LncRNA STXBP5-AS1 suppressed cervical cancer progression via targeting miR-96-5p/PTEN axis
Shiqing Shao1, Chen Wang1, Shelian Wang1
1Department of Obstetrics and Gynecology, Huaihe Hospital of Henan University, Kaifeng, Henan Province, China.
Abstract:
Long non-coding RNAs (lncRNAs) play important roles in tumor initiation and progression, including cervical cancer (CC). However, the effects and underlying mechanisms of STXBP5-AS1 in CC are still unknown. The expression of STXBP5-AS1, miR-96-5p, and PTEN in CC was explored by qRT-PCR. CCK-8 and transwell assays were used to determine the roles of STXBP5-AS1 on CC progression. Luciferase report assay and RIP assay were used to explore the correction between STXBP5-AS1, miR-96-5p and PTEN in CC. In our study, we showed that the expression of STXBP5-AS1 and PTEN was reduced while miR-96-5p expression was upregulated in CC. STXBP5-AS1 overexpression significantly reduced CC cells proliferation and invasion ability by suppressing miR-96-5p expression. MiR-96-5p promoted CC cells progression via regulating PTEN expression. Furthermore, STXBP5-AS1 was identified as a ceRNA to upregulate PTEN via sponging miR-96-5p in CC. Taken together, our findings revealed that STXBP5-AS1 might function as a ceRNA to drive CC cells proliferation and invasion via regulating miR-96-5p/PTEN axis.
Insights
Long non-coding RNA STXBP5-AS1 suppresses cervical cancer (CC) progression by inhibiting miR-96-5p. STXBP5-AS1 acts as a ceRNA to upregulate PTEN, reducing CC cell proliferation and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are implicated in tumor initiation and progression, including cervical cancer (CC).
- The specific role and molecular mechanisms of STXBP5-AS1 in CC remain largely uncharacterized.
- Understanding lncRNA functions is crucial for developing novel therapeutic strategies for cervical cancer.
Purpose of the Study:
- To investigate the expression levels of STXBP5-AS1, miR-96-5p, and PTEN in cervical cancer tissues.
- To elucidate the functional role of STXBP5-AS1 in regulating CC cell proliferation and invasion.
- To explore the underlying molecular mechanism involving STXBP5-AS1, miR-96-5p, and PTEN in CC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
- Cell Counting Kit-8 (CCK-8) and Transwell assays to assess cell proliferation and invasion.
- Luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm molecular interactions.
Main Results:
- STXBP5-AS1 and PTEN expression were downregulated, while miR-96-5p was upregulated in CC tissues.
- Overexpression of STXBP5-AS1 significantly inhibited CC cell proliferation and invasion by suppressing miR-96-5p.
- MiR-96-5p promoted CC progression by regulating PTEN, and STXBP5-AS1 functioned as a competing endogenous RNA (ceRNA) upregulating PTEN via sponging miR-96-5p.
Conclusions:
- STXBP5-AS1 acts as a tumor suppressor in cervical cancer.
- The STXBP5-AS1/miR-96-5p/PTEN axis plays a critical role in regulating CC cell proliferation and invasion.
- STXBP5-AS1 may serve as a potential therapeutic target for cervical cancer treatment.
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