scholarly journals Annexin A13 promotes tumor cell invasion in vitro and is associated with metastasis in human colorectal cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (13) ◽  
pp. 21663-21673 ◽  
Author(s):  
Guozhong Jiang ◽  
Pengju Wang ◽  
Weiwei Wang ◽  
Wencai Li ◽  
Liping Dai ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Human Colorectal Cancer

scholarly journals Inhibition of STAT5 induces G1 cell cycle arrest and reduces tumor cell invasion in human colorectal cancer cells

2009 ◽  
Vol 89 (6) ◽  
pp. 717-725 ◽  
Author(s):  
Hua Xiong ◽  
Wen-Yu Su ◽  
Qin-Chuan Liang ◽  
Zhi-Gang Zhang ◽  
Hui-Min Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Human Colorectal Cancer ◽  
Cycle Arrest ◽  
Colorectal Cancer Cells ◽  
G1 Cell Cycle Arrest ◽  
Human Colorectal Cancer Cells

C/EBPβ Promotion of MMP3-Dependent Tumor Cell Invasion and Association with Metastasis in Colorectal Cancer

2018 ◽  
Vol 22 (1) ◽  
pp. 5-10 ◽  
Author(s):  
Yuanyuan Ji ◽  
Junkuo Li ◽  
Pan Li ◽  
Li Wang ◽  
Haijun Yang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion

scholarly journals Expression of miR-106a in colorectal cancer and its relation with tumor cell invasion

2012 ◽  
Vol 20 (34) ◽  
pp. 3370
Author(s):  
Qun-Ying Ma ◽  
Xin-Ying Wang ◽  
Zhao Li ◽  
Bo Jiang ◽  
An-Gao Xu
Keyword(s):  
Colorectal Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion

scholarly journals Regulation of the Mechanism ofTWIST1Transcription by BHLHE40 and BHLHE41 in Cancer Cells

2015 ◽  
Vol 35 (24) ◽  
pp. 4096-4109 ◽  
Author(s):  
Kazuo Asanoma ◽  
Ge Liu ◽  
Takako Yamane ◽  
Yoko Miyanari ◽  
Tomoka Takao ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Invasion ◽  
Transcriptional Activity ◽  
Epithelial To Mesenchymal Transition ◽  
Tumor Cell Invasion ◽  
Dependent Manner ◽  
Promoter Regions ◽  
Mesenchymal Transition ◽  
Basal Transcriptional Activity

BHLHE40 and BHLHE41 (BHLHE40/41) are basic helix-loop-helix type transcription factors that play key roles in multiple cell behaviors. BHLHE40/41 were recently shown to be involved in an epithelial-to-mesenchymal transition (EMT). However, the precise mechanism of EMT control by BHLHE40/41 remains unclear. In the present study, we demonstrated that BHLHE40/41 expression was controlled in a pathological stage-dependent manner in human endometrial cancer (HEC). Ourin vitroassays showed that BHLHE40/41 suppressed tumor cell invasion. BHLHE40/41 also suppressed the transcription of the EMT effectorsSNAI1,SNAI2, andTWIST1. We identified the critical promoter regions ofTWIST1for its basal transcriptional activity. We elucidated that the transcription factor SP1 was involved in the basal transcriptional activity ofTWIST1and that BHLHE40/41 competed with SP1 for DNA binding to regulate gene transcription. This study is the first to report the detailed functions of BHLHE40 and BHLHE41 in the suppression of EMT effectorsin vitro. Our results suggest that BHLHE40/41 suppress tumor cell invasion by inhibiting EMT in tumor cells. We propose that BHLHE40/41 are promising markers to predict the aggressiveness of each HEC case and that molecular targeting strategies involving BHLHE40/41 and SP1 may effectively regulate HEC progression.

scholarly journals P11.65 Insights into the mechanisms of primary brain tumor invasion

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii58-iii59
Author(s):  
A Bikfalvi ◽  
T Daubon ◽  
C Billottet
Keyword(s):  
Extracellular Matrix ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Conformational Changes ◽  
Cell Invasion ◽  
Immune Cell ◽  
Tumor Cell Invasion ◽  
Migration And Invasion ◽  
Matricellular Proteins

