Correlation between SPARC, TGFβ1, Endoglin and angiogenesis mechanism in lung cancer

B. Wang, Z. Zhang, J. Tang, H. Tao, Z. Zhang

Article ID: 5307
Vol 32, Issue 6, 2018
DOI: https://doi.org/10.54517/jbrha5307
Received: 8 January 2019; Accepted: 8 January 2019; Available online: 8 January 2019; Issue release: 8 January 2019

Abstract

To study the relationship between Secreted protein, acidic and rich in cysteine (SPARC), Transforming growth factorβ1 (TGFβ1), Endoglin and angiogenesis in lung cancer, 40 cases of lung cancer specimens and 40 adjacent normal lung tissues specimens were collected and 10 cases from each were selected for preparation of tissue chip. CD34 (endothelial cell marker), Endoglin human α-Smooth muscle actin, and (α-SMA) markers were performed by immunohistochemical staining, and the immuno-phenotype and the relationship between different morphologies of the microvascular wall components were evaluated. The expression of SPARC mRNA and protein, TGFβ1 mRNA and protein and Endoglin in the remaining 30 cases of lung cancer were detected by immunohistochemistry and in-situ hybridization. The result shows that the positive rates of SPARC, TGFβ1 and Endoglin in lung cancer tissues were significantly higher than those in adjacent normal lung tissues (P less than 0.05). The expression of SPARC and TGFβ1 was negatively correlated with lung cancer. When the positive expression of SPARC increased, the micro-vessel density (MVD) marked by Endoglin decreased gradually; while the positive expression of TGFβ1 increased, MVD increased gradually, and SPARC, TGFβ1 and MVD were correlated (P less than0.05). High SPARC mRNA expression in lung cancer tissues could inhibit the progression of lung cancer, while high TGFβ1 mRNA expression can promote the progression of lung cancer and participate in the metastasis of lung cancer. To sum up, the angiogenesis of lung cancer may be related to the interaction of SPARC, TGFβ1 and Endoglin.


Keywords

lung cancer;SPARC;TGFβ1;Endoglin;angiogenesis mechanism


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Supporting Agencies



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