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Article ; Online: "

Chen, Xiang / Du, Yi-Chieh Nancy

Annals of pancreatic cancer

2022 Volume 5

Language	English
Publishing date	2022-07-10
Publishing country	China
Document type	Journal Article ; Comment
ISSN	2616-2741
ISSN (online)	2616-2741
DOI	10.21037/apc-2022-1
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Article ; Online: Orthotopic Pancreatic Tumor Mouse Models of Liver Metastasis.

Zhang, George / Du, Yi-Chieh Nancy

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1882, Page(s) 309–320

Abstract: The survival from pancreatic cancer is poor because most patients are diagnosed after the cancer has metastasized. Liver is the most common site of pancreatic cancer metastasis. Orthotopic mouse models of liver metastasis by intrasplenically injecting ... ...

Abstract	The survival from pancreatic cancer is poor because most patients are diagnosed after the cancer has metastasized. Liver is the most common site of pancreatic cancer metastasis. Orthotopic mouse models of liver metastasis by intrasplenically injecting the pancreatic tumor cells are useful in studying the molecular mechanisms of metastasis and evaluating therapeutic regimens.
MeSH term(s)	Animals ; Cell Culture Techniques/instrumentation ; Cell Culture Techniques/methods ; Cell Line, Tumor ; Culture Media, Conditioned ; Humans ; Liver/pathology ; Liver Neoplasms/pathology ; Liver Neoplasms/secondary ; Mice ; Mice, Inbred NOD ; Pancreatic Neoplasms/pathology ; Xenograft Model Antitumor Assays/instrumentation ; Xenograft Model Antitumor Assays/methods
Chemical Substances	Culture Media, Conditioned
Language	English
Publishing date	2018-10-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8879-2_27
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Article ; Online: Immunohistochemical analysis of RHAMM expression in normal and neoplastic human tissues: a cell cycle protein with distinctive expression in mitotic cells and testicular germ cells.

Chen, Yao-Tseng / Chen, Zhengming / Du, Yi-Chieh Nancy

Oncotarget

2018 Volume 9, Issue 30, Page(s) 20941–20952

Abstract: Expression of Receptor for Hyaluronic Acid Mediated Motility (RHAMM) increases cellular motility and RHAMM overexpression promotes invasive phenotype and metastasis of cancer cells. RHAMM has been suggested as a biomarker for poor prognosis in several ... ...

Abstract	Expression of Receptor for Hyaluronic Acid Mediated Motility (RHAMM) increases cellular motility and RHAMM overexpression promotes invasive phenotype and metastasis of cancer cells. RHAMM has been suggested as a biomarker for poor prognosis in several tumor types, including lung, breast, colorectal, gastric, pancreatic ductal, and ovarian cancers. RNA studies showed restricted RHAMM expression in normal tissues, but its protein expression data in tissues were limited. In light of its potential as a prognostic marker and a therapeutic target, we performed immunohistochemical analysis to systematically characterize
Language	English
Publishing date	2018-04-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.24939
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Article: Identification and characterization of metastatic factors by gene transfer into the novel RIP-Tag; RIP-tva murine model

Zhang, George / Chi, Yudan / Du, Yi-Chieh Nancy

Journal of visualized experiments. 2017 Oct. 16, , no. 128

2017

Abstract: Metastatic cancer accounts for 90% of deaths in patients with solid tumors. There is an urgent need to better understand the drivers of cancer metastasis and to identify novel therapeutic targets. To investigate molecular events that drive the ... ...

