scholarly journals Crosstalk between the canonical NF-κB and Notch signaling pathways inhibits Pparγ expression and promotes pancreatic cancer progression in mice

2011 ◽  
Vol 121 (12) ◽  
pp. 4685-4699 ◽  
Author(s):  
Eleni Maniati ◽  
Maud Bossard ◽  
Natalie Cook ◽  
Juliana B. Candido ◽  
Nia Emami-Shahri ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Notch Signaling ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Pparγ Expression

scholarly journals miR-1266 Contributes to Pancreatic Cancer Progression and Chemoresistance by the STAT3 and NF-κB Signaling Pathways

2018 ◽  
Vol 11 ◽  
pp. 142-158 ◽  
Author(s):  
Xin Zhang ◽  
Dong Ren ◽  
Xianqiu Wu ◽  
Xi Lin ◽  
Liping Ye ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathways ◽  
Cancer Progression

scholarly journals Exosome-Derived LINC00960 and LINC02470 Promote the Epithelial-Mesenchymal Transition and Aggressiveness of Bladder Cancer Cells

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1419
Author(s):  
Cheng-Shuo Huang ◽  
Jar-Yi Ho ◽  
Jung-Hwa Chiang ◽  
Cheng-Ping Yu ◽  
Dah-Shyong Yu
Keyword(s):  
Bladder Cancer ◽  
Notch Signaling ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Low Grade ◽  
High Grade ◽  
Mesenchymal Transition ◽  
Bladder Cancer Cells

Exosomes are essential for several tumor progression-related processes, including the epithelial–mesenchymal transition (EMT). Long non-coding RNAs (lncRNAs) comprise a major group of exosomal components and regulate the neoplastic development of several cancer types; however, the progressive role of exosomal lncRNAs in bladder cancer have rarely been addressed. In this study, we identified two potential aggressiveness-promoting exosomal lncRNAs, LINC00960 and LINC02470. Exosomes derived from high-grade bladder cancer cells enhanced the viability, migration, invasion and clonogenicity of recipient low-grade bladder cancer cells and activated major EMT-upstream signaling pathways, including β-catenin signaling, Notch signaling, and Smad2/3 signaling pathways. Nevertheless, LINC00960 and LINC02470 were expressed at significantly higher levels in T24 and J82 cells and their secreted exosomes than in TSGH-8301 cells. Moreover, exosomes derived from LINC00960 knockdown or LINC02470 knockdown T24 cells significantly attenuated the ability of exosomes to promote cell aggressiveness and activate EMT-related signaling pathways in recipient TSGH-8301 cells. Our findings indicate that exosome-derived LINC00960 and LINC02470 from high-grade bladder cancer cells promote the malignant behaviors of recipient low-grade bladder cancer cells and induce EMT by upregulating β-catenin signaling, Notch signaling, and Smad2/3 signaling. Both lncRNAs may serve as potential liquid biomarkers for the prognostic surveillance of bladder cancer progression.

Inhibition of Notch signaling attenuates pancreatic cancer progression

2008 ◽  
Vol 46 (09) ◽  
Author(s):  
RR Plentz ◽  
S Sankaran ◽  
BZ Stanger ◽  
PK Majumder ◽  
N Bardeesy
Keyword(s):  
Pancreatic Cancer ◽  
Notch Signaling ◽  
Cancer Progression

scholarly journals The Role of Notch Signaling and Leptin-Notch Crosstalk in Pancreatic Cancer

Medicines ◽  
2018 ◽  
Vol 5 (3) ◽  
pp. 68 ◽  
Author(s):  
Adriana Harbuzariu ◽  
Gabriela Oprea-Ilies ◽  
Ruben Gonzalez-Perez
Keyword(s):  
Pancreatic Cancer ◽  
Notch Signaling ◽  
Cancer Progression ◽  
Treatment Success ◽  
Notch Signaling Pathway ◽  
Cancer Development ◽  
Cancer Cell Proliferation ◽  
The Novel ◽  
Cancer Types

There is accumulating evidence that deregulated Notch signaling affects cancer development, and specifically pancreatic cancer (PC) progression. Notch canonical and non-canonical signaling has diverse impact on PC. Moreover, the actions of RBP-Jk (nuclear partner of activated Notch) independent of Notch signaling pathway seem to affect differently cancer progression. Recent data show that in PC and other cancer types the adipokine leptin can modulate Notch/RBP-Jk signaling, thereby, linking the pandemic obesity with cancer and chemoresistance. The potential pivotal role of leptin on PC, and its connection with Notch signaling and chemoresistance are still not completely understood. In this review, we will describe the most important aspects of Notch-RBP-Jk signaling in PC. Further, we will discuss on studies related to RBP-Jk-independent Notch and Notch-independent RPB-Jk signaling. We will also discuss on the novel crosstalk between leptin and Notch in PC and its implications in chemoresistance. The effects of leptin-Notch/RBP-Jk signaling on cancer cell proliferation, apoptosis, and drug resistance require more investigation. Data from these investigations could help to open unexplored ways to improve PC treatment success that has shown little progress for many years.

scholarly journals Leptin-Notch signaling axis is involved in pancreatic cancer progression

