ArticleCurrent medical science2021
GDF-15 Level Correlates with CMKLR1 and VEGF-A in Tumor-free Margin in Colorectal Cancer.
Article in Current medical science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Cytoplasmic LIM domain only 2 enhances tumor endothelial cell migration through integrin β1-mediated focal adhesion signaling.Acta neuropathologica communications · 2026Article
- Automatically quantifying spatial heterogeneity of immune and tumor hypoxia environment and predicting disease-free survival for patients with rectal cancer.Cancer immunology, immunotherapy : CII · 2025Article
- A Citrate Synthase Splice Variant Rewires the TCA Cycle to Promote Colorectal Cancer Progression.Cancer research · 2025Article
- GDF15 promotes gallbladder cancer progression by activating the NF-κB mediated Vascular Endothelial Growth Factor A (VEGFA) expression.American journal of cancer research · 2025Article
- Macrophages as a Source and Target of GDF-15.International journal of molecular sciences · 2024Review
- Regulation of VEGF-A expression and VEGF-A-targeted therapy in malignant tumors.Journal of cancer research and clinical oncology · 2024Review
- Role and Mechanism of Growth Differentiation Factor 15 in Chronic Kidney Disease.Journal of inflammation research · 2024Review
- B7H3 Role in Reshaping Immunosuppressive Landscape in MSI and MSS Colorectal Cancer Tumours.Cancers · 2023Article
- Predictive Value of GDF-15 and sST2 for Pulmonary Hypertension in Acute Exacerbation of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Article
- Investigation of the Disparities in Ultrasound Imaging Features of miR-323, miR-409-3p, and VEGF Expression Scales in Different Clinicopathological Features of Prostate Carcinoma and Their Correlation with Prognosis.BioMed research international · 2022Article
- A Chemerin Peptide Analog Stimulates Tumor Growth in Two Xenograft Mouse Models of Human Colorectal Carcinoma.Cancers · 2021Article
- The Concentration of CMKLR1 Expression on Clinicopathological Parameters of Colorectal Cancer: A Preliminary Study.Medicina (Kaunas, Lithuania) · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is the third most frequently diagnosed cancer worldwide, responsible for over 880 000 deaths each year. Growth/differentiation factor 15 (GDF-15) is reported to be a promising diagnostic and prognostic factor in CRC. It induces pleiotropic effects in tumor cells: proliferation, stemness, invasion and metastasis. Some studies indicate that GDF-15 may stimulate angiogenesis in malignant neoplasms. However, it has not been investigated in CRC yet. The aim of our study was to determine the level of GDF-15 and the concentrations of hypoxia-inducible factor-1α (HIF-1α), VEGF-A and chemokine-like receptor 1 (CMKLR1) in tumor and margin specimens of CRC in relation to histological grade and TNM staging. The study comprised 33 samples of tumor and margin tissues obtained from CRC patients. To assess the concentration of GDF-15, HIF-1α, VEGF-A and CMKLR1, commercially available enzyme-linked immunosorbent assay (ELISA) kits were used. We found significantly increased levels of GDF-15 and CMKLR1 in tumor tissue compared to margin tissue and higher concentrations of HIF-1α and VEGF-A in margin tissue than in tumor tissue. The levels of GDF-15 and HIF-1α were significantly correlated with VEGF-A and CMKLR1 in margin tissue. In CRC, the increased level of GDF-15 might stimulate angiogenesis through upregulation of HIF-1α, VEGF A and CMKLR1 expression. Our study is the first one to reveal the correlation between the levels of GDF-15 and CMKLR1 in CRC. The elevated levels of HIF-1α and VEGF-A in tumor-free margin tissues suggest that noncancer cells in the tumor microenvironment are an important source of proangiogenic factors.
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