4.2 Article

PVT1 Promotes Angiogenesis by Regulating miR-29c/Vascular Endothelial Growth Factor (VEGF) Signaling Pathway in Non-Small-Cell Lung Cancer (NSCLC)

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MEDICAL SCIENCE MONITOR
卷 25, 期 -, 页码 5418-5425

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INT SCIENTIFIC INFORMATION, INC
DOI: 10.12659/MSM.917601

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Angiogenesis Inducing Agents; Carcinoma, Non-Small-Cell Lung; Vascular Endothelial Growth Factor A

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Background: Lung cancer is a common tumor. Non-small-cell lung cancer (NSCLC) accounts for over 85% of lung cancer and has a high degree of malignancy. Angiogenesis plays an important role in NSCLC progression. Some studies have found that PVT1 can promote angiogenesis in tumor tissues, but the role of PVT1 in angiogenesis in NSCLC, as well as the underlying mechanism, is unclear. Material/Methods: To explore the role of PVT1 in NSCLC, qRT-PCR, Western blot, luciferase reporter assay, and ELISA were carried out for detecting the relationship among PVT1, miR-29c, and VEGF. Tube formation assay was used to assess the role of PVT1 in angiogenesis in NSCLC. Results: Our results showed that higher PVT1 was expressed in NSCLC and the elevated PVT1 was closely related to angiogenesis and poor prognosis in NSCLC. Further functional analysis showed that higher PVT1 expression could promote angiogenesis by regulating VEGF in NSCLC. Mechanistically, the luciferase reporter assay confirmed that VEGF was the targeted gene of miR-29c. In addition, we found that miR-29c is an inhibitory target of PVT1. Conclusions: We found that PVT1 promotes angiogenesis through targeting the miR-29c/VEGF signaling pathway in NSCLC.

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