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学科主题临床医学
Psoriasin overexpression confers drug resistance to cisplatin by activating ERK in gastric cancer
Li, Liting1,2; Cui, Yuxin2; Ye, Lin2; Zhao, Zehang2; Jiang, Wen G.2; Ji, Jiafu1
通讯作者Jiang, Wen G.(2) ; Ji, Jiafu(1)
关键词psoriasin gastric cancer extracellular signal-regulated kinase cisplatin
刊名INTERNATIONAL JOURNAL OF ONCOLOGY
2018-09-01
DOI10.3892/ijo.2018.4455
53期:3页:1171-1182
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]EPITHELIAL-MESENCHYMAL TRANSITION ; SQUAMOUS-CELL CARCINOMA ; BREAST-CANCER ; RAF/MEK/ERK PATHWAY ; IN-VITRO ; S100A7 ; GROWTH ; EXPRESSION ; CHEMOTHERAPY ; THERAPY
英文摘要

Psoriasin, a member of the S100 multigenic family, which is aberrantly expressed in a variety of human tumors, is considered as an attractive molecular target for cancer treatment. The present study aimed to characterize the role of psoriasin in gastric cancer (GC), the associated pathways through which it contributes to cancer development and progression, and the effect of psoriasin on cellular response to pre-operative chemotherapy in patients with GC. Expression of psoriasin mRNA and protein were analyzed using quantitative polymerase chain reaction and immunohistochemistry of gastric cancer cohorts, respectively. Gastric cancer cell models with differential expression of psoriasin were generated using stable cell lines that overexpressed psoriasin. The in vitro biological functions of the cells in response to psoriasin overexpression and to chemotherapeutic agents were assessed using various cell-based assays. Psoriasin was overexpressed in patients with advanced GC, and high psoriasin levels led to poor clinical outcomes. Increasing psoriasin expression in GC cell lines promoted cell proliferation, migration and invasion in vitro. Furthermore, psoriasin overexpression caused alterations in the levels of epithelial-mesenchymal transition-associated proteins, and activated the extracellular signal-regulated kinase signaling pathway. Additionally, higher levels of psoriasin expression were significantly associated a lack of response to neoadjuvant chemotherapy in patients with GC. Psoriasin overexpression tended to decrease the sensitivity of GC cells to cisplatin, potentially by inhibiting apoptosis or increasing the S-phase population. Taken together, these results indicate that psoriasin may be a promising therapeutic target for GC treatment, and a potential molecular marker to predict patient response to pre-operative chemotherapy.

语种英语
WOS记录号WOS:000440583100021
通讯作者邮箱jiangw@cf.ac.uk ; jijiafu@hsc.pku.edu.cn
第一作者单位Peking Univ, Canc Hosp & Inst, Dept Gastrointestinal Surg, Key Lab Carcinogenesis & Translat Res, 52 Fucheng Rd, Beijing 100142, Peoples R China ; Cardiff Univ, Sch Med, Cardiff China Med Res Collaborat, Henry Wellcome Bldg,Heath Pk, Cardiff CF14 4XN, S Glam, Wales
通讯作者单位Peking Univ, Canc Hosp & Inst, Dept Gastrointestinal Surg, Key Lab Carcinogenesis & Translat Res, 52 Fucheng Rd, Beijing 100142, Peoples R China ; Cardiff Univ, Sch Med, Cardiff China Med Res Collaborat, Henry Wellcome Bldg,Heath Pk, Cardiff CF14 4XN, S Glam, Wales
ISSN1019-6439
引用统计
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/142605
专题北京大学临床肿瘤学院_胃肠肿瘤中心
北京大学临床肿瘤学院_胃肠肿瘤中心一病区
作者单位1.Peking Univ, Canc Hosp & Inst, Dept Gastrointestinal Surg, Key Lab Carcinogenesis & Translat Res, 52 Fucheng Rd, Beijing 100142, Peoples R China;
2.Cardiff Univ, Sch Med, Cardiff China Med Res Collaborat, Henry Wellcome Bldg,Heath Pk, Cardiff CF14 4XN, S Glam, Wales
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Li, Liting,Cui, Yuxin,Ye, Lin,et al. Psoriasin overexpression confers drug resistance to cisplatin by activating ERK in gastric cancer[J]. INTERNATIONAL JOURNAL OF ONCOLOGY,2018,53(3):1171-1182.
APA Li, Liting,Cui, Yuxin,Ye, Lin,Zhao, Zehang,Jiang, Wen G.,&Ji, Jiafu.(2018).Psoriasin overexpression confers drug resistance to cisplatin by activating ERK in gastric cancer.INTERNATIONAL JOURNAL OF ONCOLOGY,53(3),1171-1182.
MLA Li, Liting,et al."Psoriasin overexpression confers drug resistance to cisplatin by activating ERK in gastric cancer".INTERNATIONAL JOURNAL OF ONCOLOGY 53.3(2018):1171-1182.
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