FEM1B enhances TRAIL-induced apoptosis in T lymphocytes and monocytes.

IF 2.8 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Chenbo Yang, Wenhui Yu, Cui Dang, Jingjing Zhang, Jiahan Lu, Jing Xue
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引用次数: 0

Abstract

FEM1B is recognized for its significant pro-apoptotic function in colorectal cancer; however, its influence and mechanisms regarding apoptosis in immune cells remain inadequately elucidated. In this study, we demonstrated that FEM1B enhances TRAIL-induced apoptosis in Molt-4, Jurkat, THP-1, and U937 cell lines. Notably, the knockdown of FEM1B in transfected cells resulted in a reversal of the observed increase in cell apoptosis. Our findings indicate that FEM1B activates caspase-3 and caspase-8, but not caspase-9, in response to TRAIL stimulation, suggesting its involvement in the extrinsic caspase-dependent apoptotic pathway. Furthermore, we found that FEM1B interacted with TRAF2 and downregulates its expression in Molt-4 and Jurkat cells, thereby diminishing TRAF2's inhibitory effect on caspase-8. In THP-1 and U937 cells, FEM1B was found to upregulate TRAIL-R2, thereby promoting TRAIL-induced apoptosis. Knockout studies in murine models further corroborated that FEM1B facilitates TRAIL-induced apoptosis. These results demonstrate that FEM1B enhances TRAIL-induced apoptosis in T lymphocytes and monocytes through a caspase-dependent mechanism involving TRAF2 or TRAIL receptors.

FEM1B增强trail诱导的T淋巴细胞和单核细胞凋亡。
FEM1B在结直肠癌中具有显著的促凋亡功能;然而,其对免疫细胞凋亡的影响及其机制尚不清楚。在这项研究中,我们证明了FEM1B促进trail诱导的Molt-4、Jurkat、THP-1和U937细胞系的凋亡。值得注意的是,转染细胞中FEM1B的敲低导致观察到的细胞凋亡增加的逆转。我们的研究结果表明,FEM1B在TRAIL刺激下激活caspase-3和caspase-8,而不是caspase-9,这表明它参与了外源性caspase依赖性凋亡途径。此外,我们发现FEM1B与TRAF2相互作用,下调其在Molt-4和Jurkat细胞中的表达,从而减弱TRAF2对caspase-8的抑制作用。在THP-1和U937细胞中,FEM1B被发现上调TRAIL-R2,从而促进trail诱导的细胞凋亡。小鼠模型的敲除研究进一步证实了FEM1B促进trail诱导的细胞凋亡。这些结果表明,FEM1B通过涉及TRAF2或TRAIL受体的caspase依赖机制增强TRAIL诱导的T淋巴细胞和单核细胞凋亡。
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来源期刊
FEBS Open Bio
FEBS Open Bio BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
5.10
自引率
0.00%
发文量
173
审稿时长
10 weeks
期刊介绍: FEBS Open Bio is an online-only open access journal for the rapid publication of research articles in molecular and cellular life sciences in both health and disease. The journal''s peer review process focuses on the technical soundness of papers, leaving the assessment of their impact and importance to the scientific community. FEBS Open Bio is owned by the Federation of European Biochemical Societies (FEBS), a not-for-profit organization, and is published on behalf of FEBS by FEBS Press and Wiley. Any income from the journal will be used to support scientists through fellowships, courses, travel grants, prizes and other FEBS initiatives.
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