PCLAF promotes neuroblastoma G1/S cell cycle progression via the E2F1/PTTG1 axis

PCLAF (PCNA clamp-associated factor), also known as PAF15/ KIAA0101, is overexpressed in most human cancers and is a predominant regulator of tumor progression. However, its biological function in neuroblastoma remains unclear. PCLAF is extremely overexpressed in neuroblastoma and is associated with...

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Published in:Cell death & disease 2022-02, Vol.13 (2), p.178-178, Article 178
Main Authors: Liu, Xiaowei, Cai, Yuanxia, Cheng, Cheng, Gu, Yaoyao, Hu, Xiaoxiao, Chen, Kai, Wu, Yeming, Wu, Zhixiang
Format: Article
Language:English
Subjects:
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Antibodies
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Cell cycle
Cell Cycle - genetics
Cell Division
Cell Line, Tumor
Cell proliferation
Cell Proliferation - genetics
E2F1 Transcription Factor - genetics
E2F1 Transcription Factor - metabolism
Gene Expression Regulation, Neoplastic
Genes, cdc
Humans
Immunology
Life Sciences
Neuroblastoma
Neuroblastoma - genetics
Neuroblastoma - pathology
Neuroblastoma cells
Pituitary tumor-transforming proteins
Signal Transduction
Therapeutic targets
Tumors
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Summary:PCLAF (PCNA clamp-associated factor), also known as PAF15/ KIAA0101, is overexpressed in most human cancers and is a predominant regulator of tumor progression. However, its biological function in neuroblastoma remains unclear. PCLAF is extremely overexpressed in neuroblastoma and is associated with poor prognosis. Through the analysis of various data sets, we found that the high expression of PCLAF is positively correlated with increased stage and high risk of neuroblastoma. Most importantly, knocking down PCLAF could restrict the proliferation of neuroblastoma cells in vitro and in vitro. By analyzing RNA-seq data, we found that the enrichment of cell cycle-related pathway genes was most significant among the differentially expressed downregulated genes after reducing the expression of PCLAF . In addition, PCLAF accelerated the G1/S transition of the neuroblastoma cell cycle by activating the E2F1/PTTG1 signaling pathway. In this study, we reveal the mechanism by which PCLAF facilitates cell cycle progression and recommend that the PCLAF/E2F1/PTTG1 axis is a therapeutic target in neuroblastoma.
ISSN:2041-4889
2041-4889
DOI:10.1038/s41419-022-04635-w