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circANKRD28 inhibits cisplatin resistance in non-small-cell lung cancer through the miR-221-3p/SOCS3 axis
Shu Song1, Yuhan Shi1, Dong Zeng1
1Department of Pathology, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Background:
Non-small-cell lung cancer (NSCLC) is a common cancer. Chemotherapeutic drug resistance limits the therapeutic effect of NSCLC and leads to a poor prognosis. As a result, new specific targets may be better identified by studying the mechanism of drug resistance to cisplatin in NSCLC.
Methods:
In the present study, we performed a quantitative real-time polymerase chain reaction and western blotting to detect mRNA and protein levels. The proliferation of cells was analyzed by a Cell Counting Kit-8 and colony formation assays. Cell invasion was measured via the Transwell assay. A scratch assay was performed to measure cell migration in cisplatin (DDP)-resistant NSCLC cells. Apoptosis of cells was examined using flow cytometry.
Results:
We found that circANKRD28 was notably decreased in NSCLC. The results showed that circANKRD28 expression was not affected, and its half-life was more than 12 h. Functional experiments revealed that circANKRD28 overexpression inhibited DDP resistance in NSCLC cells in vitro. Mechanistic findings demonstrated that circANKRD28 regulated tumor cell progression and DDP sensitivity through the miR-221-3p/SOCS3 axis.
Conclusions:
The present study revealed the regulatory effects and molecular mechanism of circANKRD28 on the development and cisplatin resistance in NSCLC, which may provide experimental basis and theoretical support to identify new targets for therapy of DDP resistance in NSCLC.
Insights
Circular RNA circANKRD28 is decreased in non-small-cell lung cancer (NSCLC) and inhibits cisplatin resistance by regulating the miR-221-3p/SOCS3 axis, offering potential therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Non-small-cell lung cancer (NSCLC) poses a significant health challenge.
- Chemotherapeutic drug resistance in NSCLC limits treatment efficacy and worsens patient prognosis.
- Understanding cisplatin resistance mechanisms is crucial for developing novel NSCLC therapies.
Purpose of the Study:
- To investigate the role of circANKRD28 in non-small-cell lung cancer (NSCLC) drug resistance.
- To elucidate the molecular mechanism underlying circANKRD28's regulation of cisplatin sensitivity in NSCLC.
- To identify potential therapeutic targets for overcoming cisplatin resistance in NSCLC.
Main Methods:
- Quantitative real-time PCR and Western blotting to assess mRNA and protein expression.
- Cell Counting Kit-8 and colony formation assays for proliferation analysis.
- Transwell and scratch assays for invasion and migration.
- Flow cytometry for apoptosis assessment.
Main Results:
- circANKRD28 expression was significantly decreased in NSCLC.
- Overexpression of circANKRD28 inhibited cisplatin (DDP) resistance in NSCLC cells.
- circANKRD28 regulates tumor progression and DDP sensitivity via the miR-221-3p/SOCS3 axis.
Conclusions:
- circANKRD28 plays a critical role in the development and cisplatin resistance of NSCLC.
- The miR-221-3p/SOCS3 axis is a key molecular pathway regulated by circANKRD28.
- circANKRD28 presents a potential therapeutic target for enhancing DDP sensitivity in NSCLC.
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