Open Access
ARTICLE
miR-101 Represses T-Cell Acute Lymphoblastic Leukemia by Targeting CXCR7/STAT3 Axis
Life Science College, Luoyang Normal University, Luoyang, Henan, P.R. China
Oncology Research 2019, 27(9), 997-1006. https://doi.org/10.3727/096504018X15439207752093
Abstract
Although miR-101 is involved in the development and progression of T-cell acute lymphoblastic leukemia (T-ALL), the underlying molecular mechanisms remain unclear. In this article, we report that miR-101 expression was inversely correlated with CX chemokine receptor 7 (CXCR7) level in T-ALL. Introducing miR-101 inhibited T-ALL cell proliferation and invasion in vitro and suppressed tumor growth and lung metastasis in vivo. CXCR7 was identified as a direct target of miR-101. The inhibitory effects of miR-101 were mimicked and counteracted by CXCR7 depletion and overexpression, respectively. Mechanistically, miR-101 targets CXCR7/STAT3 axis to reduce T-ALL growth and metastasis. Overall, these findings implied the potential application of miR-101 and CXCR7 in T-ALL treatment.Keywords
MicroRNA-101 (miR-101); CXCR7; T-cell acute lymphoblastic leukemia (T-ALL)
Cite This Article
APA Style
Yang, X., Sheng, Y. (2019). miR-101 Represses T-Cell Acute Lymphoblastic Leukemia by Targeting CXCR7/STAT3 Axis. Oncology Research, 27(9), 997–1006. https://doi.org/10.3727/096504018X15439207752093
Vancouver Style
Yang X, Sheng Y. miR-101 Represses T-Cell Acute Lymphoblastic Leukemia by Targeting CXCR7/STAT3 Axis. Oncol Res. 2019;27(9):997–1006. https://doi.org/10.3727/096504018X15439207752093
IEEE Style
X. Yang and Y. Sheng, “miR-101 Represses T-Cell Acute Lymphoblastic Leukemia by Targeting CXCR7/STAT3 Axis,” Oncol. Res., vol. 27, no. 9, pp. 997–1006, 2019. https://doi.org/10.3727/096504018X15439207752093
Copyright © 2019 The Author(s). Published by Tech Science Press.This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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