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LncRNA JPX promotes cervical cancer progression by modulating miR-25-3p/SOX4 axis
Xia Chen1, Jingxiu Yang1, Yuping Wang1
1Department of Gynaecology and Obstetrics, The Affiliated Lianyungang Oriental Hospital of Xuzhou Medical University, No. 57 Zhong'hua Rest Road, Lianyun District, Lianyungang, 222042 Jiangsu China.
Background:
The long noncoding RNA (lncRNA) JPX is a molecular switch for X-chromosome inactivation. Accumulating studies have shown that the aberrant expression and function of lncRNAs are involved in the occurrence and development of tumors. However, the functional importance and mechanism of the action of lncRNA JPX in cervical cancer (CC) remain unknown.
Method:
In this study, qRT-PCR and western blotting were used to evaluate the mRNA or protein expression of JPX, miR-25-3p and SOX4 in CC tissues and cell lines. StarBase v2.0 database, luciferase reporter assay and RNA immunoprecipitation assay were used to explore the relationship between JPX and miR-25-3p. EdU assay, CCK-8 assay and transwell assay were utilized to evaluate the proliferation, migration and invasion of CC cells. The tumor xenograft assay in nude mice was performed to demonstrate the role of the JPX/miR-25-3p/SOX4 axis in CC.
Results:
We found that JPX was markedly upregulated, whereas miR-25-3p was markedly downregulated in CC tissues and cell lines, and the expression of JPX was negatively correlated with miR-25-3p in CC tissues. Moreover, overexpression of JPX increased proliferation, migration and invasion of HeLa cells, whereas knockdown of JPX decreased proliferation, migration and invasion of HeLa cells. In contrast to JPX, overexpression of miR-25-3p decreased proliferation, migration and invasion of HeLa cells. In addition, knockdown of JPX was found to inhibit HeLa cell viability and tumor development via up-regulating the expression of miR-25-3p and inhibiting the expression of SOX4.
Conclusions:
Our study demonstrates that JPX promotes cervical cancer progression through modulating the miR-25-3p/SOX4 axis, and may serve as a potential target for CC therapy.
Insights
The long noncoding RNA JPX promotes cervical cancer by regulating miR-25-3p and SOX4. This finding suggests JPX as a potential therapeutic target for cervical cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long noncoding RNAs (lncRNAs) are implicated in tumor development.
- The role of lncRNA JPX in cervical cancer (CC) is currently unknown.
- JPX acts as a molecular switch for X-chromosome inactivation.
Purpose of the Study:
- To investigate the functional role and mechanism of lncRNA JPX in cervical cancer.
- To explore the relationship between JPX, miR-25-3p, and SOX4 in CC.
- To determine if the JPX/miR-25-3p/SOX4 axis is a potential therapeutic target for CC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and western blotting assessed JPX, miR-25-3p, and SOX4 expression.
- Bioinformatic analysis (StarBase v2.0), luciferase reporter, and RNA immunoprecipitation assays investigated the JPX-miR-25-3p interaction.
- Cell proliferation, migration, and invasion were evaluated using EdU, CCK-8, and Transwell assays.
- In vivo tumor xenograft assays in nude mice demonstrated the axis's role in CC progression.
Main Results:
- JPX was significantly upregulated, while miR-25-3p was downregulated in CC tissues and cell lines.
- JPX overexpression enhanced, and knockdown inhibited, HeLa cell proliferation, migration, and invasion.
- JPX knockdown suppressed HeLa cell viability and tumor growth by upregulating miR-25-3p and downregulating SOX4.
- JPX expression negatively correlated with miR-25-3p in CC tissues.
Conclusions:
- lncRNA JPX promotes cervical cancer progression by modulating the miR-25-3p/SOX4 axis.
- The JPX/miR-25-3p/SOX4 pathway represents a potential therapeutic target for cervical cancer.
- Understanding lncRNA JPX's mechanism offers insights into cervical cancer development.
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