Oncotarget ◽  
2016 ◽  
Vol 8 (5) ◽  
pp. 7740-7752 ◽  
Author(s):  
Adriana Harbuzariu ◽  
Antonio Rampoldi ◽  
Danielle S Daley-Brown ◽  
Pierre Candelaria ◽  
Tia L Harmon ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Notch Signaling ◽  
Cancer Progression ◽  
Signaling Axis

scholarly journals The miR-1224-5p/ELF3 Axis Regulates Malignant Behaviors of Pancreatic Cancer via PI3K/AKT/Notch Signaling Pathways

2020 ◽  
Vol Volume 13 ◽  
pp. 3449-3466 ◽  
Author(s):  
Lingming Kong ◽  
Peng Liu ◽  
Mingjun Zheng ◽  
Zhongpeng Wang ◽  
Yang Gao ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Notch Signaling ◽  
Signaling Pathways

scholarly journals Folded and Unfolded Conformations of Proteins Involved in Pancreatic Cancer: a Layman's Guide

2010 ◽  
Vol 10 ◽  
pp. 1612-1633 ◽  
Author(s):  
Jerónimo Bravo ◽  
José L. Neira
Keyword(s):  
Pancreatic Cancer ◽  
Amino Acids ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Current Knowledge ◽  
Biochemical Pathway ◽  
Natively Unfolded ◽  
Folded Proteins ◽  
Key Residues ◽  
Hub Proteins

Pancreatic cancer (PC) is one of the most difficult illnesses to treat, since the 5-year survival rate is lower than 5% in patients and no substantial advances in its treatment have been achieved in the last 20 years. Since cancer deregulation and progression are associated with changes in at least one biochemical pathway, the knowledge of the structure of the proteins involved in such routes seems to be crucial in order to understand how this cancer progresses and, more importantly, to design more efficient and rationally designed drugs. In this review, we describe the fold and structures of proteins involved in different signaling pathways that intervene during PC development and progression. In particular, we will focus on the most frequently mutated, or alternatively differently expressed, proteins in PC. The current knowledge suggests that most of the proteins carry out their function by interacting with others via specific domains and through key residues at the recognition interfaces; these amino acids are mutated in patients developing PC. Furthermore, phosphorylation seems to be a crucial regulation step along several signaling pathways. Finally, we show not only that well-folded proteins in several signaling pathways are critical in the development of PC, but also that natively unfolded “hub” proteins, able to interact with DNA or proteins, are also important in such cancer progression.

scholarly journals Exosome-transmitted LINC00960 and LINC02470 promote the epithelial-mesenchymal transition and aggressiveness of bladder cancer cells

2020 ◽  
Author(s):  
Cheng-Shuo Huang ◽  
Jar-Yi Ho ◽  
Jung-Hwa Chiang ◽  
Cheng-Ping Yu ◽  
Dah-Shyong Yu
Keyword(s):  
Bladder Cancer ◽  
Notch Signaling ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Low Grade ◽  
High Grade ◽  
Mesenchymal Transition ◽  
Bladder Cancer Cells

Abstract Background Exosomes are essential for several tumor progression-related processes, including epithelial-mesenchymal transition (EMT). Long noncoding RNAs (lncRNAs) comprise a major group of exosomal components and regulate the neoplastic development of several cancer types; however, the progressive roles of exosomal lncRNAs in bladder cancer have rarely been addressed. In this study, we identified two potential aggressiveness-promoting exosomal lncRNAs, LINC00960 and LINC02470; we found that these lncRNAs potently induced EMT during bladder cancer progression. Methods Low-grade bladder cancer cells (TSGH-8301) were treated with conditioned media or exosomes derived from high-grade bladder cancer cells (T24 or J82), and the aggressiveness-promoting effects were evaluated. Cell viability, cell migratory/invasive activities and clonogenicity were compared to assess the response to these intercellular transmissions. Exosome-transmitted lncRNA candidates were screened with bioinformatic pipelines, and their expression levels were validated in bladder cancer cells and exosomes. Two novel lncRNAs, LINC00960 and LINC02470, were selected, and their roles and regulatory mechanisms in inducing the aggressiveness of bladder cancer cells were investigated. Results Exosomes derived from high-grade bladder cancer cells enhanced the viability, migration, invasion and clonogenicity of recipient low-grade bladder cancer cells and activated major EMT-upstream signaling pathways, including β-catenin signaling, Notch signaling, and Smad2/3 signaling pathways. Nevertheless, LINC00960 and LINC02470 were expressed at significantly higher levels in T24 and J82 cells and their secreted exosomes than in TSGH-8301 cells. Moreover, exosomes derived from LINC00960 knockdown or LINC02470 knockdown T24 cells significantly attenuated the ability of exosomes to promote cell aggressiveness and activate EMT-related signaling pathways in recipient TSGH-8301 cells. Conclusion Our findings indicate that exosome-transmitted LINC00960 and LINC02470 from high-grade bladder cancer cells promotes the malignant behaviors of recipient low-grade bladder cancer cells and induces EMT by upregulating β-catenin signaling, Notch signaling, and Smad2/3 signaling. Both lncRNAs may serve as potential liquid biomarkers for the prognostic surveillance of bladder cancer progression.

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