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PeerJ. 2019 Jan 24;7:e6352. doi: 10.7717/peerj.6352. eCollection 2019.

Transcriptome profiling reveals the role of ZBTB38 knock-down in human neuroblastoma.

Chen J#1,2,3, Xing C#1,2, Yan L4, Wang Y5, Wang H6, Zhang Z1, Yu D1, Li J1, Li H7, Li J1, Cai Y2.

Author information

1
College of Life Sciences, Anhui Provincial Key Lab of the Conservation and Exploitation of Biological Resources, Anhui Normal University, WuHu, China.
2
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
3
The Secondary Hospital of Wuhu, WuHu, China.
4
Department of Radiation Oncology, Linyi People Hospital, Linyi, China.
5
The First Affiliated Hospital of Wannan Medical College, WuHu, China.
6
Taizhou 4th Hospital, Taizhou, China.
7
Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta State University, Augusta, GA, USA.
#
Contributed equally

Abstract

ZBTB38 belongs to the zinc finger protein family and contains the typical BTB domains. As a transcription factor, ZBTB38 is involved in cell regulation, proliferation and apoptosis, whereas, functional deficiency of ZBTB38 induces the human neuroblastoma (NB) cell death potentially. To have some insight into the role of ZBTB38 in NB development, high throughput RNA sequencing was performed using the human NB cell line SH-SY5Y with the deletion of ZBTB38. In the present study, 2,438 differentially expressed genes (DEGs) in ZBTB38-/- SH-SY5Y cells were obtained, 83.5% of which was down-regulated. Functional annotation of the DEGs in the Kyoto Encyclopedia of Genes and Genomes database revealed that most of the identified genes were enriched in the neurotrophin TRK receptor signaling pathway, including PI3K/Akt and MAPK signaling pathway. we also observed that ZBTB38 affects expression of CDK4/6, Cyclin E, MDM2, ATM, ATR, PTEN, Gadd45, and PIGs in the p53 signaling pathway. In addition, ZBTB38 knockdown significantly suppresses the expression of autophagy-related key genes including PIK3C2A and RB1CC1. The present meeting provides evidence to molecular mechanism of ZBTB38 modulating NB development and targeted anti-tumor therapies.

KEYWORDS:

Bioinformatics analysis; DEGs; Neuroblastoma; Transcriptome; ZBTB38

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