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Pancreatic Neoplasms: HELP
Articles by Z. Tian
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Z. Tian wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article ILC3 cells promote the proliferation and invasion of pancreatic cancer cells through IL-22/AKT signaling. 2019

Xuan, X / Zhou, J / Tian, Z / Lin, Y / Song, J / Ruan, Z / Ni, B / Zhao, H / Yang, W. ·Department of Pathophysiology, College of High Altitude Military Medicine, Third Military Medical University, Chongqing, 400038, China. · Department of Kidney, Southwest Hospital, Army Medical University (Third Military Medical University), 30 Gaotanyan Street, District Shapingba, Chongqing, 400038, China. · Institute of Immunology, PLA, Third Military Medical University, Chongqing, 400038, China. · Bellevue Christian High School, 1601 98th Ave NE, Bellevue, WA, 98004, USA. · Department of Microbial Pathogenesis and Immunology, Texas A&M University Health Science Center, College Station, TX, 77843, USA. · Department of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China. · Department of Pathophysiology, College of High Altitude Military Medicine, Third Military Medical University, Chongqing, 400038, China. 15991833423@163.com. · Department of Kidney, Southwest Hospital, Army Medical University (Third Military Medical University), 30 Gaotanyan Street, District Shapingba, Chongqing, 400038, China. zhaohw212@126.com. · Department of Dermatology, The 181th Hospital of PLA, No. 1 Xinqiaoyuan Road, Guilin, 541002, Guangxi Zhuang Autonomous Region, China. 1512638974@qq.com. ·Clin Transl Oncol · Pubmed #31203574.

ABSTRACT: PURPOSE: Type 3 innate lymphocytes (ILC3s) are reported to be involved in lung cancer, possibly by producing interleukin-22 (IL-22). However, whether ILC3s and their secreted IL-22 molecules contribute to the pathogenesis of pancreatic cancer (PC) remains unclear. To this end, in this study, we investigated the effects and possible mechanisms of ILC3s on PC pathogenesis. METHOD: The IL-22 and IL-2i2R levels and the ILC3s' frequency in cancer tissues from PC patients and in peripheral blood from PC patients and healthy controls were analyzed by flow cytometry, immunochemistry, or immunofluorescence. The effects of IL-22-induced AKT signaling on the proliferation, invasion, and migration of PC cells were examined by co-culturing PC cell lines with ILC3s isolated from PC tissues, with or without the addition of neutralizing IL-22 antibody, IL-22R antibody or AKT inhibitor. RESULTS: Our results showed that IL-22 and ILC3s were significantly upregulated in the PBMCs and cancer tissues of PC patients, and the IL-22R level was increased in PC cells. The increased frequency of ILC3s was positively correlated with the clinical features of PC patients. Co-culture experiments indicated that ILC3s promoted the proliferation, invasion, and migration of PC cell lines by secreting IL-22 to activate AKT signaling because IL-22/IL-22R or AKT blockage markedly counteracted such effects on PC cells. CONCLUSION: Our data demonstrated that ILC3s may promote PC pathogenesis through IL-22/IL-22R-AKT signaling, suggesting a potential intervention target for PC treatment in the future.

2 Article Downregulated miR-506 expression facilitates pancreatic cancer progression and chemoresistance via SPHK1/Akt/NF-κB signaling. 2016

Li, J / Wu, H / Li, W / Yin, L / Guo, S / Xu, X / Ouyang, Y / Zhao, Z / Liu, S / Tian, Y / Tian, Z / Ju, J / Ni, B / Wang, H. ·Institute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China. · Department of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · Department of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China. · Institute of Immunology PLA, Third Military Medical University, Chongqing, China. · Translational Research Laboratory, Department of Pathology, Stony Brook University, Stony Brook, NY, USA. · Department of Pathophysiology and High Altitude Pathology, Third Military Medical University, Chongqing, China. ·Oncogene · Pubmed #27065335.

ABSTRACT: The aberrant expression of microRNAs (miRNAs) has emerged as an important hallmark of cancer. However, the molecular mechanisms underlying the changes in miRNA expression remain unclear. In this study, we discovered a novel epigenetic mechanism of miR-506 regulation and investigated its functional significance in pancreatic cancer. Sequencing analysis revealed that the miR-506 promoter is highly methylated in pancreatic cancer tissues compared with non-cancerous tissues. Reduced miR-506 expression was significantly associated with clinical stage, pathologic tumor status, distant metastasis and decreased survival of pancreatic cancer patients. miR-506 inhibited cell proliferation, induced cell cycle arrest at the G1/S transition and enhanced apoptosis and chemosensitivity of pancreatic cancer cells. Furthermore, we identified sphingosine kinase 1 (SPHK1) as a novel target of miR-506, the expression of which inhibited the SPHK1/Akt/NF-κB signaling pathway, which is activated in pancreatic cancer. High SPHK1 expression was significantly associated with poor survival in a large cohort of pancreatic cancer specimens. Our data suggest that miR-506 acts as a tumor suppressor miRNA and is epigenetically silenced in pancreatic cancer. The newly identified miR-506/SPHK1 axis represents a novel therapeutic strategy for future pancreatic cancer treatment.

3 Retraction MicroRNA-215 functions as a tumor suppressor and directly targets ZEB2 in human pancreatic cancer. 2015

Li, Q W / Zhou, T / Wang, F / Jiang, M / Liu, C B / Zhang, K R / Zhou, Q / Tian, Z / Hu, K W. ·Department of Oncology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China. ·Genet Mol Res · Pubmed #26662405.

ABSTRACT: It has been shown that microRNA-215 (miR-215) is dysregulated in several human malignancies, and this correlates with tumor progression. However, its expression and function in pancreatic cancer is still unclear. The aim of this study was to explore the effects of miR-215 on pancreatic cancer formation and progression. Using quantitative RT-PCR, we detected miR-215 expression in pancreatic cancer cell lines and primary tumor tissues. The association of miR-215 expression with clinicopathological factors and prognosis was also analyzed. We then observed the effects of miR-215 on the biological behavior of pancreatic cancer cells. Lastly, the potential regulatory function of miR-215 on ZEB2 expression was investigated. miR-215 expression levels were significantly downregulated in pancreatic cancer samples and cell lines. Decreased miR-215 expression was significantly associated with large tumor size, advanced TNM stage, lymph node metastasis, vessel invasion, and lower overall survival. Multivariate regression analysis corroborated that downregulation of miR-215 was an independent unfavorable prognostic factor. Overexpression of miR-215 inhibited pancreatic cancer cell proliferation, invasion, and migration; promoted cell apoptosis in vitro; and suppressed tumorigenicity in vivo. Further, ZEB2 was confirmed as a direct target of miR-215 by using a luciferase reporter assay. These findings indicate that miR-215 may act as a tumor suppressor in pancreatic cancer cells, and could serve as a novel therapeutic target for miR-based therapy.