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Published on: March 30, 2019
The effect and mechanism of miR-607/CANT1 axis in lung squamous carcinoma
Gang Qiao1, Hai-Bo Wang2, Xiu-Na Duan3
1Department of Integrative Medicine Oncology, Zibo Bashan Wanjie Hospital, Zibo.
Abstract:
Lung squamous carcinoma (LUSC) is the second most frequent subtype of non-small cell lung cancer. Rarely gene alterations are identified in LUSC. Therefore, identifying LUSC-related genes to explain the relevant molecular mechanism is urgently needed. A potential biomarker, calcium-activated nucleotidase 1 (CANT1), was elevated in tissues of LUSC patients relative to normal cases based on the TCGA and/or GTEx database. CCK-8 and transwell tests were then implemented to measure the proliferative, invasive and migratory capacities, and showed that knockdown of CANT1 blocked LUSC cells proliferation. miR-607, predicted as an upstream factor for CANT1, was declined in LUSC using TargetScan analysis and luciferase activity test. Low miR-607 expression was related with unfavorable outcomes of LUSC patients. Moreover, miR-607 downregulation elevated cell viability, invasion and migration in LUSC cells, which was antagonized by si-CANT1. GEPIA website was accessed to estimate the relevance between CANT1 and epithelial-mesenchymal transition (EMT)-related positive factors. The protein levels of Fibronectin, Vimentin, Snail and β-catenin were altered due to the abnormal CANT1 and miR-607 expression. Together, these data unveiled that miR-607/CANT1 pair may exert a vital role in the progression of LUSC through mediating EMT process, which would furnish an available therapeutic therapy for LUSC.
Insights
Researchers identified a new molecular mechanism in lung squamous cell carcinoma (LUSC). The miR-607/CANT1 pathway regulates cancer progression and may offer new therapeutic targets for LUSC.
Area of Science:
- Oncology
- Molecular Biology
- Biomarker Discovery
Background:
- Lung squamous cell carcinoma (LUSC) is a major subtype of non-small cell lung cancer with limited identified gene alterations.
- Understanding the molecular mechanisms driving LUSC progression is crucial for developing effective treatments.
Purpose of the Study:
- To identify novel genes and molecular pathways involved in LUSC progression.
- To investigate the role of calcium-activated nucleotidase 1 (CANT1) and its upstream regulator miR-607 in LUSC.
Main Methods:
- Utilized TCGA and GTEx databases to analyze CANT1 expression in LUSC tissues.
- Performed CCK-8 and transwell assays to assess cell proliferation, invasion, and migration.
- Employed TargetScan analysis and luciferase assays to study the miR-607/CANT1 interaction.
- Analyzed epithelial-mesenchymal transition (EMT) markers using the GEPIA website.
Main Results:
- Calcium-activated nucleotidase 1 (CANT1) expression was elevated in LUSC tissues.
- Knockdown of CANT1 inhibited LUSC cell proliferation, invasion, and migration.
- miR-607 was downregulated in LUSC and associated with poor patient outcomes.
- The miR-607/CANT1 axis modulated LUSC cell behavior and EMT markers (Fibronectin, Vimentin, Snail, β-catenin).
Conclusions:
- The miR-607/CANT1 pathway plays a significant role in LUSC progression by mediating the epithelial-mesenchymal transition (EMT) process.
- This pathway represents a potential therapeutic target for LUSC treatment.
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