scholarly journals Matrix remodeling‐associated protein 8 is a marker of a subset of cancer‐associated fibroblasts in pancreatic cancer

2022 ◽  
Author(s):  
Ryosuke Ichihara ◽  
Yukihiro Shiraki ◽  
Yasuyuki Mizutani ◽  
Tadashi Iida ◽  
Yuki Miyai ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Matrix Remodeling ◽  
Cancer Associated Fibroblasts

Abstract PR-015: Cancer-associated fibroblasts sustain critical dependency of pancreatic cancer cells on exogenous lipids

2021 ◽  
Author(s):  
Charline Ogier ◽  
Alena Klochkova ◽  
Linara Gabitova ◽  
Battuya Bayarmagnai ◽  
Diana Restifo ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cancer Associated Fibroblasts ◽  
Pancreatic Cancer Cells

Abstract PR001: The splanchnic mesenchyme during fetal development is the major source of pancreatic cancer associated fibroblasts

2021 ◽  
Author(s):  
Lu Han ◽  
Yongxia Xu ◽  
Sean Sweeney ◽  
Ulyss Roesner ◽  
Melodie Parrish ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Fetal Development ◽  
Cancer Associated Fibroblasts

scholarly journals BRAF inhibitors reprogram cancer-associated fibroblasts to drive matrix remodeling and therapeutic escape in melanoma

2021 ◽  
Author(s):  
Tianyi Liu ◽  
Linli Zhou ◽  
Yao Xiao ◽  
Thomas Andl ◽  
Yuhang Zhang
Keyword(s):  
Resistance Mechanism ◽  
Tumor Stroma ◽  
Melanoma Cells ◽  
Biological Properties ◽  
Nuclear Accumulation ◽  
Matrix Remodeling ◽  
Cancer Associated Fibroblasts ◽  
Braf Inhibitors ◽  
Downstream Effector ◽  
Cellular Components

ABSTRACTThe tumor stroma and its cellular components are known to play an important role in tumor resilience towards treatment. Here, we report a novel resistance mechanism in melanoma that is elicited by BRAF inhibitors (BRAFi)-induced non-canonical nuclear β-catenin signaling in cancer-associated fibroblasts (CAFs). Our study reveals that BRAFi leads to an expanded CAF population with increased β-catenin nuclear accumulation and enhances their biological properties. This CAF subpopulation is essential for melanoma cells to grow and resist to BRAFi/MEK inhibitors (MEKi). Mechanistically, BRAFi induces BRAF and CRAF dimerization and subsequently the activation of ERK signaling in CAFs, leading to the inactivation of the β-catenin destruction complex. By RNA-Seq, periostin (POSTN) is identified as a major downstream effector of β catenin in CAFs and can compensate for the loss of β-catenin in CAFs in conferring melanoma cell BRAFi/MEKi resistance. Moreover, POSTN reactivates the ERK pathway, which is inhibited by BRAFi/MEKi, in melanoma cells through PI3K/AKT signaling. Our data underscore the roles of BRAFi-induced CAF reprogramming in matrix remodeling and therapeutic escape of melanoma cells and reveal POSTN as an important matrix target to eliminate BRAFi/MEKi resistance in melanoma.

scholarly journals Extensive desmoplasia is associated with high expression of ZEB1 in pancreatic cancer cells and cancer associated fibroblasts determine prognosis

HPB ◽  
2019 ◽  
Vol 21 ◽  
pp. S867
Author(s):  
L. Bolm ◽  
P. Bronsert ◽  
S. Cigolla ◽  
L. Käsmann ◽  
U. Wittel ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
High Expression ◽  
Cancer Associated Fibroblasts ◽  
Pancreatic Cancer Cells

scholarly journals The Role of Autophagy in Pancreatic Cancer: From Bench to the Dark Bedside

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 1063 ◽  
Author(s):  
Kıvanç Görgülü ◽  
Kalliope N. Diakopoulos ◽  
Ezgi Kaya-Aksoy ◽  
Katrin J. Ciecielski ◽  
Jiaoyu Ai ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Fine Tuning ◽  
Cancer Tissue ◽  
Dependent Manner ◽  
Cancer Associated Fibroblasts ◽  
Preneoplastic Lesions ◽  
Pancreatic Cancer Tissue ◽  
Cancer Types ◽  
Initiation Stage

Pancreatic cancer is one of the deadliest cancer types urgently requiring effective therapeutic strategies. Autophagy occurs in several compartments of pancreatic cancer tissue including cancer cells, cancer associated fibroblasts, and immune cells where it can be subjected to a multitude of stimulatory and inhibitory signals fine-tuning its activity. Therefore, the effects of autophagy on pancreatic carcinogenesis and progression differ in a stage and context dependent manner. In the initiation stage autophagy hinders development of preneoplastic lesions; in the progression stage however, autophagy promotes tumor growth. This double-edged action of autophagy makes it a hard therapeutic target. Indeed, autophagy inhibitors have not yet shown survival improvements in clinical trials, indicating a need for better evaluation of existing results and smarter targeting techniques. Clearly, the role of autophagy in pancreatic cancer is complex and many aspects have to be considered when moving from the bench to the bedside.

scholarly journals Pancreatic cancer‐secreted miR‐155 implicates in the conversion from normal fibroblasts to cancer‐associated fibroblasts

2015 ◽  
Vol 106 (10) ◽  
pp. 1362-1369 ◽  
Author(s):  
Wenjing Pang ◽  
Jiaojiao Su ◽  
Yalei Wang ◽  
Hui Feng ◽  
Xin Dai ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Associated Fibroblasts
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