Abstract	Metastatic cancer accounts for 90% of deaths in patients with solid tumors. There is an urgent need to better understand the drivers of cancer metastasis and to identify novel therapeutic targets. To investigate molecular events that drive the progression from primary cancer to metastasis, we have developed a bitransgenic mouse model, RIP-Tag; RIP-tva. In this mouse model, the rat insulin promoter (RIP) drives the expression of the SV40 T antigen (Tag) and the receptor for subgroup A avian leukosis virus (tva) in pancreatic β cells. The mice develop pancreatic neuroendocrine tumors with 100% penetrance through well-defined stages that are similar to human tumorigenesis, with stages including hyperplasia, angiogenesis, adenoma, and invasive carcinoma. Because RIP-Tag; RIP-tva mice do not develop metastatic disease, genetic alterations that promote metastasis can be identified easily. Somatic gene transfer into tva-expressing, proliferating pancreatic β premalignant lesions is achieved through intracardiac injection of avian retroviruses harboring the desired genetic alteration. A titer of >1 x 108 infectious units per ml is considered appropriate for in vivo infection. In addition, avian retroviruses can infect cell lines derived from tumors in RIP-Tag; RIP-tva mice with high efficiency. The cell lines can also be used to characterize the metastatic factors. Here we demonstrate how to utilize this mouse model and cell lines to assess the functions of candidate genes in tumor metastasis.
Keywords	Avian leukosis virus ; adenoma ; angiogenesis ; animal models ; antigens ; carcinogenesis ; carcinoma ; cell lines ; gene transfer ; genes ; humans ; hyperplasia ; insulin ; islets of Langerhans ; metastasis ; mice ; patients ; penetrance ; rats ; therapeutics
Language	English
Dates of publication	2017-1016
Size	p. e55890.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/55890
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model.

Zhang, George / Chi, Yudan / Du, Yi-Chieh Nancy

Journal of visualized experiments : JoVE

2017 , Issue 128

Abstract	Metastatic cancer accounts for 90% of deaths in patients with solid tumors. There is an urgent need to better understand the drivers of cancer metastasis and to identify novel therapeutic targets. To investigate molecular events that drive the progression from primary cancer to metastasis, we have developed a bitransgenic mouse model, RIP-Tag; RIP-tva. In this mouse model, the rat insulin promoter (RIP) drives the expression of the SV40 T antigen (Tag) and the receptor for subgroup A avian leukosis virus (tva) in pancreatic β cells. The mice develop pancreatic neuroendocrine tumors with 100% penetrance through well-defined stages that are similar to human tumorigenesis, with stages including hyperplasia, angiogenesis, adenoma, and invasive carcinoma. Because RIP-Tag; RIP-tva mice do not develop metastatic disease, genetic alterations that promote metastasis can be identified easily. Somatic gene transfer into tva-expressing, proliferating pancreatic β premalignant lesions is achieved through intracardiac injection of avian retroviruses harboring the desired genetic alteration. A titer of >1 x 10
MeSH term(s)	Animals ; Antigens, Polyomavirus Transforming/biosynthesis ; Antigens, Polyomavirus Transforming/genetics ; Avian Leukosis Virus/genetics ; Disease Models, Animal ; Gene Transfer Techniques ; Genetic Vectors/genetics ; Insulin/genetics ; Insulin-Secreting Cells/pathology ; Insulin-Secreting Cells/virology ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/pathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/virology ; Precancerous Conditions/genetics ; Precancerous Conditions/pathology ; Promoter Regions, Genetic
Chemical Substances	Antigens, Polyomavirus Transforming ; Insulin
Language	English
Publishing date	2017-10-16
Publishing country	United States
Document type	Journal Article ; Video-Audio Media ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/55890
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Article: Bcl-xL is translocated to the nucleus via CtBP2 to epigenetically promote metastasis.

Zhang, Tiantian / Li, Sha / Tan, Yingcai Adrian / Na, Joseph HyungJoon / Chen, Zhengming / Damle, Priyadarshan / Chen, Xiang / Choi, Soyoung / Mishra, Bikash / Wang, Dunrui / Grossman, Steven R / Jiang, Xuejun / Li, Yi / Chen, Yao-Tseng / Xiang, Jenny Z / Du, Yi-Chieh Nancy

bioRxiv : the preprint server for biology

2023

Abstract: Besides its mitochondria-based anti-apoptotic role, Bcl-xL also travels to the nucleus to promote cancer metastasis by upregulating global histone H3 trimethyl Lys4 (H3K4me3) and TGFβ transcription. How Bcl-xL is translocated into the nucleus and how ... ...

