scholarly journals Tumor Localization and Biodistribution with Radiolabeled Monoclonal Anbibody against Pancreatic Cancer in Tumor-Bearing Nude Mice.

1992 ◽  
Vol 168 (2) ◽  
pp. 397-401 ◽  
Author(s):  
YONG S. CHUNG ◽  
TETSUJI SAWADA ◽  
YASUYUKI KONDO ◽  
Jenny J.L. HO ◽  
YOUNG S. Kim ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Nude Mice ◽  
Tumor Localization ◽  
Tumor Bearing

scholarly journals TRPM2 promotes pancreatic cancer by PKC/MAPK pathway

2020 ◽  
Author(s):  
Rui Lin ◽  
Xunxia Bao ◽  
Hui Wang ◽  
Sibo Zhu ◽  
Zhongyan Liu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Nude Mice ◽  
Transcriptome Analysis ◽  
Cell Model ◽  
Mapk Pathway ◽  
Tissue Sample ◽  
Pancreatic Cancer Cell Line ◽  
Cancer Cell Line ◽  
Migration And Invasion ◽  
Tumor Bearing

AbstractBackgroundThe mechanism of pancreatic cancer(PA) is not fully understanded. In our last report, TRPM2 plays a promising role in pancreatic cancer. However, the mechanism of TRPM2 is still unknown in this dismal disease. This study was designed to investigate the role and mechanism of TRPM2 in pancreatic cancer.MethodsTRPM2 overexpressed and siRNA plasmid were created and transfected with pancreatic cancer cell line(BxPC-3) to construct the cell model. We employed CCK-8, Transwell, scratch wound, and nude mice tumor bearing model to investigate the role of TRPM2 in pancreatic cancer. Besides, we collected the clinical data, tumor tissue sample(TT) and para-tumor sample(TP) from the pancreatic cancer patients treated in our hospital. We analyzed the mechanism of TRPM2 in pancreatic cancer by transcriptome analysis, Westernblot, and PCR.ResultsOverexpressed TRPM2 could promote pancreatic cancer in proliferation, migration, and invasion ability in no matter the cell model or nude mice tumor bearing model. TRPM2 level is highly negative correlated to the overall survival and progression-free survival time in PA patients, however, it is significantly increased in PA tissue as the tumor stage increases. The transcriptome analysis, GSEA analysis, Westernblot, and PCR results indicates TRPM2 is highly correlated with PKC/MAPK pathways.ConclusionTRPM2 could directly activate PKCα by calcium or indirectly activate PKCε and PKCδ by increased DAG in PC, which promote PC by downstream MAPK/MEK pathway activation.

Radioimmunoscintigraphy of pancreatic cancer in tumor-bearing athymic nude mice using 99mtechnetium-labeled anti-KL-6/MUC1 antibody

2008 ◽  
Vol 26 (3) ◽  
pp. 133-139 ◽  
Author(s):  
Kenji Matsumura ◽  
Ichiro Niki ◽  
Hui Tian ◽  
Masahisa Takuma ◽  
Norio Hongo ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Nude Mice ◽  
Athymic Nude Mice ◽  
Tumor Bearing

scholarly journals TRPM2 promotes pancreatic cancer by PKC/MAPK pathway

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Rui Lin ◽  
Xunxia Bao ◽  
Hui Wang ◽  
Sibo Zhu ◽  
Zhongyan Liu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Wound Healing ◽  
Western Blot ◽  
Nude Mice ◽  
Transcriptome Analysis ◽  
Cell Model ◽  
Mapk Pathway ◽  
Migration And Invasion ◽  
Tumor Bearing ◽  
Scratch Wound

