Hsa_circ_0000190 Promotes NSCLC Cell Resistance to Cisplatin via the Modulation of the miR-1253/IL-6 Axis

Background. This study explored the mechanistic basis for nonsmall cell lung cancer (NSCLC) cisplatin (DDP) treatment resistance in an effort to define effective approaches to abrogating the emergence of such chemoresistance. Methods. Analyses of NSCLC expression of hsa_circ_0000190, miR-1253, and i...

Full description

Saved in:
Bibliographic Details
Main Authors: Hua He, Tian Li
Format: Article
Language:English
Published: Wiley 2024-01-01
Series:Analytical Cellular Pathology
Online Access:http://dx.doi.org/10.1155/2024/6647810
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832558635574624256
author Hua He
Tian Li
author_facet Hua He
Tian Li
author_sort Hua He
collection DOAJ
description Background. This study explored the mechanistic basis for nonsmall cell lung cancer (NSCLC) cisplatin (DDP) treatment resistance in an effort to define effective approaches to abrogating the emergence of such chemoresistance. Methods. Analyses of NSCLC expression of hsa_circ_0000190, miR-1253, and interleukin 6 (IL-6) were conducted via a quantitative real-time polymerase chain reaction (qPCR) approach, while the ability of these tumor cells to resist DDP treatment was evaluated with a CCK-8 assay. Interactions between different RNA molecules were assessed using both RNA immunoprecipitation and dual-luciferase reporter assays. Results. NSCLC cell lines and tissues resistant to DDP were found to express higher levels of hsa_circ_0000190, and knocking down this circRNA in NSCLC cells was associated with greater sensitivity to DDP exposure. Further research identified miR-1253 as a hsa_circ_0000190 target, with the ability of hsa_circ_0000190 knockdown to restore DDP sensitivity being largely attributable to the ability of this circRNA to suppress miR-1253 activity. IL-6 was identified as a major miR-1253 target in this context, with miR-1253 regulating chemoresistance in NSCLC cells in part by preventing IL-6 upregulation. Conclusion. Together, these data suggest that hsa_circ_0000190 can promote DDP chemoresistance in NSCLC cells through its ability to modulate miR-1253/IL-6 axis activity, highlighting a novel pathway that can be targeted in an effort to guide the more effective diagnosis and management of DDP-resistant tumors.
format Article
id doaj-art-10f7be6d5f3d4c5aa2ec3875a3d3a4e5
institution Kabale University
issn 2210-7185
language English
publishDate 2024-01-01
publisher Wiley
record_format Article
series Analytical Cellular Pathology
spelling doaj-art-10f7be6d5f3d4c5aa2ec3875a3d3a4e52025-02-03T01:31:53ZengWileyAnalytical Cellular Pathology2210-71852024-01-01202410.1155/2024/6647810Hsa_circ_0000190 Promotes NSCLC Cell Resistance to Cisplatin via the Modulation of the miR-1253/IL-6 AxisHua He0Tian Li1Department of RespiratoryDepartment of RespiratoryBackground. This study explored the mechanistic basis for nonsmall cell lung cancer (NSCLC) cisplatin (DDP) treatment resistance in an effort to define effective approaches to abrogating the emergence of such chemoresistance. Methods. Analyses of NSCLC expression of hsa_circ_0000190, miR-1253, and interleukin 6 (IL-6) were conducted via a quantitative real-time polymerase chain reaction (qPCR) approach, while the ability of these tumor cells to resist DDP treatment was evaluated with a CCK-8 assay. Interactions between different RNA molecules were assessed using both RNA immunoprecipitation and dual-luciferase reporter assays. Results. NSCLC cell lines and tissues resistant to DDP were found to express higher levels of hsa_circ_0000190, and knocking down this circRNA in NSCLC cells was associated with greater sensitivity to DDP exposure. Further research identified miR-1253 as a hsa_circ_0000190 target, with the ability of hsa_circ_0000190 knockdown to restore DDP sensitivity being largely attributable to the ability of this circRNA to suppress miR-1253 activity. IL-6 was identified as a major miR-1253 target in this context, with miR-1253 regulating chemoresistance in NSCLC cells in part by preventing IL-6 upregulation. Conclusion. Together, these data suggest that hsa_circ_0000190 can promote DDP chemoresistance in NSCLC cells through its ability to modulate miR-1253/IL-6 axis activity, highlighting a novel pathway that can be targeted in an effort to guide the more effective diagnosis and management of DDP-resistant tumors.http://dx.doi.org/10.1155/2024/6647810
spellingShingle Hua He
Tian Li
Hsa_circ_0000190 Promotes NSCLC Cell Resistance to Cisplatin via the Modulation of the miR-1253/IL-6 Axis
Analytical Cellular Pathology
title Hsa_circ_0000190 Promotes NSCLC Cell Resistance to Cisplatin via the Modulation of the miR-1253/IL-6 Axis
title_full Hsa_circ_0000190 Promotes NSCLC Cell Resistance to Cisplatin via the Modulation of the miR-1253/IL-6 Axis
title_fullStr Hsa_circ_0000190 Promotes NSCLC Cell Resistance to Cisplatin via the Modulation of the miR-1253/IL-6 Axis
title_full_unstemmed Hsa_circ_0000190 Promotes NSCLC Cell Resistance to Cisplatin via the Modulation of the miR-1253/IL-6 Axis
title_short Hsa_circ_0000190 Promotes NSCLC Cell Resistance to Cisplatin via the Modulation of the miR-1253/IL-6 Axis
title_sort hsa circ 0000190 promotes nsclc cell resistance to cisplatin via the modulation of the mir 1253 il 6 axis
url http://dx.doi.org/10.1155/2024/6647810
work_keys_str_mv AT huahe hsacirc0000190promotesnsclccellresistancetocisplatinviathemodulationofthemir1253il6axis
AT tianli hsacirc0000190promotesnsclccellresistancetocisplatinviathemodulationofthemir1253il6axis