scholarly journals Metastatic colorectal cancer cells maintain the TGFβ program and use TGFBI to fuel angiogenesis

Theranostics ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 1626-1640
Author(s):  
Barbara Chiavarina ◽  
Brunella Costanza ◽  
Roberto Ronca ◽  
Arnaud Blomme ◽  
Sara Rezzola ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Cancer Cells ◽  
Colorectal Cancer Cells

Cell-SELEX-based selection of aptamers that recognize distinct targets on metastatic colorectal cancer cells

Biomaterials ◽  
2014 ◽  
Vol 35 (25) ◽  
pp. 6998-7007 ◽  
Author(s):  
Wan-Ming Li ◽  
Tao Bing ◽  
Jia-Yi Wei ◽  
Zhe-Zhou Chen ◽  
Di-Hua Shangguan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Cancer Cells ◽  
Colorectal Cancer Cells ◽  
Selection Of

Proteome analysis of metastatic colorectal cancer cells recognized by the lectin Helix pomatia agglutinin (HPA)

PROTEOMICS ◽  
2007 ◽  
Vol 7 (22) ◽  
pp. 4082-4089 ◽  
Author(s):  
Julien Saint-Guirons ◽  
Elton Zeqiraj ◽  
Udo Schumacher ◽  
Pamela Greenwell ◽  
Miriam Dwek
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Cancer Cells ◽  
Helix Pomatia ◽  
Proteome Analysis ◽  
Helix Pomatia Agglutinin ◽  
Colorectal Cancer Cells

scholarly journals Exosome-Derived ADAM17 Promotes Liver Metastasis in Colorectal Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Jinbing Sun ◽  
Zhihua Lu ◽  
Wei Fu ◽  
Kuangyi Lu ◽  
Xiuwen Gu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Metastatic Niche ◽  
Colorectal Cancer Cells ◽  
Niche Formation ◽  
Underlying Mechanisms

Exosomes derived from cancer cells are deemed important drivers of pre-metastatic niche formation at distant organs, but the underlying mechanisms of their effects remain largely unknow. Although the role of ADAM17 in cancer cells has been well studied, the secreted ADAM17 effects transported via exosomes are less understood. Herein, we show that the level of exosome-derived ADAM17 is elevated in the serum of patients with metastatic colorectal cancer as well as in metastatic colorectal cancer cells. Furthermore, exosomal ADAM17 was shown to promote the migratory ability of colorectal cancer cells by cleaving the E-cadherin junction. Moreover, exosomal ADAM17 overexpression as well as RNA interference results highlighted its function as a tumor metastasis-promoting factor in colorectal cancer in vitro and in vivo. Taken together, our current work suggests that exosomal ADAM17 is involved in pre-metastatic niche formation and may be utilized as a blood-based biomarker of colorectal cancer metastasis.

scholarly journals Parthenolide Induces Oxidative Stress and Impedes Cell Migration by Suppressing Wnt Pathway and Epithelial-Mesenchymal-Transition (EMT) in HCT-116 Metastatic Colorectal Cancer Cells

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 2313-2323
Author(s):  
Sananda Dey ◽  
Nensina Murmu ◽  
Mijanur R Molla ◽  
Sandeep K Dash ◽  
Biplab Giri
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Metastatic Colorectal Cancer ◽  
Cancer Cells ◽  
Metastatic Cancer ◽  
Pcr Analysis ◽  
Mesenchymal Transition ◽  
Anti Cancer ◽  
Colorectal Cancer Cells ◽  
Hct 116

Colorectal cancer (CRC) is a vital cause of cancer morbidity and mortality. 50% of CRC patients suffer from an aggressive metastatic disease which ultimately fallout in death. In metastatic cancer, tumour cells migrate, invade, and finally colonise to the distant organ by degrading their attachments with the extracellular matrix. Parthenolide (PTL) is a secondary metabolite of feverfew (Tanacetum parthenium) plant. It shows its cytotoxic effect towards cancer cells via different cellular signalling pathways like inhibition of NF-κB, STAT3, MAPK, JNK pathways, activation of p53 etc. In the present study, we have assessed anti-cancer and anti-metastatic potential of PTL against human HCT-116 metastatic colorectal cancer cells. Analysis of cellular oxidative status (GSH/GSSG) of PTL treated HCT-116 cells showed a significant decrease (p<0.05) in GSH level while GSSG level was increased significantly (p<0.05) on PTL treatment. PTL also increased the amount of intracellular reactive oxygen species. The qRT-PCR analysis revealed that PTL down-regulates c-fos, c-jun and N-cadherin expression and up-regulates E-cadherin expression indicating inhibition of cell migration and metastasis by EMT pathway. PTL inhibited the MMP-9 expression in a dose-dependent fashion and inhibited cancer cell migration by regulating Wnt/β-catenin signalling through the up-regulation of DKK-1 protein expression indicating PTL has a promising anti-cancer potential against HCT-116 metastatic colorectal carcinoma cells. 

scholarly journals Interleukin Receptor Antagonist Inhibits Matastatic Potential by Down-Regulating CXCL12/CXCR4 Signaling Axis in Colorectal Cancer

2021 ◽  
Author(s):  
Jiachi Ma ◽  
Wanqing Liang ◽  
Yaosheng Qiang ◽  
Lei Li ◽  
Jun Du ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Stromal Cells ◽  
Metastatic Potential ◽  
Colorectal Cancer Cell ◽  
Colorectal Cancer Cells ◽  
Ht 29 ◽  
High Liver

Abstract Background: The aim of this study was to investigate the co-operative role of CXCR4/ CXCL12 axis and IL-1Ra in metastatic processes mechanism by interactions between colorectal cancer cells and stromal cells in their microenvironment. Methods: Expression of IL-1a, CXCL12 and CXCR4 mRNA and proteins were determined by RT-PCR and Western blot. The effect of secreted level of CXCL12 by IL-1Ra on fibroblasts was measured by ELISA. CXCL12 regulate metastatic potential of colorectal cancer was evaluated by proliferation, invasion and angiogenesis assays, respectively, in which invasion and angiogenesis assays used an in vitro system consisting of co-cultured colorectal cells and stromal cells. Results: IL-1a was expressed in high liver metastatic colorectal cancer cell lines (HT-29 and WiDr). The colorectal cancer cell-derived IL-1a and rIL-1a significantly promoted CXCL12 expression by fibroblasts, and this enhancing effect can be significantly inhibited by IL-1Ra (P<0.01). CXCL12 not only enhanced the migration and proliferation of human umbilical vein endothelial cells (HUVECs), but also significantly enhanced angiogenesis (P<0.01). Furthermore, the high liver-metastatic colorectal cancer cell line (HT-29), which secretes IL-1a, significantly enhanced angiogenesis compared to the low liver-metastatic cell line (CaCo-2), which does not produce IL-1a (P<0.01). On the contrary, IL-1Ra can significantly inhibit migration, proliferation and angiogenesis (P<0.01). Conclusion: Autocrine IL-1a and paracrine CXCL12 co-enhances the metastatic potential of colorectal cancer cells; IL-1Ra can inhibit the metastatic potential of colorectal cancer cells via decrease IL-1a/CXCR4/CXCL12 signaling pathways.

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