IGF2BP1/ORC1 Axis Influences Nonsmall Cell Lung Cancer Progression via m6A Methylation Modification
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View abstract on PubMed
Summary
This summary is machine-generated.The ORC1 gene is upregulated in non-small cell lung cancer (NSCLC), promoting tumor growth. IGF2BP1 enhances ORC1 stability via m6A modification, driving NSCLC progression and highlighting the IGF2BP1/ORC1 axis as a therapeutic target.
Area Of Science
- Molecular Biology
- Oncology
- Epigenetics
Background
- The role of ORC1 in cancer, particularly lung cancer, is not fully understood.
- Epigenetic modifications regulated by ORC1 in non-small cell lung cancer (NSCLC) progression require systematic analysis.
Purpose Of The Study
- To investigate the expression and function of ORC1 in NSCLC.
- To explore the regulatory relationship between ORC1, m6A modification, and IGF2BP1 in NSCLC progression.
Main Methods
- Bioinformatics analysis of ORC1 expression and m6A modification in NSCLC.
- Validation using clinical samples and cell experiments.
- In vitro and in vivo assays including RNA pulldown, MeRIP-qPCR, mRNA stability, cell cycle, apoptosis, and xenograft mouse models.
Main Results
- ORC1 was significantly upregulated in NSCLC tissues and cells.
- Silencing ORC1 inhibited NSCLC cell proliferation.
- IGF2BP1 enhanced ORC1 mRNA stability through m6A modification, promoting tumor proliferation and apoptosis resistance.
- The IGF2BP1/ORC1 axis was identified as a key driver of NSCLC progression.
Conclusions
- ORC1 plays a crucial role in NSCLC proliferation.
- IGF2BP1 promotes NSCLC progression by stabilizing ORC1 mRNA via m6A modification.
- The IGF2BP1/ORC1 axis represents a potential therapeutic target for NSCLC.
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