[Potential molecular mechanism of lncRNAs HOTAIR in malignant metastasis of esophageal cancer]
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View abstract on PubMed
Summary
This summary is machine-generated.Cancer-associated fibroblast exosomes carrying HOTAIR promote esophageal cancer metastasis. Knocking down HOTAIR in these exosomes reduces cancer cell proliferation, migration, and invasion by regulating glycolysis.
Area Of Science
- Molecular oncology
- Cell biology
- Cancer research
Context
- Esophageal squamous cell carcinoma (ESCC) is a significant global health concern with high metastatic potential.
- Cancer-associated fibroblasts (CAFs) play a crucial role in tumor microenvironment modulation and cancer progression.
- Exosomes are key mediators of intercellular communication, transferring biomolecules between cells.
Purpose
- To investigate the molecular mechanism by which exosomes derived from CAFs (CAFs-Exo) carrying lncRNA HOTAIR promote ESCC metastasis.
- To determine the role of HOTAIR in CAFs-Exo and its impact on ESCC cell proliferation, migration, invasion, and glycolysis.
Summary
- CAFs-Exo significantly promoted proliferation, migration, and invasion of ESCC cells compared to normal fibroblast exosomes (NFs-Exo).
- CAFs-Exo treatment altered epithelial-mesenchymal transition (EMT) markers, increasing N-cadherin and decreasing E-cadherin.
- Exosomal HOTAIR levels were significantly higher in CAFs-Exo than NFs-Exo. Knockdown of HOTAIR in ESCC cells reduced proliferation, migration, invasion, and key glycolytic indicators (HK2, ECAR, ATP/ADP ratio).
Impact
- This study identifies exosomal HOTAIR from CAFs as a critical driver of ESCC metastasis.
- The findings suggest that targeting exosomal HOTAIR could be a potential therapeutic strategy for inhibiting ESCC progression and metastasis.
- Understanding the role of CAFs-Exo in regulating cancer cell glycolysis provides new insights into metabolic reprogramming in cancer.
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