LOC644656 promotes cisplatin resistance in cervical cancer by recruiting ZNF143 and activating the transcription of E6-AP.
Cell Signal
; 117: 111115, 2024 05.
Article
in En
| MEDLINE
| ID: mdl-38395183
ABSTRACT
Cisplatin resistance remains a persistent challenge in cervical cancer (CC) treatment. Molecular biomarkers have garnered attention for their association with cisplatin resistance in various diseases. Long non-coding RNAs (lncRNAs) exert significant influence on CC development. This study explores the role of LOC644656 in regulating cisplatin resistance in CC. Parental and cisplatin-resistant CC cells underwent cisplatin treatment. Functional assays assessed cell proliferation and apoptosis under different conditions. RNA pull-down with mass spectrometry, along with literature review, elucidated the interaction between LOC644656, ZNF143, and E6-AP. Mechanistic assays analyzed the relationship between different factors. RT-qPCR and western blot quantified RNA and protein levels, respectively. In vivo models validated E6-AP's function. Results revealed LOC644656 overexpression in cisplatin-resistant CC cells, exacerbating cell growth. LOC644656 recruited ZNF143 to activate E6-AP transcription, promoting cisplatin resistance in CC. In conclusion, LOC644656 positively modulates E6-AP expression via ZNF143-mediated transcriptional activation, contributing to cisplatin resistance in CC.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Trans-Activators
/
Uterine Cervical Neoplasms
/
Cisplatin
/
Drug Resistance, Neoplasm
/
MicroRNAs
/
Ubiquitin-Protein Ligases
Limits:
Female
/
Humans
Language:
En
Journal:
Cell Signal
/
Cell. signal
/
Cellular signalling
Year:
2024
Document type:
Article
Affiliation country:
China
Country of publication:
United kingdom