LOC644656 promotes cisplatin resistance in cervical cancer by recruiting ZNF143 and activating the transcription of E6-AP.
Cell Signal
; 117: 111115, 2024 05.
Article
en 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.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Transactivadores
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Neoplasias del Cuello Uterino
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Cisplatino
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Resistencia a Antineoplásicos
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MicroARNs
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Ubiquitina-Proteína Ligasas
Límite:
Female
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Humans
Idioma:
En
Año:
2024
Tipo del documento:
Article