Selected article for: "activator signal transducer and cell cycle"

Author: Liu, Chenguang; Yu, Fangqin; Ma, Runsheng; Zhang, Lele; Du, Gongbo; Niu, Dongpeng; Yin, Detao
Title: Cep63 knockout inhibits the malignant phenotypes of papillary thyroid cancer cell line TPC-1
  • Cord-id: xhsdbk2j
  • Document date: 2021_7_21
  • ID: xhsdbk2j
    Snippet: The present study was designed to observe the expression of the centrosomal protein 63 in papillary thyroid cancer (PTC) tissues and cells and to explore the clinical significance of Cep63 expression in PTC. Primary PTC tissues and matched normal thyroid tissues were collected, and the Cep63 expression level was determined by reverse transcription-quantitative PCR and western blotting. A stable Cep63-knockout cell line was constructed to assess the proliferation, invasion, migration and apoptosi
    Document: The present study was designed to observe the expression of the centrosomal protein 63 in papillary thyroid cancer (PTC) tissues and cells and to explore the clinical significance of Cep63 expression in PTC. Primary PTC tissues and matched normal thyroid tissues were collected, and the Cep63 expression level was determined by reverse transcription-quantitative PCR and western blotting. A stable Cep63-knockout cell line was constructed to assess the proliferation, invasion, migration and apoptosis abilities in vitro. A subcutaneous tumorigenesis model was established in nude mice to evaluate the effect of Cep63 on tumor growth and proliferation in vivo. Western blotting was used to explore the relevant signaling pathways. The results revealed that the expression level of Cep63 in PTC tissues was significantly increased. The proliferation, invasion and migration abilities of TPC-1 cells were decreased after Cep63 knockout, and silencing of Cep63 resulted in TPC-1 cell cycle arrest in the S phase. Mechanistically, Cep63 knockout inhibited the activation of the Janus kinase/signal transducer and activator of transcription 3 signaling pathway. In conclusion, Cep63 knockout significantly inhibited biological functions of TPC-1 cells in vitro and in vivo, indicating that Cep63 may be an important oncogene of PTC.

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