CDK8 mediated colon cancer growth in the liver through downregulation of matrix metalloproteinase (MMP) inhibitor TIMP3 via TGFβ/SMAD-driven expression of a TIMP3-targeting microRNA, miR-181b, along with induction of Mmp3 in murine or MMP9 in human colon cancer cells via Wnt/β-catenin-driven transcription.
AFAP1-AS1 knockdown also increased the expression of E-cadherin and ZO-1 while inhibited the expression of Vimentin, MMP9, ZEB1 and β-catenin, suggesting that AFAP1-AS1 is involved in the epithelial-mesenchymal transition (EMT) process of CC.
DNM3 may weaken the malignant behavior of colon cancer and may have promoted the invasion and migration of colon cancer by regulating the expression of MMP-2 and MMP-9.
Extensive imaging studies using a mouse model of human colon cancer revealed that the overexpression of MMP-9 and abnormal microenvironmental pH quantitatively visualized by this dual-ratiometric probe are spatially heterogeneous and synergistically guide the tumor invasion in vivo.
Transcriptional and posttranscriptional levels of CaMKIIin tissue samples and MMP2, MMP9 and TIMP-1 expression in the human colon cancer cell line HCT116 were assessed by qRT-PCR and western blot.
In addition, it was also observed that miR-7 regulated the proliferation and migration of CC by regulating the protein expression of FAK, therefore, regulating the expression of matrix metalloproteinase (MMP)-2 and MMP-9. miR-7 inhibited the proliferation and migration of CC cells by regulating FAK.
These results implicate the key role of CCR1 in colon cancer metastasis in this mouse model, and explain why both MMP9 and MMP2 are essential as genetically demonstrated previously.
We compared IP-MRM to ELISA for the analysis of six colon cancer biomarker candidates (metalloproteinase inhibitor 1 (TIMP1), cartilage oligomeric matrix protein (COMP), thrombospondin-2 (THBS2), endoglin (ENG), mesothelin (MSLN) and matrix metalloproteinase-9 (MMP9)) in plasma from colon cancer patients and noncancer controls.
In comparison with the colon cancer cell lines incubated in 5% CO(2) only, the invasive ability of cells increased in all the colon cancer cell lines subjected to incubation in 20% CO(2) followed by incubation in 5% CO(2), with a concomitant increase in the mRNA expressions of matrix metalloproteinase-2 (MMP2) and MMP9.
In the present study, we demonstrated the role of exogenous NO levels in the regulation of MMP2 and MMP9 (gelatinases A and B) in colon cancer cell line WiDr and its inhibition with emodin (a naturally occurring anthraquinone).
Matrix metalloproteinases (MMPs), in particular MMP-2 and MMP-9, are involved in colon cancer progression and metastasis due to their ability to degrade extracellular matrix (ECM) components.