NPHS2-6 drives cervical squamous cell carcinoma (CSCC) progression via hsa-miR-1323/SMC1B axis to activate PI3K-Akt pathway

Fen Li; Yan Wang; Mengke Wen; Gulibiya Aizezi; Jinrui Yuan; Tongjunnan Zhou; Guqun Shen

Ayuda

NPHS2-6 drives cervical squamous cell carcinoma (CSCC) progression via hsa-miR-1323/SMC1B axis to activate PI3K-Akt pathway

Fen Li ^[2] ; Yan Wang ^[1] ; Mengke Wen ^[2] ; Gulibiya Aizezi ^[2] ; Jinrui Yuan ^[2] ; Tongjunnan Zhou ^[2] ; Guqun Shen ^[2]
1. [1] Xinjiang Medical University
  
  Xinjiang Medical University
  
  China
2. [2] The Second Department of Gynecology, Affiliated Tumor Hospital of Xinjiang Medical University, 789 Suzhou East Street, Urumqi, Xinjiang Province, China
Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 26, Nº. 1, 2024, págs. 245-259
Idioma: inglés
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Resumen
- 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.