Cervical cancer (CC) is one of the most common malignant tumors. This study analyzed the impact of protein tyrosine phosphatase, receptor type B (PTPRB) on malignant behavior of CC and explored its possible molecular mechanism. RT-PCR, western blot and Immunohistochemistry were applied to examine the expression of PTPRB in CC specimens and cells. Aberrant PTPRB expression in CC and survival outcomes were constructed using The Cancer Genome Atlas (TCGA) database and tissue microarray cervical squamous cell carcinoma cohort. Cultured human CC cells were assayed for viability, apoptosis, migration, and invasion in vitro and in vivo. Kyoto Encyclopedia of Genes and Genomes (KEGG) assays and gene set enrichment analysis (GSEA) assays were used to delve into PTPRB-related pathways using TCGA datasets. The levels of proteins associated with the epithelial-mesenchymal transition (EMT) pathway and modulated by PTPRB were examined through Western blot. We found that the levels of PTPRB in CC tissues and cells were distinctly up-regulated. PTPRB was also an unfavorable prognostic factor for CC patients. Functionally, PTPRB knockdown exhibits tumorsuppressive function via reducing cell proliferation and metastasis and inducing cell apoptosis. KEGG assays and GSEA assays suggested PTPRB overexpression was associated with several tumor-related pathways. The results of Western blot assays suggested that N-cadherin was decreased in the PTPRBknockdown CC cells, while E-cadherin was increased. Overall, PTPRB is highly expressed in CC and can effectively enhance the proliferation, metastasis and EMT process of tumor cells. PTPRB is expected to be a therapeutic target for CC.

Long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) exerts a pro-oncogenic role in several cancers, whereas its underlying regulatory mechanism in papillary thyroid carcinoma (PTC) progression remains unknown. This research mainly explored the roles of NEAT1 in PTC development. Quantitative real-time polymerase-chain reaction (qRT-PCR) was applied to measure NEAT1, miR-524-5p, and inhibitor of DNA binding 1 (ID1) expression in PTC tissues and cells. Western blot was conducted for detecting the protein levels. MTT, transwell, and flow cytometry assays were applied to assess cell proliferation, metastasis, and apoptosis in PTC cells in vitro . The PTC xenograft tumor model was used for investigating the role of NEAT1 in vivo . Dual-luciferase reporter assay was utilized for confirming the interaction between miR-524-5p and NEAT1 or ID1. In PTC tissues and cells, NEAT1 was significantly up-regulated. NEAT1 silencing blocked cell proliferation, metastasis, and facilitated apoptosis in vitro and impeded xenograft tumor growth in vivo . Bioinformatics prediction revealed the existence of binding sites between NEAT1 and miR-524-5p. Besides, ID1 was confirmed as a direct target to miR-524-5p, and the enhancement of ID1 reversed the regulation of miR-524-5p upregulation on cell progression. In addition, NEAT1 promoted PTC development by regulating ID1 expression via sponging miR-524-5p in PTC. In summary, we demonstrate that NEAT1 advanced the process of PTC by miR-524-5p/ID1 axis, which may enhance our comprehension of PTC pathogenesis.

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