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Updated: Jun 22, 2025
Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
CircPDSS1 (hsa_circ_0017998) silencing induces ferroptosis in non-small-cell lung cancer cells by modulating the
Ling Wu1, Ni Li2, Linwen Zhu2
1Women and Children's Hospital of Ningbo University, Ningbo, Zhejiang 315000, China.
Background:
Circular RNAs (circRNAs) regulate the tumorigenesis of non-small-cell lung cancer (NSCLC). CircPDSS1 (hsa_circ_0017998) has been newly discovered, and its role in NSCLC remains elusive. We aimed to investigate the functional roles and downstream targets of circPDSS1 in NSCLC cells.
Materials And Methods:
Cellular viabilities were measured through the Cell Counting Kit-8 (CCK-8) assay, whereas cell death was assessed through flow cytometry. The lactate dehydrogenase activity, malondialdehyde levels, ferrous iron, and reactive oxygen species were measured using commercial assay kits. The interaction between circPDSSA/ microRNA-137 (miR-137) and miR-137/solute carrier family 7 member 11 (SLC7A11) was assayed through a dual luciferase activity assay. Finally, the mRNA and protein levels were measured using real-time reverse transcriptase-polymerase chain reaction and western blots, respectively.
Results:
CircPDSS1 expression was upregulated in NSCLC cells, compared with healthy lung cells. CircPDSS1 silencing suppressed the viability of NSCLC cells. Additionally, circPDSS1 knockdown induced ferroptosis rather than other types of cell death in NSCLC cells. Mechanically, circPDSS1 functions as a "sponge" to inversely control miR-137 expression, which directly targets SLC7A11. Moreover, circPDSS1 silencing causes the downregulation of glutathione peroxidase 4 (GPX4) and glutamate-cysteine ligase catalytic subunit (GCLC).
Conclusions:
Targeting the circPDSS1/miR-137/SLC7A11/GPX4/GCLC axis may be a promising strategy to kill NSCLC cells.
Insights
Circular RNAs (circRNAs) like circPDSS1 promote non-small-cell lung cancer (NSCLC) by sponging miR-137, leading to increased cell viability. Targeting this circPDSS1/miR-137 pathway may offer a new strategy for NSCLC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Circular RNAs (circRNAs) are implicated in non-small-cell lung cancer (NSCLC) tumorigenesis.
- The specific role of the newly identified circPDSS1 in NSCLC remains largely unknown.
- Investigating circPDSS1's function and targets is crucial for understanding NSCLC progression.
Purpose of the Study:
- To elucidate the functional significance of circPDSS1 in NSCLC.
- To identify downstream molecular targets regulated by circPDSS1.
- To explore the potential of circPDSS1 as a therapeutic target in NSCLC.
Main Methods:
- Cell viability assessed using Cell Counting Kit-8 (CCK-8) assay.
- Cell death analyzed via flow cytometry.
- Expression levels of circRNAs, microRNAs, and proteins measured by RT-qPCR and Western blot.
- Luciferase reporter assays used to confirm interactions between circPDSS1, miR-137, and SLC7A11.
Main Results:
- CircPDSS1 expression is significantly upregulated in NSCLC cells compared to healthy lung cells.
- Silencing circPDSS1 inhibits NSCLC cell viability and induces ferroptosis.
- CircPDSS1 acts as a molecular sponge for miR-137, negatively regulating its expression.
- MiR-137 directly targets SLC7A11, and circPDSS1 knockdown downregulates GPX4 and GCLC.
Conclusions:
- CircPDSS1 promotes NSCLC cell viability and inhibits ferroptosis.
- The circPDSS1/miR-137/SLC7A11 axis plays a critical role in NSCLC progression.
- Targeting the circPDSS1/miR-137/SLC7A11/GPX4/GCLC pathway presents a potential therapeutic strategy for NSCLC.
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