Abstract We have made progress in unravelling the mechanisms of tumor cell invasion by focusing the attention on two molecular pathways including chemokines and extracellular matrix molecules. Chemokines are important mediators of cell signaling that operate both on normal cells and tumor cells and in the immune-cell compartment (Billottet et al, 2013). Among the chemokine receptors, CXCR3 mediate diverse biological functions and comes in two major isoforms the A and B isoform. We found that ligand affinities and conformational changes are very different for the A and B form. We have recently elucidated the role and mechanism of CXCR3A in GBM invasion (Boyé et al, 2017b). We demonstrated that agonist stimulation enhances in vitro cell migration and invasion in GBM cells. A major finding was that CXCR3A forms a complex with the trafficking receptor Lipoprotein-related receptor-1 (LRP1). Silencing of LRP1 leads to an increase in the magnitude of ligand-induced conformational change with CXCR3-A focalized at the cell membrane, leading to sustained receptor activity and increase in the migration. This was also clinically validated. Our study defines LRP1 as a new regulator of CXCR3 and indicates that targeting CXCR3-A in GBM may constitute a promising strategy to halt tumor cell invasion. The extracellular matrix (ECM) has morphogenic roles in tumors. Important ECM components are the matricellular proteins, called thrombospondins(THBS1-5) (Adams and Lawler 2011). We recently elucidated the complex role of THSB1 in GBM invasion (Daubon et al.2019). Global expression analysis revealed that THBS1 is up-regulated in GBMs and associated with a poor prognosis. We, furthermore, demonstrated that THBS1 did not activate TGFβ in GBM but that TGFβ1 induced the expression of THBS1 via SMAD3. Furthermore, GBM invasion is compromised when THBS1 is silenced in tumor cells. Thus, our data clearly show that THBS1 is not only involved in the regulation of angiogenesis in GBM, but also impacts the invasive behaviour of glioma cells by interacting with a molecule called CD47 expressed on the surface of GBM cells. RNA-sequencing after microdissection of central and peripheral tumour areas in a human PDX model demonstrated that THBS1 was the gene with the highest connectivity in the peripheral invasive tumour areas. Taken together, these data indicate that THBS1 plays important role in the infiltrative process in GBM. REFERENCES: Adams JC, Lawler J. Cold Spring Harb Perspect Biol. 2011;3:a009712 Billottet C, Quemener C, Bikfalvi A. Biochim Biophys Acta. 2013;1836:287- Boyé K et al. Sci Rep. 2017;7:10703 Boyé K et al. Nat Commun. 2017;8:1571 Daubon T et al, Nature Communications. Nat Commun. 2019 Mar 8;10(1):1146 Murphy-Ullrich JE, Poczatek M. Cytokine Growth Factor Rev. 2000 11:59

Association of CXCR1 and 2 expressions with gastric cancer metastasis in ex vivo and tumor cell invasion in vitro

Cytokine ◽  
2014 ◽  
Vol 69 (1) ◽  
pp. 6-13 ◽  
Author(s):  
Zhen Li ◽  
Ying Wang ◽  
Suiwei Dong ◽  
Chunlei Ge ◽  
Yanbin Xiao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Cancer Metastasis ◽  
Ex Vivo ◽  
Tumor Cell Invasion

scholarly journals Characterization of a synthetic peptide from type IV collagen that promotes melanoma cell adhesion, spreading, and motility.

1990 ◽  
Vol 111 (1) ◽  
pp. 261-270 ◽  
Author(s):  
M K Chelberg ◽  
J B McCarthy ◽  
A P Skubitz ◽  
L T Furcht ◽  
E C Tsilibary
Keyword(s):  
Cell Adhesion ◽  
Tumor Cell ◽  
Melanoma Cell ◽  
Cell Invasion ◽  
Synthetic Peptide ◽  
Type Iv Collagen ◽  
Cell Types ◽  
Tumor Cell Invasion ◽  
Type Iv

The adhesion and motility of tumor cells on basement membranes is a central consideration in tumor cell invasion and metastasis. Basement membrane type IV collagen directly promotes the adhesion and migration of various tumor cell types in vitro. Our previous studies demonstrated that tumor cells adhered and spread on surfaces coated with intact type IV collagen or either of the two major enzymatically purified domains of this protein. Only one of these major domains, the pepsin-generated major triple helical fragment, also supported tumor cell motility in vitro, implicating the involvement of the major triple helical region in type IV collagen-mediated tumor cell invasion in vivo. The present studies extend our previous observations using a synthetic peptide approach. A peptide, designated IV-H1, was derived from a continuous collagenous region of the major triple helical domain of the human alpha 1(IV) chain. This peptide, which has the sequence GVKGDKGNPGWPGAP, directly supported the adhesion, spreading, and motility of the highly metastatic K1735 M4 murine melanoma cell line, as well as the adhesion and spreading of other cell types, in a concentration-dependent manner in vitro. Furthermore, excess soluble peptide IV-H1, or polyclonal antibodies directed against peptide IV-H1, inhibited type IV collagen-mediated melanoma cell adhesion, spreading, and motility, but had no effect on these cellular responses to type I collagen. The full complement of cell adhesion, spreading, and motility promoting activities was dependent upon the preservation of the three prolyl residues in the peptide IV-H1 sequence. These studies indicate that peptide IV-H1 represents a cell-specific adhesion, spreading, and motility promoting domain that is active within the type IV collagen molecule.

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