Abstract
Cervical cancer (CC) is a huge threat to the health of women worldwide. Long non-coding RNA plasmacytoma variant translocation 1 gene (PVT1) was proved to be associated with the development of diverse human cancers, including CC. Nevertheless, the exact mechanism of PVT1 in CC progression remains unclear. Levels of PVT1, microRNA-503 (miR-503), and ADP ribosylation factor-like protein 2 (ARL2) were measured by quantitative reverse transcription-polymerase chain reaction or western blot assay. 3-(4,5)-Dimethylthiazole-2-y1)-2,5-biphenyl tetrazolium bromide (MTT) and flow cytometry were used to examine cell viability and apoptosis, respectively. For migration and invasion detection, transwell assay was performed. The interaction between miR-503 and PVT1 or ARL2 was shown by dual luciferase reporter assay. A nude mouse model was constructed to clarify the role of PVT1 in vivo. PVT1 and ARL2 expressions were increased, whereas miR-503 expression was decreased in CC tissues and cells. PVT1 was a sponge of miR-503, and miR-503 targeted ARL2. PVT1 knockdown suppressed proliferation, migration, and invasion of CC cells, which could be largely reverted by miR-503 inhibitor. In addition, upregulated ARL2 could attenuate si-PVT1-mediated anti-proliferation and anti-metastasis effects on CC cells. Silenced PVT1 also inhibited CC tumor growth in vivo. PVT1 knockdown exerted tumor suppressor role in CC progression via the miR-503/ARL2 axis, at least in part.
Highlights
Cervical cancer (CC) is the third most common cancer and the fourth most deadly malignancy among women in the world, with approximately 5.30 × 105 new CC cases and 2.75 × 105 CC-induced deaths every year [1,2]
We observed an obvious upregulation of plasmacytoma variant translocation 1 gene (PVT1) expression in CC tissues and cell lines, and silencing of PVT1 restricted cell proliferation, migration and invasion in vitro, as well as inhibited tumor growth in vivo
We further explored the targeted relationship among PVT1, miR-503, and ADP-ribosylation factor-like protein 2 (ARL2) and draw the conclusion that PVT1 directly targeted miR-503 and that ARL2 was the direct target of miR-503
Summary
Cervical cancer (CC) is the third most common cancer and the fourth most deadly malignancy among women in the world, with approximately 5.30 × 105 new CC cases and 2.75 × 105 CC-induced deaths every year [1,2]. Prognosis and treatment approaches of CC have developed greatly. Routine treatment methods, including surgery, chemotherapy, and radiotherapy, have not obviously elevated the 5-year survival rate of advanced patients, because of metastasis, recurrence, and drug resistance [3,4]. LINC00511 served as an oncogene in CC, and it had the potential to be an efficient biomarker and therapeutic target for patients with CC [8]. A former study indicated that lncRNA CCHE1 was considerably upregulated in CC tumor tissues, and it was identified as a prognostic biomarker and novel treatment target [9]. LncRNA plasmacytoma variant translocation 1 gene (PVT1), located at 8q24.21, was significantly upregulated and identified as an oncogene in the progression of diverse human
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