Prominin 2 decreases cisplatin sensitivity in non-small cell lung cancer and is modulated by CTCC binding factor
Article Category: Research Article
Pubblicato online: 04 set 2023
Pagine: 325 - 336
Ricevuto: 21 dic 2022
Accettato: 21 giu 2023
DOI: https://doi.org/10.2478/raon-2023-0033
Parole chiave
© 2023 Jiyang Tang et al., published by Sciendo
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 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.
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.
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.