Ontology highlight
ABSTRACT:
Materials and methods: We used small interfering RNA (siRNA) technology to knock down LEF1 in Jurkat cells and then compared the gene expression levels in the LEF1 knockdown cells with non-targeting siRNA-transfected and non-transfected cells by employing microarray analysis.
Results: We identified DHRS2, a tumor suppressor gene, as the most significantly downregulated gene in LEF1 knockdown cells, and we further confirmed its downregulation by real-time quantitative polymerase chain reaction (qRT-PCR) in mRNA and at protein level by western blotting.
Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.
SUBMITTER: S?rma Ekmekci S
PROVIDER: S-EPMC7702649 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
Sırma Ekmekci Sema S Emrence Zeliha Z Abacı Neslihan N Sarıman Melda M Salman Burcu B Ekmekci Cumhur Gökhan CG Güleç Çağrı Ç
Turkish journal of haematology : official journal of Turkish Society of Haematology 20200626 4
<h4>Objective</h4>T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease resulting from the accumulation of genetic changes that affect the development of T-cells. The precise role of lymphoid enhancer-binding factor 1 (<i>LEF1</i>) in T-ALL has been controversial since both overexpression and inactivating <i>LEF1</i> mutations have been reported to date. Here, we investigate the potential gene targets of <i>LEF1</i> in the Jurkat human T-cell leukemia cell line.<h4>Materials and m ...[more]