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NPHS2-6 drives cervical squamous cell carcinoma (CSCC) progression via hsa-miR-1323/SMC1B axis to activate PI3K-Akt pathway.
Li, Fen; Wang, Yan; Wen, Mengke; Aizezi, Gulibiya; Yuan, Jinrui; Zhou, Tongjunnan; Shen, Guqun.
Afiliação
  • Li F; The Second Department of Gynecology, Affiliated Tumor Hospital of Xinjiang Medical University, 789 Suzhou East Street, Urumqi, 830011, Xinjiang Province, China.
  • Wang Y; Key Laboratory of Oncology of Xinjiang Uyghur Autonomous Region, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, 830011, China.
  • Wen M; The Second Department of Gynecology, Affiliated Tumor Hospital of Xinjiang Medical University, 789 Suzhou East Street, Urumqi, 830011, Xinjiang Province, China.
  • Aizezi G; The Second Department of Gynecology, Affiliated Tumor Hospital of Xinjiang Medical University, 789 Suzhou East Street, Urumqi, 830011, Xinjiang Province, China.
  • Yuan J; The Second Department of Gynecology, Affiliated Tumor Hospital of Xinjiang Medical University, 789 Suzhou East Street, Urumqi, 830011, Xinjiang Province, China.
  • Zhou T; The Second Department of Gynecology, Affiliated Tumor Hospital of Xinjiang Medical University, 789 Suzhou East Street, Urumqi, 830011, Xinjiang Province, China.
  • Shen G; The Second Department of Gynecology, Affiliated Tumor Hospital of Xinjiang Medical University, 789 Suzhou East Street, Urumqi, 830011, Xinjiang Province, China. sgq1228@tom.com.
Clin Transl Oncol ; 26(1): 245-259, 2024 Jan.
Article em En | MEDLINE | ID: mdl-37322227
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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Carcinoma de Células Escamosas / Neoplasias do Colo do Útero / MicroRNAs Limite: Animals / Female / Humans Idioma: En Revista: Clin Transl Oncol Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China País de publicação: Itália

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Carcinoma de Células Escamosas / Neoplasias do Colo do Útero / MicroRNAs Limite: Animals / Female / Humans Idioma: En Revista: Clin Transl Oncol Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China País de publicação: Itália