LncRNA TYMSOS stimulates immune escape and the advancement of cervical squamous cell carcinoma by regulating miR-134-5p/KRAS expression.
LncRNAs can regulate related miRNAs and participate in the regulation of tumorigenesis, progression, and immune escape in tumors.
To examine the clinical and functional impact of lncRNA TYMSOS in the advancement and immune escape of cervical cancer.
The abundances of TYMSOS in cervical squamous cell carcinoma (CSCC) patients were detected using RT-qPCR and verified by bioinformatic analysis. The functional impact of TYMSOS in cervical cancer cells was assessed by CCK-8 and Transwell assays. ELISA assay was utilized to determine the amounts of IFN-γ and TNF-α released. The CytoTox 96 non-radioactive cytotoxicity assay was conducted to measure the cytotoxicity of NK92 cells against cervical cancer cells. The interaction among TYMSOS, miR-134-5p, and KRAS was assessed by dual-luciferase reporter assay, RNA pull-down, and RIP assays.
TYMSOS and KRAS were upregulated while miR-134-5p was decreased in CSCC patients. Serum TYMSOS levels had predictive value for CSCC patients and tumor tissue TYMSOS had prognostic value in predicting progression-free survival. Silencing TYMSOS repressed cell proliferation, migration, and invasion abilities, while enhancing the cytotoxic activity of NK cells against cervical cancer cells and stimulated the release of IFN-γ and TNF-α. miR-134-5p was a target of TYMSOS and KRAS was a potential target of miR-134-5p. Interference of KRAS abolished the effects of miR-134-5p on the malignant behaviors and killing influence of NK92 cells to cervical cancer cells.
Increased TYMSOS was linked to adverse prognosis, malignant progression, and immune escape in cervical cancer by modulating miR-134-5p/KRAS axis.
To examine the clinical and functional impact of lncRNA TYMSOS in the advancement and immune escape of cervical cancer.
The abundances of TYMSOS in cervical squamous cell carcinoma (CSCC) patients were detected using RT-qPCR and verified by bioinformatic analysis. The functional impact of TYMSOS in cervical cancer cells was assessed by CCK-8 and Transwell assays. ELISA assay was utilized to determine the amounts of IFN-γ and TNF-α released. The CytoTox 96 non-radioactive cytotoxicity assay was conducted to measure the cytotoxicity of NK92 cells against cervical cancer cells. The interaction among TYMSOS, miR-134-5p, and KRAS was assessed by dual-luciferase reporter assay, RNA pull-down, and RIP assays.
TYMSOS and KRAS were upregulated while miR-134-5p was decreased in CSCC patients. Serum TYMSOS levels had predictive value for CSCC patients and tumor tissue TYMSOS had prognostic value in predicting progression-free survival. Silencing TYMSOS repressed cell proliferation, migration, and invasion abilities, while enhancing the cytotoxic activity of NK cells against cervical cancer cells and stimulated the release of IFN-γ and TNF-α. miR-134-5p was a target of TYMSOS and KRAS was a potential target of miR-134-5p. Interference of KRAS abolished the effects of miR-134-5p on the malignant behaviors and killing influence of NK92 cells to cervical cancer cells.
Increased TYMSOS was linked to adverse prognosis, malignant progression, and immune escape in cervical cancer by modulating miR-134-5p/KRAS axis.