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The Frontiers of Society, Science and Technology, 2020, 2(11); doi: 10.25236/FSST.2020.021119.

Downregulating Lunar1 to “Notch-Down” the Progression of Human t-All


Qitong Luan

Corresponding Author:
Qitong Luan

Gaston Day School


T-ALL is one of the most common types of leukemia with a high lethality rate. The effective leukemia treatment CAR-T therapy is difficult to be applied on T-ALL. Previous studies has reported that the Notch-regulated lncRNA LUNAR1 upregulates IGF1R, which increases the cell proliferation in T-ALL cell lines. The silencing of LUNAR1 will downregulate the expression of IGF1 R and reduce T-ALL cell proliferation. This study investigates the effect of knocking down LUNAR1 using LUNAR1 siRNA on T-ALL treatment, in both in vitro and in vivo conditions. The experiments will use know human leukemia cell lines, a variety of pediatric primary thymus surgical samples and peripheral blood samples, murine cell lines, and Xenograft Murine Models. There are three most possible results: (1) Knockdown of LUNAR1 inhibit the T-ALL cell proliferation in both in vitro and in vivo cell lines; (2) Knockdown of LUNAR1 only inhibit the T-ALL cell proliferation in in vitro cell cultures; (3) Knockdown of LUNAR1 only inhibit the T-ALL cell proliferation in determined human and murine T-ALL cell lines. The result of this study will provide important information for the future clinical trial of LUNAR1 knockdown therapy. Future studies should focus on improving the in vivo delivery methods and finding more LUNAR1 drug inhibitors, as well as exploring the specific gene regulation mechanism of LUNAR1 in detail.


T-all, Notch pathway, Lncrna, Lunar1, Igf1 r, Sirna therapy

Cite This Paper

Qitong Luan. Downregulating Lunar1 to “Notch-Down” the Progression of Human t-All. The Frontiers of Society, Science and Technology (2020) Vol. 2 Issue 11: 132-137. https://doi.org/10.25236/FSST.2020.021119.


[1] Grabher, C., H. von Boehmer, A.T. Look (2006). Notch 1 activation in the molecular pathogenesis of T-cell acute lymphoblastic leukaemia. Nature Reviews Cancer, vol.6, no.5, pp.347-359.

[2] Fleischer, L.C., H.T. Spencer, S.S. Raikar (2019). Targeting T cell malignancies using CAR-based immunotherapy: challenges and potential solutions. Journal of Hematology & Oncology, vol.12, no.1, pp.141.

[3] Medyouf, H., et al (2011). High-level IGF1R expression is required for leukemia-initiating cell activity in T-ALL and is supported by Notch signaling. The Journal of experimental medicine, vol.208, no.9, pp.1809-1822.

[4] Trimarchi, T., et al (2014). Genome-wide mapping and characterization of Notch-regulated long noncoding RNAs in acute leukemia. Cell, vol.158, no.3, pp.593-606.

[5] Wang, X., et al (2019). Novel lncRNA-IUR suppresses Bcr-Abl-induced tumorigenesis through regulation of STAT5-CD71 pathway. Molecular Cancer, vol.18, no.1, pp.84.

[6] Gopalakrishnapillai, A., et al (2016). Generation of Pediatric Leukemia Xenograft Models in NSG-B2m Mice: Comparison with NOD/SCID Mice. Frontiers in oncology, no.6, pp.162-162.

[7] Palomero, T., et al (2006). CUTLL1, a novel human T-cell lymphoma cell line with t (7;9) rearrangement, aberrant NOTCH1 activation and high sensitivity to γ-secretase inhibitors. Leukemia, vol.20, no.7, pp.1279-1287.

[8] Pajcini, K.V., et al (2017). MAFB enhances oncogenic Notch signaling in T cell acute lymphoblastic leukemia. Science Signaling, vol.10, no.505, pp.6846.