ArticleInvestigational new drugs2013
Expression of matrix macromolecules and functional properties of EGF-responsive colon cancer cells are inhibited by panitumumab.
Article in Investigational new drugs, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Non-Integrin Laminin Receptors: Shedding New Light and Clarity on Their Involvement in Human Diseases.International journal of molecular sciences · 2025Review
- Integrative analysis revealed that distinct cuprotosis patterns reshaped tumor microenvironment and responses to immunotherapy of colorectal cancer.Frontiers in immunology · 2023Article
- Ramucirumab combination with sorafenib enhances the inhibitory effect of sorafenib on HepG2 cancer cells.Scientific reports · 2022Article
- Syndecan-4 affects myogenesis via Rac1-mediated actin remodeling and exhibits copy-number amplification and increased expression in human rhabdomyosarcoma tumors.Cellular and molecular life sciences : CMLS · 2022Article
- Syndecan-4 as a Pathogenesis Factor and Therapeutic Target in Cancer.Biomolecules · 2021Review
- Heparan sulfate proteoglycans as targets for cancer therapy: a review.Cancer biology & therapy · 2020Review
- The impact of RNA binding motif protein 4-regulated splicing cascade on the progression and metabolism of colorectal cancer cells.Oncotarget · 2015Article
- Study on extracellular matrix metalloproteinase inducer and human epidermal growth factor receptor-2 protein expression in papillary thyroid carcinoma using a quantum dot-based immunofluorescence technique.Experimental and therapeutic medicine · 2015Article
- Syndecan-1 expression is associated with tumor size and EGFR expression in colorectal carcinoma: a clinicopathological study of 230 cases.International journal of medical sciences · 2015Article
- Cell-matrix interactions: focus on proteoglycan-proteinase interplay and pharmacological targeting in cancer.The FEBS journal · 2014Review
- Hypomethylation of the MMP7 promoter and increased expression of MMP7 distinguishes the basal-like breast cancer subtype from other triple-negative tumors.Breast cancer research and treatment · 2014Article
- Syndecans as modulators and potential pharmacological targets in cancer progression.Frontiers in oncology · 2014Review
- Preparation and toxicological assessment of functionalized carbon nanotube-polymer hybrids.PloS one · 2014Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epidermal growth factor receptor (EGFR) is a member of the HER family receptors and its activation induced by its natural ligand EGF results in colon cancer growth and progression. Panitumumab (pmAb) is a fully human IgG2 anti-EGFR antibody that blocks the EGFR actions. In the present study, we evaluated the effects of pmAb on the EGF-mediated cellular responses in a panel of colon cancer cells (HCT-8, HT-29, DLD-1 and HCT-116). HCT-1116 and DLD-1 cells showed no significant EGF-dependent cell proliferation; HT-29 and HCT-8 exhibited an EGF-dependent proliferation, with HCT-8 cells to be the most responsive with significant EGFR phosphorylation upon treatment with EGF. The effects of pmAb were then evaluated in the most EGF-responsive cells, HCT-8. In that respect, pmAb impedes the signaling cascade mediated by EGFR intracellular phosphorylation and activity of focal adhesion kinase (FAK) as well as the EGF-induced invasive and migratory potential of colon cancer cells. At the level of matrix effectors implicated in colon cancer progression we report that pmAb is a potent inhibitor of constitute and EGF-mediated gene expression of certain matrix effectors, such as membrane-type 1 metalloproteinase (MT1-MMP), extracellular metalloproteinases inducer (EMMPRIN), urokinase plasminogen activator (uPA) and syndecan-4. The obtained data demonstrated that pmAb is a specific blocker of EGF-mediated EGFR activation, resulting in a significant inhibition of colon cancer cell proliferation in early stages of growth, migration and invasiveness as well as of matrix effector implicated in cancer progression.
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