scholarly journals Expression of core 3 synthase in human pancreatic cancer cells suppresses tumor growth and metastasis

2013 ◽  
pp. n/a-n/a ◽  
Author(s):  
Prakash Radhakrishnan ◽  
Paul M. Grandgenett ◽  
Ashley M. Mohr ◽  
Stephanie K. Bunt ◽  
Fang Yu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Tumor Growth And Metastasis

scholarly journals Long noncoding RNA SOX2OT promotes pancreatic cancer cell migration and invasion through destabilizing FUS protein via ubiquitination

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yan Wang ◽  
Xiong-Fei Zhang ◽  
Dong-Yan Wang ◽  
Yi Zhu ◽  
Lei Chen ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Migration ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Migration ◽  
Pancreatic Cancer Cells ◽  
Tumor Growth And Metastasis ◽  
Fus Protein

AbstractPancreatic cancer is a highly aggressive and lethal digestive system malignancy. Our previous studies revealed the correlation of high levels of lncRNA SOX2OT expression with patients’ poor survival outcomes, the promoting role of SOX2OT in proliferation and cycle progression of pancreatic cancer cells, and the in vivo binding of SOX2OT to RNA binding protein FUS, which destabilized the protein expression of FUS. However, the mechanism of SOX2OT binding and inhibiting FUS protein stability remains unclear. In this study, we performed RNA pull-down, cycloheximide-chase, and ubiquitination assays to determine the effect of SOX2OT on FUS ubiquitination, and explored the specific regulatory mechanism of SOX2OT–FUS axis in pancreatic cancer cell migration, invasion, in vivo tumor growth, and metastasis through RNA sequencing. We found that SOX2OT binds to FUS through its 5′ and 3′ regions, resulting in FUS ubiquitination and degradation. The SOX2OT–FUS regulatory axis promotes migration, invasion, tumor growth, and metastasis ability of pancreatic cancer cells. The in-depth elaboration of the SOX2OT–FUS regulatory axis in pancreatic cancer may clarify the mechanism of action of SOX2OT and provide new ideas for pancreatic cancer treatment.

scholarly journals Long Noncoding RNA JHDM1D-AS1 Promotes Tumor Growth by Regulating Angiogenesis in Response to Nutrient Starvation

2017 ◽  
Vol 37 (18) ◽  
Author(s):  
Ayano Kondo ◽  
Aya Nonaka ◽  
Teppei Shimamura ◽  
Shogo Yamamoto ◽  
Tetsuo Yoshida ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Nutrient Starvation ◽  
Human Pancreatic Cancer ◽  
Tumor Xenografts ◽  
Pancreatic Cancer Cells

ABSTRACT Long noncoding RNAs play a pivotal role in tumor progression, but their role in cancer cells in the nutrient-starved tumor microenvironment remains unknown. Here, we show that a nutrient starvation-responsive long noncoding RNA, JHDM1D antisense 1 (JHDM1D-AS1), promotes tumorigenesis by regulating angiogenesis in response to nutrient starvation. Expression of JHDM1D-AS1 was increased in cancer cells. In addition, expression of JHDM1D-AS1 was increased in clinical tumor samples compared to that in normal tissue. Stable expression of JHDM1D-AS1 in human pancreatic cancer (PANC-1 and AsPC-1) cells promoted cell growth in vitro. Remarkably, these JHDM1D-AS1-expressing cells showed a significant increase in tumor growth in vivo that was associated with increased formation of CD31+ blood vessels and elevated infiltration of CD11b+ macrophage lineage cells into tumor tissues. Genome-wide analysis of tumor xenografts revealed that expression of genes for tumor-derived angiogenic factors such as hHGF and hFGF1 concomitant with host-derived inflammation-responsive genes such as mMmp3, mMmp9, mS100a8, and mS100a9 was increased in tumor xenografts of JHDM1D-AS1-expressing pancreatic cancer cells, leading to a poor prognosis. Our results provide evidence that increased JHDM1D-AS1 expression under nutrient starvation accelerates tumor growth by upregulating angiogenesis, thus laying the foundation for improved therapeutic strategies.

scholarly journals RNA Interference Targeting Aurora Kinase A Suppresses Tumor Growth and Enhances the Taxane Chemosensitivity in Human Pancreatic Cancer Cells

2005 ◽  
Vol 65 (7) ◽  
pp. 2899-2905 ◽  
Author(s):  
Tatsuo Hata ◽  
Toru Furukawa ◽  
Makoto Sunamura ◽  
Shinichi Egawa ◽  
Fuyuhiko Motoi ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Rna Interference ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Aurora Kinase ◽  
Human Pancreatic Cancer ◽  
Aurora Kinase A ◽  
Pancreatic Cancer Cells ◽  
Kinase A

scholarly journals An Inhibitor of GSK3B and HDACs Kills Pancreatic Cancer Cells and Slows Pancreatic Tumor Growth and Metastasis in Mice

2018 ◽  
Vol 155 (6) ◽  
pp. 1985-1998.e5 ◽  
Author(s):  
Mouad Edderkaoui ◽  
Chintan Chheda ◽  
Badr Soufi ◽  
Fouzia Zayou ◽  
Robert W. Hu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Pancreatic Tumor ◽  
Pancreatic Cancer Cells ◽  
Tumor Growth And Metastasis

In Vitro and In Vivo Antitumor Efficacy of Docetaxel and Sorafenib Combination in Human Pancreatic Cancer Cells

2010 ◽  
Vol 999 (999) ◽  
pp. 1-11
Author(s):  
P. Ulivi ◽  
C. Arienti ◽  
W. Zoli ◽  
M. Scarsella ◽  
S. Carloni ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Antitumor Efficacy ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells
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