Abstract	Besides its mitochondria-based anti-apoptotic role, Bcl-xL also travels to the nucleus to promote cancer metastasis by upregulating global histone H3 trimethyl Lys4 (H3K4me3) and TGFβ transcription. How Bcl-xL is translocated into the nucleus and how nuclear Bcl-xL regulates H3K4me3 modification are not understood. Here, we report that C-terminal Binding Protein 2 (CtBP2) binds Bcl-xL via its N-terminus and translocates Bcl-xL into the nucleus. Knockdown of CtBP2 by shRNA decreases the nuclear portion of Bcl-xL and reverses Bcl-xL-induced cell migration and metastasis in mouse models. Furthermore, knockout of CtBP2 suppresses Bcl-xL transcription. The binding between Bcl-xL and CtBP2 is required for their interaction with MLL1, a histone H3K4 methyltransferase. Pharmacologic inhibition of MLL1 enzymatic activity reverses Bcl-xL-induced H3K4me3 and TGFβ mRNA upregulation as well as cell invasion. Moreover, cleavage under targets and release using nuclease (CUT&RUN) coupled with next generation sequencing reveals that H3K4me3 modifications are particularly enriched in the promotor region of genes encoding TGFβ and its signaling pathway in the cancer cells overexpressing Bcl-xL. Altogether, the metastatic function of Bcl-xL is mediated by its interaction with CtBP2 and MLL1.
Language	English
Publishing date	2023-04-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.26.538373
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Article ; Online: Expression of the Receptor for Hyaluronic Acid-Mediated Motility (RHAMM) in Endometrial Cancer is Associated With Adverse Histologic Parameters and Tumor Progression.

Schatz-Siemers, Nina / Chen, Yao-Tseng / Chen, Zhengming / Wang, Dunrui / Ellenson, Lora H / Du, Yi-Chieh Nancy

Applied immunohistochemistry & molecular morphology : AIMM

2020 Volume 28, Issue 6, Page(s) 453–459

Abstract: Endometrial cancer is one of the most common gynecologic malignancies worldwide. Only 2 agents have been approved by Food and Drug Administration for endometrial cancer since 1971. There is a need to identify molecular targets to treat advanced ... ...

