<abstract xmlns="http://www.w3.org/1999/xhtml">

<sec><h3>Background</h3>
<p>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.</p>
</sec>
<sec><h3>Patients and methods</h3>
<p>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. <italic>In vivo</italic> experiments confirmed the role of PROM2 in NSCLC.</p>
</sec>
<sec><h3>Results</h3>
<p>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. <italic>In vivo</italic> experiments confirmed that PROM2 knockdown could inhibit tumor growth and increase the sensitivity of tumor cells to cisplatin.</p>
</sec>
<sec><h3>Conclusions</h3>
<p>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.</p>
</sec>
</abstract>

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.

Prominin 2 decreases cisplatin sensitivity in non-small cell lung cancer and is modulated by CTCC binding factor

The Third Affiliated Hospital of ZunYi Medical University (The First People's Hospital of ZunYi)

Radiology and Oncology

This work is licensed under the Creative Commons Attribution 4.0 International License.

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...

Prominin 2 decreases cisplatin sensitivity in non-small cell lung cancer and is modulated by CTCC binding factor

Article Category: Research Article

Data publikacji: 04 wrz 2023

Zakres stron: 325 - 336

Otrzymano: 21 gru 2022

Przyjęty: 21 cze 2023

DOI: https://doi.org/10.2478/raon-2023-0033

Słowa kluczowe
non-small cell lung cancer, PROM2, cisplatin, drug resistance, CTCF

© 2023 Jiyang Tang et al., published by Sciendo

This work is licensed under the Creative Commons Attribution 4.0 International License.

Prominin 2 decreases cisplatin sensitivity in non-small cell lung cancer and is modulated by CTCC binding factor

Article Category: Research Article

Data publikacji: 04 wrz 2023

Zakres stron: 325 - 336

Otrzymano: 21 gru 2022

Przyjęty: 21 cze 2023

DOI: https://doi.org/10.2478/raon-2023-0033

Słowa kluczowenon-small cell lung cancer, PROM2, cisplatin, drug resistance, CTCF

© 2023 Jiyang Tang et al., published by Sciendo

This work is licensed under the Creative Commons Attribution 4.0 International License.

Słowa kluczowe
non-small cell lung cancer, PROM2, cisplatin, drug resistance, CTCF