scholarly journals CTGF drives autophagy, glycolysis and senescence in cancer-associated fibroblasts via HIF1 activation, metabolically promoting tumor growth

Cell Cycle ◽  
2012 ◽  
Vol 11 (12) ◽  
pp. 2272-2284 ◽  
Author(s):  
Claudia Capparelli ◽  
Diana Whitaker-Menezes ◽  
Carmela Guido ◽  
Renee Balliet ◽  
Timothy G. Pestell ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cancer Associated Fibroblasts

scholarly journals Cancer-Associated Fibroblasts: Their Characteristics and Their Roles in Tumor Growth

Cancers ◽  
2015 ◽  
Vol 7 (4) ◽  
pp. 2443-2458 ◽  
Author(s):  
Kazuyoshi Shiga ◽  
Masayasu Hara ◽  
Takaya Nagasaki ◽  
Takafumi Sato ◽  
Hiroki Takahashi ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cancer Associated Fibroblasts

scholarly journals Cancer-associated fibroblasts stimulate primary tumor growth and metastatic spread in an orthotopic prostate cancer xenograft model

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Johannes Linxweiler ◽  
Turkan Hajili ◽  
Christina Körbel ◽  
Carolina Berchem ◽  
Philip Zeuschner ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Growth ◽  
Primary Tumor ◽  
Xenograft Model ◽  
Metastatic Spread ◽  
Cancer Associated Fibroblasts ◽  
Primary Tumor Growth

scholarly journals Gallbladder cancer-associated fibroblasts promote vasculogenic mimicry formation and tumor growth in gallbladder cancer via upregulating the expression of NOX4, a poor prognosis factor, through IL-6-JAK-STAT3 signal pathway

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Mu-Su Pan ◽  
Hui Wang ◽  
Kamar Hasan Ansari ◽  
Xin-Ping Li ◽  
Wei Sun ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Gallbladder Cancer ◽  
Molecular Mechanism ◽  
Poor Prognosis ◽  
Vasculogenic Mimicry ◽  
Tube Formation ◽  
Signal Pathway ◽  
Cancer Associated Fibroblasts

Abstract Background Cancer-associated fibroblasts (CAFs) and vasculogenic mimicry (VM) play important roles in the occurrence and development of tumors. However, the relationship between CAFs and VM formation, especially in gallbladder cancer (GBC) has not been clarified. In this study, we investigated whether gallbladder CAFs (GCAFs) can promote VM formation and tumor growth and explored the underlying molecular mechanism. Methods A co-culture system of human GBC cells and fibroblasts or HUVECs was established. VM formation, proliferation, invasion, migration, tube formation assays, CD31-PAS double staining, optic/electron microscopy and tumor xenograft assay were used to detect VM formation and malignant phenotypes of 3-D co-culture matrices in vitro, as well as the VM formation and tumor growth of xenografts in vivo, respectively. Microarray analysis was used to analyze gene expression profile in GCAFs/NFs and VM (+)/VM (−) in vitro. QRT-PCR, western blotting, IHC and CIF were used to detected NOX4 expression in GCAFs/NFs, 3-D culture/co-culture matrices in vitro, the xenografts in vivo and human gallbladder tissue/stroma samples. The correlation between NOX4 expression and clinicopathological and prognostic factors of GBC patients was analyzed. And, the underlying molecular mechanism of GCAFs promoting VM formation and tumor growth in GBC was explored. Results GCAFs promote VM formation and tumor growth in GBC; and the finding was confirmed by facts that GCAFs induced proliferation, invasion, migration and tube formation of GBC cells in vitro, and promoted VM formation and tumor growth of xenografts in vivo. NOX4 is highly expressed in GBC and its stroma, which is the key gene for VM formation, and is correlated with tumor aggression and survival of GBC patients. The GBC patients with high NOX4 expression in tumor cells and stroma have a poor prognosis. The underlying molecular mechanism may be related to the upregulation of NOX4 expression through paracrine IL-6 mediated IL-6/JAK/STAT3 signaling pathway. Conclusions GCAFs promote VM formation and tumor growth in GBC via upregulating NOX4 expression through the activation of IL-6-JAK-STAT3 signal pathway. NOX4, as a VM-related gene in GBC, is overexpressed in GBC cells and GCAFs, which is related to aggression and unfavorable prognosis of GBC patients.

