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Prominin 2 decreases cisplatin sensitivity in non-small cell lung cancer and is modulated by CTCC binding factor
Jiyang Tang1, Dejun Shu1, Zhimin Fang1
1Department of Thoracic Surgery, The Third Affiliated Hospital of ZunYi Medical University (The First People's Hospital of ZunYi), Zunyi, Guizhou, China.
Background:
Non-small cell lung cancer (NSCLC) is the major pathological type of lung cancer and accounts for the majority of lung cancer-related deaths worldwide. We investigated the molecular mechanism of prominin 2 (PROM2) involved in cisplatin resistance in NSCLC.
Patients And Methods:
The GEO database was analyzed to obtain differential genes to target PROM2. Immunohistochemistry and western blotting were used to detect protein expression levels. To examine the role of PROM2 in NSCLC, we overexpressed or knocked down PROM2 by transfection of plasmid or small interfering RNA. In functional experiments, CCK8 was used to detect cell viability. Cell migration and invasion and apoptosis were detected by transwell assay and flow cytometry, respectively. Mechanistically, the regulation of PROM2 by CTCF was detected by ChIP-PCR. In vivo experiments confirmed the role of PROM2 in NSCLC.
Results:
GEO data analysis revealed that PROM2 was up-regulated in NSCLC, but its role in NSCLC remains unclear. Our clinical samples confirmed that the expression of PROM2 was markedly increased in NSCLC tissue. Functionally, Overexpression of PROM2 promotes cell proliferation, migration and invasion, and cisplatin resistance. CTCF up-regulates PROM2 expression by binding to its promoter region. In vivo experiments confirmed that PROM2 knockdown could inhibit tumor growth and increase the sensitivity of tumor cells to cisplatin.
Conclusions:
PROM2 up-regulation in NSCLC can attenuate the sensitivity of NSCLC cells to cisplatin and promote the proliferation, migration and invasion of tumor cells. PROM2 may provide a new target for the treatment of NSCLC.
Insights
Prominin 2 (PROM2) is elevated in non-small cell lung cancer (NSCLC), promoting tumor growth and cisplatin resistance. Reducing PROM2 may enhance NSCLC treatment sensitivity.
Area of Science:
- Oncology
- Molecular Biology
Background:
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality globally.
- The molecular mechanisms underlying cisplatin resistance in NSCLC require further elucidation.
Purpose of the Study:
- To investigate the role of prominin 2 (PROM2) in the development of cisplatin resistance in NSCLC.
- To explore the regulatory mechanism of PROM2 expression in NSCLC.
Main Methods:
- Analysis of GEO database for differential gene expression.
- Immunohistochemistry and Western blotting to assess PROM2 protein levels.
- Cellular assays (CCK8, Transwell, flow cytometry) to evaluate proliferation, migration, invasion, and apoptosis.
- Chromatin immunoprecipitation PCR (ChIP-PCR) to determine CTCF binding to the PROM2 promoter.
- In vivo studies in a mouse model.
Main Results:
- PROM2 expression is significantly upregulated in NSCLC tissues.
- Overexpression of PROM2 enhances NSCLC cell proliferation, migration, invasion, and cisplatin resistance.
- CTCF acts as a transcription factor, upregulating PROM2 by binding to its promoter region.
- Knockdown of PROM2 inhibits tumor growth and increases sensitivity to cisplatin in vivo.
Conclusions:
- Upregulated PROM2 in NSCLC contributes to cisplatin resistance and promotes tumor progression.
- PROM2 represents a potential therapeutic target for improving NSCLC treatment outcomes.
