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LINC01133 promotes the progression of cervical cancer via regulating miR-30a-5p/FOXD1.

Authors
  • Zhang, Dan1
  • Zhang, Yuyang2
  • Sun, Xiuyun1
  • 1 Department of Gynecology, General Hospital of Fushun Mining Bureau of Liaoning Health Industry Group, Fushun, Liaoning Province, China. , (China)
  • 2 The Second Department of Oncology, General Hospital of Fushun Mining Bureau of Liaoning Health Industry Group, Fushun, Liaoning Province, China. , (China)
Type
Published Article
Journal
Asia-Pacific journal of clinical oncology
Publication Date
Oct 20, 2020
Identifiers
DOI: 10.1111/ajco.13451
PMID: 33078907
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The prognosis of patients with recurrent or metastatic cervical cancer (CC) remains poor, and its incidence is especially high in developing countries. Multiple long noncoding RNAs are recently identified as crucial oncogenic factors or tumor suppressors. In this study, we explored the function and mechanism of LINC01133 during the progression of CC. Expression levels of LINC01133 and miR-30a-5p in 50 CC tissue samples were measured using quantitative real-time polymerase chain reaction. Immunohistochemistry and Western blot analysis were used to detect the expression of oncogene forkhead box D1 (FOXD1). The association between pathological indices and the expression level of LINC01133 was also analyzed. Human CC cell lines HeLa and SiHa were used as cell models. CCK-8 and bromodeoxyuridine assays were used to assess the effect of LINC01133 on CC cell line proliferation. Flow cytometry was used to study the effect of LINC01133 on CC apoptosis. Transwell assay was conducted to detect the effect of LINC01133 on migration and invasion. Furthermore, luciferase reporter assay was used to confirm the targeting relationship between miR-30a-5p to LINC01133. We observed that LINC01133 expression in CC clinical samples was significantly increased, with high expression associated with higher T stage and negative HPV infection of the patients. Its overexpression remarkably accelerated proliferation and metastasis of CC cells, with reduced apoptosis. LINC01133 knockdown suppressed the malignant phenotypes of CC cells. Overexpression of LINC01133 significantly reduced the expression of miR-30a-5p by sponging it and enhanced the expression of FOXD1. We report the overexpression of LINC01133 in CC sample and cell lines, which correlated with unfavorable pathological indices. LINC01133 was a sponge of tumor suppressor miR-30a-5p, and it enhanced the expression of FOXD1 indirectly and functioned as an oncogenic lncRNA in CC. © 2020 John Wiley & Sons Australia, Ltd.

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