Fibrillar Type I Collagen Matrices Enhance Metastasis/Invasion of Ovarian Epithelial Cancer Via β1 Integrin and PTEN Signals

Shen, Yishan; Shen, Rong; Ge, Lili; Zhu, Qi; Li, Fengshan

doi:10.1097/igc.0b013e318263ef34

Cited by 34 publications

(48 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Along with this finding, a paper has shown that fibrosis with type I collagen enrichment at the metastatic site can trigger the dormant-to-proliferative switch in dormant tumor cells leading to metastatic disease [44]. Recently, Shen and colleagues showed that fibrillar type I collagen is important in affecting the invasion of aggressive ovarian cancer cells [45] and Nguyen-Ngoc et al demonstrated metastatic mammary tumors to preferentially disseminate in specific ECM microenvironment containing also type I collagen [46]. More interestingly, transcriptomic dissection of OTSCC patient samples has revealed enhancements in e.g.…”

Section: Discussionmentioning

confidence: 97%

Human Bone Marrow Mesenchymal Stem Cells Induce Collagen Production and Tongue Cancer Invasion

et al. 2013

View full text Add to dashboard Cite

Tumor microenvironment (TME) is an active player in carcinogenesis and changes in its composition modify cancer growth. Carcinoma-associated fibroblasts, bone marrow-derived multipotent mesenchymal stem cells (BMMSCs), and inflammatory cells can all affect the composition of TME leading to changes in proliferation, invasion and metastasis formation of carcinoma cells. In this study, we confirmed an interaction between BMMSCs and oral tongue squamous cell carcinoma (OTSCC) cells by analyzing the invasion progression and gene expression pattern. In a 3-dimensional myoma organotypic invasion model the presence of BMMSCs inhibited the proliferation but increased the invasion of OTSCC cells. Furthermore, the signals originating from OTSCC cells up-regulated the expression of inflammatory chemokines by BMMSCs, whereas BMMSC products induced the expression of known invasion linked molecules by carcinoma cells. Particularly, after the cell-cell interactions, the chemokine CCL5 was abundantly secreted from BMMSCs and a function blocking antibody against CCL5 inhibited BMMSC enhanced cancer invasion area. However, CCL5 blocking antibody did not inhibit the depth of invasion. Additionally, after exposure to BMMSCs, the expression of type I collagen mRNA in OTSCC cells was markedly up-regulated. Interestingly, also high expression of type I collagen N-terminal propeptide (PINP) in vivo correlated with the cancer-specific mortality of OTSCC patients, whereas there was no association between cancer tissue CCL5 levels and the clinical parameters. In conclusion, our results suggest that the interaction between BMMSC and carcinoma cells induce cytokine and matrix molecule expression, of which high level of type I collagen production correlates with the prognosis of OTSCC patients.

show abstract

Section: Discussionmentioning

confidence: 97%

Human Bone Marrow Mesenchymal Stem Cells Induce Collagen Production and Tongue Cancer Invasion

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Collagen remodeling by compaction is an important process for maintenance of tissue homeostasis [58][59][60] particularly following wound healing [61,62] and during scar formation [63,64], and is a hallmark of the invasive behavior of cancer cells as they migrate through connective tissues [65][66][67]. PAK1 has been implicated in cell behavior that affects matrix remodeling including the ability of cells to generate extensions [31,68], ECM contraction [35], membrane ruffling [69] and the secretion of matrix metalloproteinases [70].…”

Section: Discussionmentioning

confidence: 99%

PAK1 is involved in sensing the orientation of collagen stiffness gradients in mouse fibroblasts

Pinto

Mohammadi

Lee

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

View full text Add to dashboard Cite

Migrating cells sense variations of stiffness in connective tissue matrices but how cells detect and respond to stiffness orientation is not defined. We examined cell extension formation on collagen with underlying support (vertical stiffness gradient) or on collagen laterally supported by nylon (lateral stiffness gradient). At 6 h after plating, cells plated on laterally-supported collagen exhibited >2-fold more abundant and ~2-fold longer cell extensions than cells plated on collagen with underlying support. We examined whether p21-activated kinase 1 (PAK1) influences extension formation that is dependent on the orientation of support. At 6 h after plating on collagen with underlying support, wild-type cell extensions were 40% shorter than PAK1 knockdown cells. In contrast, on laterally-supported collagen, wild-type cell extensions were 2-fold longer than PAK1 knockdown cells. In cells plated on laterally-supported collagen, there were ~2-fold reductions of collagen fiber alignment and compaction in PAK1 knockdown cells compared with wild-type cells. PAK1 knockdown did not affect collagen fiber alignment or compaction by cells plated on collagen with underlying support. Wild-type cells with lateral support of collagen exhibited 3-fold increases of phospho-myosin staining at 6h, which was 2-fold lower in PAK1 knockdown cells. In contrast, cells on collagen with underlying support showed no increase of phospho-myosin staining at any times. PAK1 knockdown did not affect α2 or β1 integrin expression or function. We conclude that PAK1 is involved in the ability of cells to sense the orientation of stiffness in collagen substrates and generate contractile forces that affect cell extension formation.

show abstract

“…Type 1 collagen might have another supportive role as a scaffold of CD133‐positive GSCs to invade surrounding tissue. Type 1 collagen enhances invasion of some other cancers via integrin‐stimulated phosphoinositide 3‐kinase (PI3K)/Akt pathway . Akt signal is deeply involved in cell migration with matrix metalloprotease 9 in GBM .…”

Section: Discussionmentioning

confidence: 99%

Type 1 collagen as a potential niche component for CD133‐positive glioblastoma cells

et al. 2014

View full text Add to dashboard Cite

Cancer stem cells are thought to be closely related to tumor p rogression and recurrence, making them attractive therapeutic targets. Stem cells of various tissu es exist within n ich es main taining their stemness. Glioblastoma stem cells (GSCs) a re located to tu mo r cap illaries, perivascular niche, which are cons idered to have important ro le in maintaining GSCs . There were some extracellu lar matrixes (ECM) on th e perivascular connective tissu e, includin g type1 co llagen. We here evalu ated wheth er type1 collagen has a potential of niche fo r GSCs. Imu nohistochemical staining of type1 collagen and CD133 , one o f the GSCs markers , on gliob lasto ma (GBM) tissues showed CD133-positive cells were located in immed iate proximity to typ e1 collagen aro und tu mor vessels. We cultured human GBM cell lines, U87MG and GBM cells obtained from fresh surgical tissu es, T472 and T555, with serum-containin g med ium (SCM) or serum -free medium with some growth facto rs (SFM) and in non-coated (No n-coat) or type1 collag en-coated cell line cultu red in the Col/SFM had Capabilities of sp here formation and tumo rigenesis. Type1 co llagen was fou nd in the perivascular area and showed a p ossibility to maintain GSCs. These fin dings su ggest th at type1 collagen could be one impo rtant co mponent of niche fo r CD133 p ositive GSCs and main tain GSCs in adheren t cultu re.

show abstract

Fibrillar Type I Collagen Matrices Enhance Metastasis/Invasion of Ovarian Epithelial Cancer Via β1 Integrin and PTEN Signals

Cited by 34 publications

References 21 publications

Human Bone Marrow Mesenchymal Stem Cells Induce Collagen Production and Tongue Cancer Invasion

Human Bone Marrow Mesenchymal Stem Cells Induce Collagen Production and Tongue Cancer Invasion

PAK1 is involved in sensing the orientation of collagen stiffness gradients in mouse fibroblasts

Type 1 collagen as a potential niche component for CD133‐positive glioblastoma cells

Contact Info

Product

Resources

About