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Published on: August 2, 2024
LncRNA MEG3 suppressed the progression of ovarian cancer via sponging miR-30e-3p and regulating LAMA4 expression
Yang Liu1, Yangchun Xu2, Lei Ding3
1Department of Radiation Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, 450008 Henan China.
Background:
Ovarian cancer (OC) is a common female reproductive malignancy with a high mortality rate. Although LAMA4 was observed to be downregulated in OC cells, its mechanism in regulating OC metastasis is still unknown. This study aimed to investigate the effect of LAMA4 and its mechanism on OC.
Methods:
To achieve this aim, a microarray analysis was performed to screen out the key genes involved in OC pathogenesis. Western-blot and qRT-PCR assays were also carried out to detect protein and mRNA expressions, respectively. A luciferase reporter assay was further used to confirm the direct interaction of miR-30e-3p with MEG3, and the direct interaction of miR-30e-3p with LAMA4 mRNA. Cytological experiments (CCK8, colony formation assay, wound-healing assay etc.) were then performed to explore the roles of miR-30e-3p, MEG3, and LAMA4 in OC cells.
Results:
After carrying out microarray analysis, LAMA4 was confirmed as a key gene associated with OC pathogenesis. Research results proved that miR-30e-3p was markedly upregulated, while MEG3 and LAMA4 were noticeably downregulated in OC tissues and cells. The overexpression of LAMA4 significantly impaired the proliferation, migration, and invasion of OC cells. However, the upregulation of MEG3 increased the expression of LAMA4 by sponging miR-30e-3p, which alleviated the malignancy of OC cells.
Conclusions:
Observations showed that forced LAMA4 overexpression could inhibit OC progression, which was regulated by MEG3 via sponging miR-30e-3p. The findings of this research could provide new insights into the mechanism by which MEG3 and LAMA4 exert their anti-oncogenic roles in OC progression.Trial registration Not applicable.
Insights
Laminin subunit alpha-4 (LAMA4) overexpression inhibits ovarian cancer (OC) progression. MEG3 regulates LAMA4 by sponging miR-30e-3p, alleviating OC malignancy.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Ovarian cancer (OC) is a prevalent malignancy with high mortality.
- The role of Laminin subunit alpha-4 (LAMA4) in OC metastasis remains unclear, despite its observed downregulation.
- This study investigates LAMA4's mechanism in OC progression.
Purpose of the Study:
- To identify key genes in OC pathogenesis.
- To elucidate the regulatory mechanism of LAMA4 in OC.
- To explore the anti-oncogenic roles of MEG3 and LAMA4 in OC.
Main Methods:
- Microarray analysis to screen key genes in OC.
- Western blot and qRT-PCR to assess gene and protein expression.
- Luciferase reporter assays to confirm interactions between miR-30e-3p, MEG3, and LAMA4 mRNA.
- Cellular assays (CCK8, colony formation, wound healing) to evaluate the functions of miR-30e-3p, MEG3, and LAMA4.
Main Results:
- LAMA4 identified as a key gene in OC pathogenesis.
- miR-30e-3p upregulated, while MEG3 and LAMA4 downregulated in OC tissues/cells.
- LAMA4 overexpression significantly inhibited OC cell proliferation, migration, and invasion.
- MEG3 upregulation increased LAMA4 expression by sponging miR-30e-3p, reducing OC malignancy.
Conclusions:
- Forced LAMA4 overexpression inhibits OC progression.
- MEG3 regulates LAMA4 via sponging miR-30e-3p, contributing to anti-oncogenic effects in OC.
- Findings offer new insights into the anti-cancer mechanisms of MEG3 and LAMA4 in OC progression.
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