Abstract	Endometrial cancer is one of the most common gynecologic malignancies worldwide. Only 2 agents have been approved by Food and Drug Administration for endometrial cancer since 1971. There is a need to identify molecular targets to treat advanced endometrial cancer. The receptor for hyaluronic acid-mediated motility (RHAMM) is upregulated in various types of cancer. Here, we aimed to determine the clinical significance of RHAMM expression in endometrial cancer. Two hundred twenty-five cases of endometrial cancer, including serous and endometrioid types, and 8 cases of normal endometrium were used for studying RHAMM protein levels. The Cancer Genome Atlas database was also queried for RHAMM mRNA expression in endometrial cancer. Increased expression of RHAMM protein was seen in endometrial cancer compared with no or weak expression in normal endometrium. RHAMM expression positively correlated with tumor grade. RHAMM expression was significantly increased in endometrial serous carcinomas, which are high-grade, aggressive types of endometrial cancer, compared with the relatively less aggressive endometrioid carcinomas. RHAMM expression also correlated with the presence of lymphovascular invasion. RHAMM mRNA expression correlated with decreased survival in The Cancer Genome Atlas cohort. Therefore, increased RHAMM expression in endometrial cancer is associated with high-grade tumors and is indicative of more aggressive behavior. These findings suggest RHAMM as a prognostic factor in endometrial cancer and as a potential therapeutic target in advanced endometrial cancer for future studies.
MeSH term(s)	Biomarkers, Tumor/metabolism ; Biopsy ; Carcinoma, Endometrioid/metabolism ; Carcinoma, Endometrioid/mortality ; Carcinoma, Endometrioid/pathology ; Carcinoma, Endometrioid/secondary ; Cohort Studies ; Databases, Factual ; Disease Progression ; Endometrial Neoplasms/genetics ; Endometrial Neoplasms/metabolism ; Endometrial Neoplasms/mortality ; Endometrial Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Hyaluronan Receptors/genetics ; Hyaluronan Receptors/metabolism ; Lymphatic Metastasis ; Neoplasm Grading ; Prognosis ; Up-Regulation
Chemical Substances	Biomarkers, Tumor ; Hyaluronan Receptors
Language	English
Publishing date	2020-04-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1473273-7
ISSN	1533-4058 ; 1062-3345 ; 1541-2016
ISSN (online)	1533-4058
ISSN	1062-3345 ; 1541-2016
DOI	10.1097/PAI.0000000000000763
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Article ; Online: miR-431 Promotes Metastasis of Pancreatic Neuroendocrine Tumors by Targeting DAB2 Interacting Protein, a Ras GTPase Activating Protein Tumor Suppressor.

Zhang, Tiantian / Choi, Soyoung / Zhang, Tuo / Chen, Zhengming / Chi, Yudan / Huang, Shixia / Xiang, Jenny Z / Du, Yi-Chieh Nancy

The American journal of pathology

2020 Volume 190, Issue 3, Page(s) 689–701

Abstract: The incidence of pancreatic neuroendocrine tumor (PNET) is increasing, and it presents with various clinical manifestations and an unfavorable survival rate. A better understanding of the drivers of PNET tumorigenesis is urgently needed. Distinct miRNA ... ...

Abstract	The incidence of pancreatic neuroendocrine tumor (PNET) is increasing, and it presents with various clinical manifestations and an unfavorable survival rate. A better understanding of the drivers of PNET tumorigenesis is urgently needed. Distinct miRNA signatures have been identified for different stages of tumorigenesis in both human and mouse PNETs. The functions of these miRNAs are poorly understood. miR-431 is the most up-regulated miRNA in the metastatic signature. However, it is unknown whether miR-431 contributes to metastasis of PNETs. Herein, we show that miR-431 overexpression activates Ras/extracellular signal-regulated kinase (Erk) signaling and promotes epithelial-mesenchymal transition, migration/invasion in vitro, and metastasis in both xenograft and spontaneous mouse models of PNET. Treatment of PNET cells with Erk inhibitor or locked nucleic acids sequestering miR-431 inhibits invasion. Four target prediction modules and dual-luciferase reporter assays were used to identify potential mRNA targets of miR-431. A Ras GTPase activating protein tumor suppressor (RasGAP), DAB2 interacting protein (DAB2IP), was discovered as an miR-431 target. Overexpression of DAB2IP's rat homolog, but not its mutant defective in Ras GTPase activating protein activity, reverses miR-431's effect on promoting invasion, Erk phosphorylation, and epithelial-mesenchymal transition of PNETs. Taken together, miR-431 silences DAB2IP to active Ras/Erk and promote metastasis of PNETs. miR-431 may be targeted to manage metastatic PNETs.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Carcinogenesis ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; MAP Kinase Signaling System ; Male ; Mice ; MicroRNAs/genetics ; Neoplasm Metastasis ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/pathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Rats ; ras GTPase-Activating Proteins/genetics ; ras GTPase-Activating Proteins/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; DAB2 protein, human ; Dab2 protein, mouse ; MIRN431 microRNA, human ; MIRN431 microRNA, mouse ; MicroRNAs ; ras GTPase-Activating Proteins
Language	English
Publishing date	2020-01-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2019.11.007
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Article ; Online: p53 and p16

Azzopardi, Stephanie / Pang, Sharon / Klimstra, David S / Du, Yi-Chieh Nancy

Neoplasia (New York, N.Y.)

