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Anti-LRP/LR specific antibody IgG1-iS18 significantly impedes adhesion and invasion in early and late stage colorectal carcinoma cells.

ABSTRACT: Cancer is a highly complex disease that has become one of the leading causes of death globally. Metastasis, a major cause of cancer deaths, requires two crucial events known as adhesion and invasion. The 37kDa/67kDa laminin receptor [laminin receptor precursor/high-affinity laminin receptor (LRP/LR)] enhances these two steps, consequently aiding in cancer progression. In this study, the role of LRP/LR in adhesion and invasion of early (SW-480 & HT-29) and late (DLD-1) stage colorectal cancer cells has been investigated. Western blotting revealed that early and late stage colorectal cancer cells contained significantly higher total LRP/LR levels compared to poorly invasive MCF-7 breast cancer control cells. Flow cytometry revealed that all three stages of colorectal cancer displayed significantly higher cell surface LRP/LR levels. Furthermore, upon treatment of the colorectal cancer cells with the anti-LRP/LR specific antibody IgG1-iS18, adhesion to laminin-1 was significantly reduced in all three stages. Each stage's invasive potential was determined using the Matrigel™ invasion assay, which revealed that invasion is significantly impeded in all three colorectal cancer stages when the cells are incubated with IgG1-iS18. In addition, Pearson's correlation coefficients propose that both total and cell surface LRP/LR levels are directly proportional to the adhesive and invasive potential of all three stages of colorectal cancer. Hence, these findings indicate the potential for the use of the IgG1-iS18 antibody as a promising therapeutic tool for colorectal cancer patients of early and late stage.

SUBMITTER: Vania L

PROVIDER: S-EPMC5082296 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature

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Anti-LRP/LR specific antibody IgG1-iS18 significantly impedes adhesion and invasion in early and late stage colorectal carcinoma cells.

Vania Leila L Chetty Carryn J CJ Ferreira Eloise E Weiss Stefan F T SFT

Molecular medicine (Cambridge, Mass.) 20160908

Cancer is a highly complex disease that has become one of the leading causes of death globally. Metastasis, a major cause of cancer deaths, requires two crucial events known as adhesion and invasion. The 37kDa/67kDa laminin receptor [laminin receptor precursor/high-affinity laminin receptor (LRP/LR)] enhances these two steps, consequently aiding in cancer progression. In this study, the role of LRP/LR in adhesion and invasion of early (SW-480 & HT-29) and late (DLD-1) stage colorectal cancer cel ...[more]

PMID: 27611822

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Project description:NELL-1, an osteoinductive protein, has been shown to regulate skeletal ossification. Interestingly, an interstitial 11p14.1-p15.3 deletion involving the Nell-1 gene was recently reported in a patient with short stature and delayed fontanelle closure. Here we sought to define the role of Nell-1 in endochondral ossification by investigating Nell-1-specific inactivation in Col2α1-expressing cell lineages. Nell-1flox/flox ; Col2α1-Cre+ (Nell-1Col2α1 KO) mice were generated for comprehensive analysis. Nell-1Col2α1 KO mice were born alive but displayed subtle femoral length shortening. At 1 and 3 months postpartum, Nell-1 inactivation resulted in dwarfism and premature osteoporotic phenotypes. Specifically, Nell-1Col2α1 KO femurs and tibias exhibited significantly reduced length, bone mineral density (BMD), bone volume per tissue volume (BV/TV), trabecular number/thickness, cortical volume/thickness/density, and increased trabecular separation. The decreased bone formation rate revealed by dynamic histomorphometry was associated with altered numbers and/or function of osteoblasts and osteoclasts. Furthermore, longitudinal observations by in vivo micro-CT showed delayed and reduced mineralization at secondary ossification centers in mutants. Histologically, reduced staining intensities of Safranin O, Col-2, Col-10, and fewer BrdU-positive chondrocytes were observed in thinner Nell-1Col2α1 KO epiphyseal plates along with altered distribution and weaker expression level of Ihh, Patched-1, PTHrP, and PTHrP receptor. Primary Nell-1Col2α1 KO chondrocytes also exhibited decreased proliferation and differentiation, and its downregulated expression of the Ihh-PTHrP signaling molecules can be partially rescued by exogenous Nell-1 protein. Moreover, intranuclear Gli-1 protein and gene expression of the Gli-1 downstream target genes, Hip-1 and N-Myc, were also significantly decreased with Nell-1 inactivation. Notably, the rescue effects were diminished/reduced with application of Ihh signaling inhibitors, cyclopamine or GANT61. Taken together, these findings suggest that Nell-1 is a pivotal modulator of epiphyseal homeostasis and endochondral ossification. The cumulative chondrocyte-specific Nell-1 inactivation significantly impedes appendicular skeletogenesis resulting in dwarfism and premature osteoporosis through inhibiting Ihh signaling and predominantly altering the Ihh-PTHrP feedback loop. © 2018 American Society for Bone and Mineral Research.

Dataset Information

Anti-LRP/LR specific antibody IgG1-iS18 significantly impedes adhesion and invasion in early and late stage colorectal carcinoma cells.

Publications

Anti-LRP/LR specific antibody IgG1-iS18 significantly impedes adhesion and invasion in early and late stage colorectal carcinoma cells.

Similar Datasets

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