MiR-124 down-regulation is critical for cancer associated fibroblasts-enhanced tumor growth of oral carcinoma

2017 ◽  
Vol 351 (1) ◽  
pp. 100-108 ◽  
Author(s):  
Xia Li ◽  
Qinqiao Fan ◽  
Jinyun Li ◽  
Jing Song ◽  
Yangcong Gu
Keyword(s):  
Tumor Growth ◽  
Oral Carcinoma ◽  
Cancer Associated Fibroblasts ◽  
Down Regulation

scholarly journals RhoA knockout fibroblasts lose tumor-inhibitory capacity in vitro and promote tumor growth in vivo

2017 ◽  
Vol 114 (8) ◽  
pp. E1413-E1421 ◽  
Author(s):  
Twana Alkasalias ◽  
Andrey Alexeyenko ◽  
Katharina Hennig ◽  
Frida Danielsson ◽  
Robert Jan Lebbink ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Tumor Cell ◽  
Rho Gtpase ◽  
Focal Adhesions ◽  
Cancer Associated Fibroblasts ◽  
Inhibitory Capacity ◽  
Promote Tumor Growth ◽  
Pc3 Cells

Fibroblasts are a main player in the tumor-inhibitory microenvironment. Upon tumor initiation and progression, fibroblasts can lose their tumor-inhibitory capacity and promote tumor growth. The molecular mechanisms that underlie this switch have not been defined completely. Previously, we identified four proteins overexpressed in cancer-associated fibroblasts and linked to Rho GTPase signaling. Here, we show that knocking out the Ras homolog family member A (RhoA) gene in normal fibroblasts decreased their tumor-inhibitory capacity, as judged by neighbor suppression in vitro and accompanied by promotion of tumor growth in vivo. This also induced PC3 cancer cell motility and increased colony size in 2D cultures. RhoA knockout in fibroblasts induced vimentin intermediate filament reorganization, accompanied by reduced contractile force and increased stiffness of cells. There was also loss of wide F-actin stress fibers and large focal adhesions. In addition, we observed a significant loss of α-smooth muscle actin, which indicates a difference between RhoA knockout fibroblasts and classic cancer-associated fibroblasts. In 3D collagen matrix, RhoA knockout reduced fibroblast branching and meshwork formation and resulted in more compactly clustered tumor-cell colonies in coculture with PC3 cells, which might boost tumor stem-like properties. Coculturing RhoA knockout fibroblasts and PC3 cells induced expression of proinflammatory genes in both. Inflammatory mediators may induce tumor cell stemness. Network enrichment analysis of transcriptomic changes, however, revealed that the Rho signaling pathway per se was significantly triggered only after coculturing with tumor cells. Taken together, our findings in vivo and in vitro indicate that Rho signaling governs the inhibitory effects by fibroblasts on tumor-cell growth.

scholarly journals Pancreatic Cancer Associated Fibroblasts (CAF): Under-Explored Target for Pancreatic Cancer Treatment

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1347 ◽  
Author(s):  
Jeffrey Norton ◽  
Deshka Foster ◽  
Malini Chinta ◽  
Ashley Titan ◽  
Michael Longaker
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Growth ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Parenchymal Cell ◽  
Surgical Techniques ◽  
Treatment Strategies ◽  
The United States ◽  
Cancer Associated Fibroblasts ◽  
Cancer Cell Growth

Pancreatic cancer is the 4th leading cause of cancer deaths in the United States. The pancreatic cancer phenotype is primarily a consequence of oncogenes disturbing the resident pancreas parenchymal cell repair program. Many solid tumor types including pancreatic cancer have severe tumor fibrosis called desmoplasia. Desmoplastic stroma is coopted by the tumor as a support structure and CAFs aid in tumor growth, invasion, and metastases. This stroma is caused by cancer associated fibroblasts (CAFs), which lay down extensive connective tissue in and around the tumor cells. CAFs represent a heterogeneous population of cells that produce various paracrine molecules such as transforming growth factor-beta (TGF-beta) and platelet derived growth factors (PDGFs) that aid tumor growth, local invasion, and development of metastases. The hard, fibrotic shell of desmoplasia serves as a barrier to the infiltration of both chemo- and immunotherapy drugs and host immune cells to the tumor. Although there have been recent improvements in chemotherapy and surgical techniques for management of pancreatic cancer, the majority of patients will die from this disease. Therefore, new treatment strategies are clearly needed. CAFs represent an under-explored potential therapeutic target. This paper discusses what we know about the role of CAFs in pancreatic cancer cell growth, invasion, and metastases. Additionally, we present different strategies that are being and could be explored as anti-CAF treatments for pancreatic cancer.

Abstract A41: SOX11 transcriptionally regulates a cytokine-based gene signature in lung cancer-associated fibroblasts (LCAF) to promote tumor growth

2012 ◽  
Vol 18 (3 Supplement) ◽  
pp. A41-A41
Author(s):  
Silvestre Vicent ◽  
Anna K. Gillespie ◽  
Dedeepya Vakaa ◽  
Purvesh Khatri ◽  
Ron Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Gene Signature ◽  
Cancer Associated Fibroblasts ◽  
Promote Tumor Growth
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