2016 Volume 18, Issue 10, Page(s) 610–617

Abstract: In human studies and mouse models, the contributions of p53 and ... ...

Abstract	In human studies and mouse models, the contributions of p53 and p16
MeSH term(s)	Animals ; Cell Transformation, Neoplastic/genetics ; Cyclin-Dependent Kinase Inhibitor p16/deficiency ; Cyclin-Dependent Kinase Inhibitor p19/deficiency ; Disease Models, Animal ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Kaplan-Meier Estimate ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Neoplastic Stem Cells/metabolism ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/mortality ; Neuroendocrine Tumors/pathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/mortality ; Pancreatic Neoplasms/pathology ; Phenotype ; Prognosis ; Tumor Burden ; Tumor Suppressor Protein p53/deficiency
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p16 ; Cyclin-Dependent Kinase Inhibitor p19 ; Tumor Suppressor Protein p53
Language	English
Publishing date	2016-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2016.08.003
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Article ; Online: (-)-Oleocanthal and (-)-oleocanthal-rich olive oils induce lysosomal membrane permeabilization in cancer cells.

Goren, Limor / Zhang, George / Kaushik, Susmita / Breslin, Paul A S / Du, Yi-Chieh Nancy / Foster, David A

PloS one

2019 Volume 14, Issue 8, Page(s) e0216024

Abstract: Oleocanthal (oleocanthal) is a phenolic compound found in varying concentrations in extra virgin olive oil oleocanthal has been shown to be active physiologically, benefiting several diseased states by conferring anti-inflammatory and neuroprotective ...

Abstract	(-)-Oleocanthal (oleocanthal) is a phenolic compound found in varying concentrations in extra virgin olive oil oleocanthal has been shown to be active physiologically, benefiting several diseased states by conferring anti-inflammatory and neuroprotective benefits. Recently, we and other groups have demonstrated its specific and selective toxicity toward cancer cells; however, the mechanism leading to cancer cell death is still disputed. The current study demonstrates that oleocanthal, as well as naturally oleocanthal-rich extra virgin olive oils, induced damage to cancer cells' lysosomes leading to cellular toxicity in vitro and in vivo. Lysosomal membrane permeabilization following oleocanthal treatment in various cell lines was assayed via three complementary methods. Additionally, we found oleocanthal treatment reduced tumor burden and extended lifespan of mice engineered to develop pancreatic neuroendocrine tumors. Finally, following-up on numerous correlative studies demonstrating consumption of olive oil reduces cancer incidence and morbidity, we observed that extra virgin olive oils naturally rich in oleocanthal sharply reduced cancer cell viability and induced lysosomal membrane permeabilization while oleocanthal-poor oils did not. Our results are especially encouraging since tumor cells often have larger and more numerous lysosomes, making them especially vulnerable to lysosomotropic agents such as oleocanthal.
MeSH term(s)	Aldehydes/administration & dosage ; Animals ; Apoptosis ; Brain Neoplasms/drug therapy ; Brain Neoplasms/pathology ; Cell Membrane Permeability/drug effects ; Cyclopentane Monoterpenes/administration & dosage ; Lysosomes/drug effects ; Lysosomes/metabolism ; Mice ; Necrosis ; Neuroectodermal Tumors, Primitive/drug therapy ; Neuroectodermal Tumors, Primitive/pathology ; Olive Oil/administration & dosage ; Phenols/administration & dosage ; Plant Oils/administration & dosage ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Aldehydes ; Cyclopentane Monoterpenes ; Olive Oil ; Phenols ; Plant Oils ; oleocanthal (AC7QO6038O)
Language	English
Publishing date	2019-08-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0216024
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