NPHS2-6 drives cervical squamous cell carcinoma (CSCC) progression via hsa-miR-1323/SMC1B axis to activate PI3K-Akt pathway
Clin. transl. oncol. (Print)
; 26(1): 245-259, jan. 2024.
Artigo
em Inglês
| IBECS
| ID: ibc-229163
Biblioteca responsável:
ES1.1
Localização: ES15.1 - BNCS
ABSTRACT
Purpose A substantial amount of evidence demonstrates suggests that long non-coding RNAs (lncRNAs) play a key role in the progression of various malignancies, cervical squamous cell carcinoma (CSCC) included. In our study, we deeply investigated the role and molecular mechanism of lncRNA NPHS2-6 in CSCC. Methods The expression level of gene and protein expression were measured by qRT-PCR and western blot. To test the cell proliferation and cell metastasis ability, we carried out the CCK-8 experiment, clone formation assay, transwell assay and wound healing, respectively. The interactivity among NPHS2-6, miR-1323 and SMC1B were co demonstrated using the bioinformatics tool, dual-luciferase reporter system, and RNA pulldown assay. The subcutaneous tumor model of nude mice was established to verify the results of previous studies at the in vivo. NPHS2-6 was upregulated in CSCC tissues and cells. Results NPHS2-6 deficiency significantly inhibited CSCC cell growth and EMT in vitro. In addition, NPHS2-6 deficiency also inhibited the growth of CSCC xenograft tumors in mice in vivo. Importantly, NPHS2-6 was a competing endogenous RNA (ceRNA) to increases SMC1B levels by binding to miR-1323, leading to activate the PI3K/Akt pathway, thereby exacerbating tumorigenesis of CSCC. Conclusions In conclusion, NPHS2-6/miR-1323/SMC1B/PI3K/Akt signaling accelerates the progression of CSCC, providing a new direction for the treatment strategy of CSCC (AU)
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Espanha
Base de dados:
IBECS
Assunto principal:
Neoplasias Uterinas
/
Carcinoma de Células Escamosas
/
MicroRNAs
Limite:
Animais
Idioma:
Inglês
Revista:
Clin. transl. oncol. (Print)
Ano de publicação:
2024
Tipo de documento:
Artigo
Instituição/País de afiliação:
Xinjiang Medical University/China