Effect of MXRA7 on the Biological Functions of Acute B Lymphoblastic Leukemia Cell Line REH.
10.19746/j.cnki.issn.1009-2137.2023.01.008
- Author:
Kun-Peng MA
1
;
Zhen-Jiang SUN
1
;
Ying SHEN
1
;
Yi-Qiang WANG
1
;
Dan-Dan LIN
2
Author Information
1. The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Medical College, Soochow University, Suzhou 215000, Jiangsu Province, China.
2. The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Medical College, Soochow University, Suzhou 215000, Jiangsu Province, China.E-mail: szlindd@163.com.
- Publication Type:Journal Article
- Keywords:
acute B lymphoblastic leukemia;
cell apoptosis;
drug sensitivity;
matrix remodeling associated 7
- MeSH:
Humans;
Apoptosis;
Cell Line, Tumor;
Cell Proliferation;
Cytarabine;
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma;
Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism*
- From:
Journal of Experimental Hematology
2023;31(1):50-56
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To discover the relationship between matrix remodeling associated 7 (MXRA7) and acute B lymphoblastic leukemia (B-ALL), and explore the effect of MXRA7 on the biological functions of B-ALL cell line REH.
METHODS:The expression of MXRA7 in blood diseases was searched and analyzed through BloodSpot database. Real-time qPCR was used to detect the expression level of MXRA7 in B-ALL cell line 697 and REH cells. Lentivirus-mediated shRNA interference technology was utilized to knock down the expression of MXRA7 in REH cells. The effects of MXRA7 on the biological functions of REH cells were studied by in vitro experiments. Cell proliferation was detected by CCK-8 assay, cell cycle was detected by PI staining, cell apoptosis was detected by Annexin V and 7-AAD staining, and the expression of apoptosis pathway related proteins was detected by Western blot.
RESULTS:Database analysis showed that MXRA7 was highly expressed in B-ALL patients, and real-time qPCR results showed that MXRA7 was also highly expressed in cell lines 697 and REH cells. Knockdown of MXRA7 in REH cells inhibited the cell proliferation and increased the percentage of G0/G1 phase cells. After treatment with cytarabine, the apoptotic ratio was increased in MXRA7-impaired REH cells, and the activation of caspase-3 and caspase-9 were also increased.
CONCLUSION:Knockdown of MXRA7 can reduce the malignancy of REH cells by inhibiting the cell proliferation and increasing the sensitivity of REH cells to cytarabine. These results indicate MXRA7 may be as a novel target for the treatment of B-ALL, and the potential usefulness of MXRA7 in B-ALL deserves further investigation.
