25917-25931 | ONCOTARGET | IF: 5.008
WoS CC Cited Count: 26
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Abstract :

Sulforaphane (SFN), a natural compound derived from broccoli/broccoli sprouts, has been demonstrated to be used as an antitumor agent in different types of cancers. However, its antitumor effect in thyroid cancer remains largely unknown. The aim of the study was to investigate the therapeutic potential of SFN for thyroid cancer and explore the mechanisms underlying antitumor effects of SFN by in vitro and in vivo studies. Our data demonstrated that SFN significantly inhibited thyroid cancer cell proliferation in a dose-and time-dependent manner, induced G2/M phase cell cycle arrest and apoptosis, and inhibited thyroid cancer cell migration and invasion by suppressing epithelial-mesenchymal transition (EMT) process and expression of Slug, Twist, MMP-2 and -9. Mechanically, SFN inhibited thyroid cancer cell growth and invasiveness through repressing phosphorylation of Akt, enhancing p21 expression by the activation of Erk and p38 signaling cascades, and promoting mitochondrial-mediated apoptosis via reactive oxygen species (ROS)-dependent pathway. Growth of xenograft tumors derived from thyroid cancer cell line FTC133 in nude mice was also significantly inhibited by SFN. Importantly, we did not find significant effect of SFN on body weight and liver function of mice. Collectively, we for the first time demonstrate that SFN is a potentially effective antitumor agent for thyroid cancer.

Keyword :

signaling pathways reactive oxygen species (ROS) sulforaphane (SFN) thyroid cancer

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GB/T 7714 Wang, Liping , Tian, Zhufang , Yang, Qi et al. Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway [J]. | ONCOTARGET , 2015 , 6 (28) : 25917-25931 .
MLA Wang, Liping et al. "Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway" . | ONCOTARGET 6 . 28 (2015) : 25917-25931 .
APA Wang, Liping , Tian, Zhufang , Yang, Qi , Li, Heng , Guan, Haixia , Shi, Bingyin et al. Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway . | ONCOTARGET , 2015 , 6 (28) , 25917-25931 .
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Frequent amplification of AIB1, a critical oncogene modulating major signaling pathways, is associated with poor survival in gastric cancer SCIE
期刊论文 | 2015 , 6 (16) , 14344-14359 | ONCOTARGET | IF: 5.008
WoS CC Cited Count: 10
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Amplified in breast cancer 1 (AIB1) is a member of p160 steroid receptor coactivator (SRC) family that mediates the transcriptional activities of nuclear receptors and other transcription factors. It acts as a major oncogene in diverse cancers, whereas biological function of AIB1 in gastric cancer remains largely unclear. This study was designed to explore the role of AIB1 in gastric tumorigenesis and its potential as a useful prognostic marker and therapeutic target in this cancer. Our data demonstrated that AIB1 was significantly up-regulated in gastric cancer tissues as compared with control subjects. Moreover, AIB1 amplification was found in 47 of 133 (35.3%) gastric cancer cases, but not in control subjects. AIB1 amplification was positively associated with its protein expression, and was significantly correlated with poor patient survival. AIB1 knockdown in gastric cancer cells dramatically inhibited cell proliferation, invasiveness and tumorigenic potential in nude mice, and induced cell cycle arrest and apoptosis. Mechanically, AIB1 promotes gastric cancer cell proliferation, survival and invasiveness through modulating major signaling pathways such as ErbB and Wnt/beta-catenin pathways. Collectively, these findings suggest that AIB1 plays an important role in the pathogenesis of gastric cancer and represents a potential prognostic marker and therapeutic target for this cancer.

Keyword :

gastric cancer poor prognosis signaling pathways genomic amplification AIB1

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GB/T 7714 Shi, Jing , Liu, Wei , Sui, Fang et al. Frequent amplification of AIB1, a critical oncogene modulating major signaling pathways, is associated with poor survival in gastric cancer [J]. | ONCOTARGET , 2015 , 6 (16) : 14344-14359 .
MLA Shi, Jing et al. "Frequent amplification of AIB1, a critical oncogene modulating major signaling pathways, is associated with poor survival in gastric cancer" . | ONCOTARGET 6 . 16 (2015) : 14344-14359 .
APA Shi, Jing , Liu, Wei , Sui, Fang , Lu, Rong , He, Qingyuan , Yang, Qi et al. Frequent amplification of AIB1, a critical oncogene modulating major signaling pathways, is associated with poor survival in gastric cancer . | ONCOTARGET , 2015 , 6 (16) , 14344-14359 .
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Epithelial cell-derived periostin functions as a tumor suppressor in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14ARF/Mdm2 signaling pathway SCIE PubMed
期刊论文 | 2014 , 13 (18) , 2962-2974 | CELL CYCLE | IF: 4.565
WoS CC Cited Count: 17
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Periostin is usually considered as an oncogene in diverse human cancers, including breast, prostate, colon, esophagus, and pancreas cancers, whereas it acts as a tumor suppressor in bladder cancer. In gastric cancer, it has been demonstrated that periglandular periostin expression is decreased whereas stromal periostin expression is significantly increased as compared with normal gastric tissues. Moreover, periostin produced by stromal myofibroblasts markedly promotes gastric cancer cell growth. These observations suggest that periostin derived from different types of cells may play distinct biological roles in gastric tumorigenesis. The aim of this study was to explore the biological functions and related molecular mechanisms of epithelial cell-derived periostin in gastric cancer. Our data showed that periglandular periostin was significantly down-regulated in gastric cancer tissues as compared with matched normal gastric mucosa. In addition, its expression in metastatic lymph nodes was significantly lower than that in their primary cancer tissues. Our data also demonstrated that periglandular periostin expression was negatively associated with tumor stage. More importantly, restoration of periostin expression in gastric cancer cells dramatically suppressed cell growth and invasiveness. Elucidation of the mechanisms involved revealed that periostin restoration enhanced Rb phosphorylation and sequentially activated the transcription of E2F1 target gene p14(ARF), leading to Mdm2 inactivation and the stabilization of p53 and E-cadherin proteins. Strikingly, these effects of periostin were abolished upon Rb deletion. Collectively, we have for the first time demonstrated that epithelial cell-derived periostin exerts tumor-suppressor activities in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14(ARF)/Mdm2 signaling pathway.

Keyword :

E2F1 pathway E-cadherin Gastric cancer Rb Mdm2 periostin p53

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GB/T 7714 Lv, Hongjun , Liu, Rui , Fu, Jiao et al. Epithelial cell-derived periostin functions as a tumor suppressor in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14ARF/Mdm2 signaling pathway [J]. | CELL CYCLE , 2014 , 13 (18) : 2962-2974 .
MLA Lv, Hongjun et al. "Epithelial cell-derived periostin functions as a tumor suppressor in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14ARF/Mdm2 signaling pathway" . | CELL CYCLE 13 . 18 (2014) : 2962-2974 .
APA Lv, Hongjun , Liu, Rui , Fu, Jiao , Yang, Qi , Shi, Jing , Chen, Pu et al. Epithelial cell-derived periostin functions as a tumor suppressor in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14ARF/Mdm2 signaling pathway . | CELL CYCLE , 2014 , 13 (18) , 2962-2974 .
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