RBPMS-AS1 sponges miR-19a-3p to restrain cervical cancer cells via enhancing PLCL1-mediated pyroptosis
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View abstract on PubMed
Summary
This summary is machine-generated.RBPMS-AS1 enhances pyroptosis and inhibits cervical cancer (CC) cell growth by sponging miR-19a-3p and upregulating PLCL1. This mechanism suppresses proliferation and epithelial-mesenchymal transition (EMT) in CC.
Area Of Science
- Molecular Oncology
- Cancer Biology
- Epigenetics
Background
- Cervical cancer (CC) remains a significant global health concern.
- Enhancing pyroptosis, a programmed cell death pathway, shows promise in inhibiting tumor cell proliferation and epithelial-mesenchymal transition (EMT).
Purpose Of The Study
- To identify key molecular players modulating pyroptosis in cervical squamous cell carcinoma (CESC).
- To elucidate the regulatory network involving RBPMS-AS1, miR-19a-3p, and PLCL1 in CC progression.
Main Methods
- Bioinformatic prediction and intersection analysis of microRNAs (miRNAs) sponged by RBPMS-AS1 and targeting PLCL1.
- Dual-luciferase reporter assays to confirm targeting relationships.
- In vitro assays including CCK-8, colony formation, qRT-PCR, and Western blot to assess cell viability, proliferation, and protein/gene expression.
Main Results
- RBPMS-AS1 and PLCL1 were found to be downregulated, while miR-19a-3p was upregulated in CESC tissues.
- RBPMS-AS1 overexpression suppressed CC cell proliferation, EMT markers (N-cadherin, vimentin), and miR-19a-3p expression, while increasing E-cadherin, PLCL1, and pyroptosis-related proteins (IL-1β, caspase-1, GSDMD).
- The effects of RBPMS-AS1 overexpression were reversed by miR-19a-3p, indicating a competitive sponging mechanism. A negative interplay was also confirmed between PLCL1 and miR-19a-3p.
Conclusions
- RBPMS-AS1 acts as a molecular sponge for miR-19a-3p, thereby relieving the inhibition on PLCL1.
- This regulatory axis promotes PLCL1-mediated pyroptosis, leading to the repression of cervical cancer cell growth and EMT.
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