当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Alternative splicing of Ikaros regulates the FUT4/LeX-α5β1 integrin-FAK axis in acute lymphoblastic leukemia.

Alternative splicing of Ikaros regulates the FUT4/LeX-α5β1 integrin-FAK axis in acute lymphoblastic leukemia.

Abstract：

:Unveiling the mechanism of the relapse of acute lymphoblastic leukemia (ALL) is the key to improve the prognosis of ALL and remains a huge challenge. Glycan-based interactions play a vital role in immune surveillance, cell-cell adhesion and cell-matrix interaction, contributing to treatment failure in tumor. However, the glycan essential for leukemia development and its upstream regulatory mechanism by oncogenic drivers were rarely reported. Here, we demonstrated that LeX, a well-characterized cancer-related glycan epitope, strengthened the cell-matrix interaction via glycosylating α5β1 integrin under the control of the driver oncogenic Ikaros isoform (IK6) in ALL. By analyzing the expression profile of Ikaros and the level of FUT4/LeX in clinical samples, we found that FUT4/LeX was positively correlated with dysfunctional Ikaros isoforms. IK1 (Full length Ikaros) regulates the level of FUT4 as a transcription repressor, while IK6 abolished the wild-type Ikaros mediated transcriptional repression and resulted in higher level of FUT4 expression. Moreover, we demonstrated that FUT4 could activate α5β1-mediated sequential signal transduction and accelerate adhesion and invasion between integrin α5β1 in leukemia cells and fibronectin in extracellular matrix (ECM) via increasing glycosylation. Together, our study provides a new insight into the mechanisms by which Ikaros mutation induced ALL cells invasion and a potential strategy for drug-resistance ALL by blocking LeX in combination with common chemotherapy.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Yi L,Hu Q,Zhou J,Liu Z,Li H

doi

10.1016/j.bbrc.2019.01.064

subject

Has Abstract

pub_date

2019-02-26 00:00:00

pages

128-134

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)30078-6

journal_volume

510

pub_type

杂志文章

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