SATB1 promotes the malignant of human non-Hodgkin lymphoma by activating the ribonucleotide reductase
small subunit M2.
- Author:
Dayong YAN
1
;
Wei WANG
2
Author Information
1. Department of Oral and Maxillofacial Surgery, Zhengzhou Central Hospital Affi liated to Zhengzhou University,Zhengzhou 450007, China yandayong2001@163.com.
2. Department of Oral and Maxillofacial Surgery, School of Stomatology, Harbin Medical University, Harbin 150001, China.
- Publication Type:Journal Article
- MeSH:
Cell Cycle Proteins;
genetics;
physiology;
Cell Movement;
genetics;
Cell Proliferation;
genetics;
Down-Regulation;
Gene Expression Regulation, Neoplastic;
genetics;
Humans;
Lymph Nodes;
chemistry;
Lymphoma, Non-Hodgkin;
Matrix Attachment Region Binding Proteins;
genetics;
physiology;
Neoplasm Invasiveness;
genetics;
Oncogenes;
genetics;
physiology;
RNA, Messenger;
RNA, Small Interfering;
Ribonucleoside Diphosphate Reductase;
Ribonucleotide Reductases;
genetics;
physiology;
Signal Transduction;
Transcription Factors;
Transcriptional Activation;
Transfection;
Tumor Cells, Cultured;
Up-Regulation
- From:
Journal of Central South University(Medical Sciences)
2016;41(11):1155-1162
- CountryChina
- Language:Chinese
-
Abstract:
To explore the role of the special AT rich sequence binding protein-1 (SATB1) and ribonucleotide reductase M2 (RRM2) in enhancing malignant progression of non-Hodgkin lymphoma (NHL).
Methods: A total of 42 NHL and 42 chronic lymphadenitis patients were recruited. The protein expressions of SATB1 and RRM2 in cervical lymph nodes were determined by Western blot. After overexpression of SATB1, siSATB1 or siRRM2, the mRNA levels of SATB1 and RRM2 in cells were analyzed via RT-PCR, the cell proliferation was evaluated via MTT and EdU assays, while the migration and invasion of cells were assessed by transwell assays.
Results: Compared with chronic lymphadenitis, the expressions of SATB1 and RRM2 in NHL patients were up-regulated. There was positive correlation between SATB1 and RRM2 in NHL patients. RRM2 mRNA level was up-regulated after transfection of SATB1 and down-regulated after transfection of siSATB1. Overexpression of SATB1 increased tumor cell proliferation, migration and invasion, while knockdown of RRM2 reversed those phenomena.
Conclusion: SATB1 functions as an oncogene and promotes tumor cell proliferation, migration and invasion by up-regulation of RRM2 in NHL.
