Abstract
This study aims to explore the effects of microRNA-126 (miR-126) on tumor proliferation and angiogenesis of hepatocellular carcinoma (HCC) by targeting EGFL7. HCC tissues and adjacent normal tissues were obtained from 71 HCC patients. Immunohistochemistry (IHC) was conducted to detect expressions of EGFL7 and VEGF and the micro-vessel density (MVD). HCC cell lines were collected and assigned into the blank, miR-126 mimics, miR-126 inhibitors, miR-126 mimics negative control (NC), miR-126 inhibitors NC, si-EGFL7, and miR-126 inhibitors + si-EGFL7 groups. Expressions of miR-126 and EGFL7 mRNA were detected by qRT-PCR assay. The protein expressions of EGFL7 and VEGF were measured by Western blotting. MTT assay was used to measure the proliferation of HCC cells. Tumor xenograft model in nude mice was utilized to evaluate the influence of miR-126 on tumor growth. HCC tissues had higher miR-126 expression and lower EGFL7 mRNA expression than adjacent normal tissues. Compared with the blank, miR-126 mimic NC, miR-126 inhibitor NC and miR-126 inhibitors + si-EGFL7 groups, the protein expressions of EGFL7 and VEGF and cell proliferation were reduced in the miR-126 mimics and si-EGFL7 groups, while the opposite trend was found in the miR-126 inhibitors group. Compared with the blank and miR-126 inhibitors + siRNA-EGFL7 groups, tumor size, tumor weight, and MVD of transplanted tumors in nude mice were significantly reduced in the miR-126 mimics and siRNA-EGFL7 groups, while the opposite trend was found in the miR-126 inhibitors group. In conclusion, miR-126 could inhibit tumor proliferation and angiogenesis of HCC by down-regulating EGFL7 expression.
Highlights
Fast growth, high degrees of malignancy and metastasis, and high recurrence rate after surgical resection lead to poor outcomes for hepatocellular carcinoma (HCC) patients [1]
This study aims to explore the effects of microRNA-126 on tumor proliferation and angiogenesis of hepatocellular carcinoma (HCC) by targeting epidermal growth factor like domain 7 (EGFL7)
Our study investigated the relationship between miR-126 and EGFL7, as well as the effects of miR-126 on tumor proliferation and angiogenesis of HCC
Summary
High degrees of malignancy and metastasis, and high recurrence rate after surgical resection lead to poor outcomes for hepatocellular carcinoma (HCC) patients [1]. HCC is triggered by inactivation of tumor suppressor genes and abnormal activation of proto-oncogenes in liver cells, aberrantly regulating several signaling pathways that form complex molecular regulatory networks through “cross talk” to promote tumorigenesis [4]. Angiogenesis plays an important role in tumor formation, providing nutrients to tumor cells and promoting tumor growth and metastasis [5] Analyzing genes and pathways involved in HCC tumorigenesis and angiogenesis will reveal genetic changes important for improving HCC patient outcomes and enhancing diagnostic accuracy [6]. MiR126 is abundant in endothelial cells and can modulate blood vessel development and production through regulation of locally-expressed genes [8]. In the present study, we studied the effects of miR-126 on tumor proliferation and angiogenesis of HCC by targeting EGFL7
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