LncRNA ROR promotes proliferation, immune escape, and polarization of M2 macrophages in thyroid cancer by activating the PI3K/AKT pathway
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View abstract on PubMed
Summary
This summary is machine-generated.Long non-coding RNA ROR (Linc-ROR) is elevated in thyroid cancer patients and linked to poorer outcomes. Silencing Linc-ROR inhibits tumor growth and immune evasion, suggesting it as a therapeutic target.
Area Of Science
- Endocrinology
- Oncology
- Molecular Biology
Background
- Thyroid cancer is the leading endocrine malignancy.
- Long non-coding RNAs (LncRNAs) play critical roles in cancer progression.
- LncRNA ROR (Linc-ROR) has demonstrated tumor-regulatory functions in various cancers.
Purpose Of The Study
- To investigate the role and mechanism of Linc-ROR in thyroid cancer.
- To determine the association between Linc-ROR levels and clinicopathological features.
- To explore Linc-ROR's impact on tumor growth, immune escape, and macrophage polarization.
Main Methods
- Quantification of Linc-ROR levels in 70 thyroid cancer patients.
- Assessment of cell viability using CCK-8 assays.
- Xenograft tumor models for evaluating tumor growth.
- Flow cytometry for CD8+ T cell analysis.
- ELISA assays for cytokine detection (IL-10, IFN-γ, TNF-β).
Main Results
- Linc-ROR levels were significantly elevated in thyroid cancer patients.
- Higher Linc-ROR expression correlated with poor survival, lymph node metastasis, and advanced TNM stage.
- Linc-ROR silencing suppressed thyroid cancer cell proliferation and tumor growth.
- Silenced Linc-ROR reduced immune escape and M2 macrophage polarization.
- The PI3K/AKT signaling pathway mediated Linc-ROR's effects.
Conclusions
- Linc-ROR is upregulated in thyroid cancer and associated with adverse prognostic factors.
- Linc-ROR inhibition hinders tumor progression and modulates the tumor immune microenvironment.
- Linc-ROR, potentially via PI3K/AKT signaling, represents a promising therapeutic target for thyroid cancer.
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