AbstractThe mechanism of pancreatic cancer (PA) is not fully understanded. In our last report, TRPM2 plays a promising role in pancreatic cancer. However, the mechanism of TRPM2 is still unknown in this dismal disease. This study was designed to investigate the role and mechanism of TRPM2 in pancreatic cancer. TRPM2 overexpressed and siRNA plasmid were created and transfected with pancreatic cancer cell line (BxPC-3) to construct the cell model. We employed CCK-8, Transwell, scratch wound, and nude mice tumor-bearing model to investigate the role of TRPM2 in pancreatic cancer. Besides, we collected the clinical data, tumor tissue sample (TT) and para-tumor sample (TP) from the pancreatic cancer patients treated in our hospital. We analyzed the mechanism of TRPM2 in pancreatic cancer by transcriptome analysis, western blot, and PCR. We blocked the downstream PKC/MEK pathway of TRPM2 to investigate the mechanism of TRPM2 in pancreatic cancer by CCK8, scratch wound healing, and transwell assays. Overexpressed TRPM2 could promote pancreatic cancer in proliferation, migration, and invasion ability in no matter the cell model or nude mice tumor-bearing model. TRPM2 level is highly negative correlated to the overall survival and progression-free survival time in PA patients, however, it is significantly increased in PA tissue as the tumor stage increases. The transcriptome analysis, GSEA analysis, western-blot, and PCR results indicate TRPM2 is highly correlated with PKC/MAPK pathways. The experiments of PKC/MEK inhibitors added to TRPM2 overexpressed BxPC-3 cell showed that significant inhibition of PA cells happened in CCK8, transwell, and wound-healing assay. TRPM2 may directly activate PKCα by calcium or indirectly activate PKCε and PKCδ by increased DAG in PA, which promote PA by downstream MAPK/MEK pathway activation.

scholarly journals Fraction B From Catfish Epidermal Secretions Kills Pancreatic Cancer Cells, Inhibits CD44 Expression and Stemness, and Alters Cancer Cell Metabolism

2021 ◽  
Vol 12 ◽  
Author(s):  
Jassim M. Al-Hassan ◽  
Daoyan Wei ◽  
Sharmistha Chakraborty ◽  
Tara Conway ◽  
Patrea Rhea ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Glutamine Metabolism ◽  
Stem Cell Marker ◽  
Control Group ◽  
Potential Candidate ◽  
Cd44 Expression ◽  
Tumor Bearing ◽  
Pancreatic Cancer Cells

Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer related death in western countries. The successful treatment of PDAC remains limited. We investigated the effect of Fraction B, which is a fraction purified from catfish (Arius bilineatus, Val.) skin secretions containing proteins and lipids, on PDAC biology both in-vivo and in-vitro. We report here that Fraction B potently suppressed the proliferation of both human and mouse pancreatic cancer cells in vitro and significantly reduced the growth of their relevant xenograft (Panc02) and orthotopic tumors (human Panc-1 cells) (p < 0.05). The Reverse Phase Protein Array (RPPA) data obtained from the tumor tissues derived from orthotopic tumor bearing mice treated with Fraction B showed that Fraction B altered the cancer stem cells related pathways and regulated glucose and glutamine metabolism. The down-regulation of the cancer stem cell marker CD44 expression was further confirmed in Panc-1 cells. CBC and blood chemistry analyses showed no systemic toxicity in Fraction B treated Panc-1 tumor bearing mice compared to that of control group. Our data support that Fraction B is a potential candidate for PDAC treatment.

LINC01133 hampers the development of gastric cancer through increasing SST via binding to microRNA-576-5p

Epigenomics ◽  
2021 ◽  
Author(s):  
Leiyi Zhang ◽  
Ke Pan ◽  
Zhongkun Zuo ◽  
Fei Ye ◽  
Ding Cao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Growth ◽  
Nude Mice ◽  
Therapeutic Targets ◽  
Loss Of Function ◽  
Gain Of Function ◽  
Tumor Bearing ◽  
New Therapeutic Targets ◽  
Low Expression ◽  
Development Of Gastric Cancer

Aim: Our study aimed at investigating how LINC01133 functions in gastric cancer (GC) progression. Materials & methods: Gain-of-function and loss-of-function approaches were applied to analyze the effects of LINC01133, microRNA-576-5p (miR-576-5p) and somatostatin (SST) on the biological behaviors of GC cells and in tumor-bearing nude mice. Results: GC tissues and cells showed low expression of LINC01133, and LINC01133 overexpression decreased malignant phenotypes of GC cells. Moreover, LINC01133 upregulated SST through binding to miR-576-5p. Overexpressing miR-576-5p or suppressing SST reversed the functions of LINC01133 in biological potentials of GC cells and tumor growth. Conclusion: LINC01133 overexpression may inhibit GC development by downregulation of miR-576-5p and upregulation of SST, which suggests new therapeutic targets for GC.

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