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Circ_0030411 aggravates cisplatin-resistance in non-small cell lung cancer by serving as a miR-495-3p sponge to
Jing Zhang1, Xiaohai Cui1, Hangying Qu1
1Department of Thoracic Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Abstract:
Circular RNAsplay important modulators in cisplatin (DDP) resistant non-small cell lung cancer (NSCLC). Herein, the role and mechanism of circ_0030411 in DDP-resistant NSCLC was explored. Circ_0030411, miR-495-3p, CCND1, PCNA, Bax, E-cadherin, and ki-67 expression were examined byqRT-PCR, western blot and IHC. DDP resistance, cell proliferation, apoptosis, and motility were assessed usingCCK, EdU flow cytometry, and transwell. Xenograft tumour model was established to explore the role of circ_0030411 in DDP-resistant NSCLC. Interaction between miR-495-3p and circ_0030411 or CCND1 wasverified via luciferase reporterand RIP. Circ_0030411 and CCND1 were increased in DDP-resistant NSCLC tissues and cells, andmiR-495-3p level was decreased. Circ_0030411 knockdown hindered cell growth, migration, invasion, in DDP-resistant NSCLC cells, and improved DDP sensitivityof NSCLC in vivo. Mechanistically, circ_0030411 acted as a sponge of miR-495-3p to affect CCND1expression. Circ_0030411 facilitated DDP resistance by regulating the miR-495-3p/CCND1 axis, highlighting a promising target for NSCLC patients.
Insights
Circular RNA circ_0030411 promotes cisplatin resistance in non-small cell lung cancer (NSCLC) by sponging miR-495-3p and upregulating CCND1. Targeting this axis may improve NSCLC treatment sensitivity.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Circular RNAs (circRNAs) are key regulators in drug-resistant cancers.
- Cisplatin resistance in non-small cell lung cancer (NSCLC) poses a significant clinical challenge.
- The specific role of circ_0030411 in cisplatin-resistant NSCLC remains largely unexplored.
Purpose of the Study:
- To investigate the function and mechanism of circ_0030411 in cisplatin-resistant NSCLC.
- To elucidate the regulatory pathway involving circ_0030411, miR-495-3p, and CCND1.
- To assess the therapeutic potential of targeting circ_0030411 in NSCLC.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blot, and immunohistochemistry (IHC) for gene expression analysis.
- Cell Counting Kit (CCK), EdU incorporation, and transwell assays to evaluate cell proliferation, apoptosis, and motility.
- Luciferase reporter assays and RNA immunoprecipitation (RIP) to confirm molecular interactions.
- Xenograft tumor models in vivo to assess the effect on tumor growth and drug sensitivity.
Main Results:
- Circ_0030411 and CCND1 expression were elevated, while miR-495-3p was decreased in cisplatin-resistant NSCLC tissues and cells.
- Knockdown of circ_0030411 suppressed proliferation, migration, and invasion, and enhanced cisplatin sensitivity in NSCLC cells and in vivo.
- Circ_0030411 functions as a molecular sponge for miR-495-3p, thereby regulating CCND1 expression.
- The miR-495-3p/CCND1 axis was identified as a key mechanism through which circ_0030411 promotes cisplatin resistance.
Conclusions:
- Circ_0030411 significantly contributes to cisplatin resistance in NSCLC by modulating the miR-495-3p/CCND1 pathway.
- Circ_0030411 represents a potential diagnostic biomarker and therapeutic target for overcoming drug resistance in NSCLC patients.
- Targeting the circ_0030411/miR-495-3p/CCND1 axis offers a promising strategy for improving NSCLC treatment outcomes.
