Anti-apoptotic function of Xbp1 as an IL-3 signaling molecule in hematopoietic cells

Kurata, Morito; Yamazaki, Yukari; Kanno, Yohei; Ishibashi, Sachiko; Takahara, Tomoko; Kitagawa, Masanobu; Nakamura, Takuro

doi:10.1038/cddis.2011.1

Cited by 69 publications

(61 citation statements)

References 28 publications

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“…In addition, Western Blot analysis revealed that pretreatment with LY294002 abolished the IL‐17A induced up‐regulation of PI3K and AKT either total protein levels or phosphorylated protein levels respectively (* P < 0.05, ** P < 0.01) (Figure C and D). These results were similar to the results from previous studies using the same inhibitor . Taken together, the results demonstrated that the IL‐17A promoted GBM cell migration and invasion were dependent on MMP‐2/9 and Twist via activating PI3K/AKT signalling pathway.…”

Section: Resultssupporting

confidence: 90%

IL‐17A promotes cell migration and invasion of glioblastoma cells via activation of PI3K/AKT signalling pathway

Zheng

Diao

Wang

et al. 2018

J Cellular Molecular Medi

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Glioblastomas (GBMs) are the most common of both benign and malignant primary brain tumours, in which the inflammatory and immunologic abnormalities are involved. Interleukin‐17A (IL‐17A) plays an important role in various inflammatory diseases and cancers. Several recent studies revealed that the expression of IL‐17A was overexpressed in human GBMs tissue. However, the accurate role of IL‐17A in GBMs remains unclear. In this study, we aimed to explore the effect of IL‐17A on cell migration and invasion of GBMs and the mechanism by which the effects occurred. We found that exogenous IL‐17A promoted significantly cell migration and invasion abilities in two GBMs cell lines (U87MG and U251) in a time‐dependent manner. In addition, the protein expressions of PI3K, Akt and MMP‐2/9 were increased in the GBMs cells challenged by IL‐17A. Furthermore, a tight junction protein ZO‐1 was down‐regulated but Twist and Bmi1 were up‐regulated. Treatment with a PI3K inhibitor (LY294002) significantly reduced the abilities of both migration and invasion in U87MG and U251 cells. LY294002 treatment also attenuated the IL‐17A causing increases of protein levels of PI3K, AKT, MMP‐2/9, Twist and the decreases of protein level of ZO‐1 in the U87MG and U251 cells. Taken together, we concluded that IL‐17A promotes the GBM cells migration and invasion via PI3K/AKT signalling pathway. IL‐17A and its related signalling pathways may be potential therapeutic targets for GBM.

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Section: Resultssupporting

confidence: 90%

IL‐17A promotes cell migration and invasion of glioblastoma cells via activation of PI3K/AKT signalling pathway

Zheng

Diao

Wang

et al. 2018

J Cellular Molecular Medi

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“…To date, it is unclear whether and how XBP1s might inhibit apoptosis. There are only two reports linking XBP1s with dedicated pro-or anti-apoptotic target genes, namely downregulation of BH3-only protein BIM (Kurata et al, 2011) or upregulation of BCL-2 (Gomez et al, 2007), respectively, and neither of these studies addressed protection from ER stress (Gomez et al, 2007;Kurata et al, 2011). In general, XBP1s-mediated protection during ER stress might rather be related to enhancement of ER folding capacity and stimulation of ERAD and/or protein secretion.…”

Section: Ire1 At the Crossroad Of Survival-death Decisionsmentioning

confidence: 99%

The unfolded protein response at the crossroads of cellular life and death during endoplasmic reticulum stress

Jäger

Bertrand

Gorman

et al. 2012

Biology of the Cell

187

139

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One of the early cellular responses to endoplasmic reticulum (ER) stress is the activation of the unfolded protein response (UPR). ER stress and the UPR are both implicated in numerous human diseases and pathologies. In spite of this, our knowledge of the molecular mechanisms that regulate cell fate following ER stress is limited. The UPR is initiated by three ER transmembrane receptors: PKR-like ER kinase (PERK), activating transcription factor (ATF) 6 and inositol-requiring enzyme 1 (IRE1). These proteins sense the accumulation of unfolded proteins and their activation triggers specific adaptive responses to resolve the stress. Intriguingly, the very same receptors can initiate signalling pathways that lead to apoptosis when the attempts to resolve the ER stress fail. In this review, we describe the known pro-apoptotic signalling pathways emanating from activated PERK, ATF6 and IRE1 and discuss how their signalling switches from an adaptive to a pro-apoptotic response. ER stress and unfolded protein responseThe endoplasmic reticulum (ER) is a threedimensional cellular network of extensive interlinked membranous tubules, sacs and flattened cisternae. It spans from the nuclear envelope to the secretory vesicles. The morphology and the extent of the ER network organisation very much depend on the predominant function(s) of any given cell type. The ER participates in a variety of cellular functions such as synthesis and sorting of secretory and membrane proteins, biosynthesis of phospholipids, cholesterol, steroids, degradation of glycogen, detoxification reactions and maintenance of intracellular calcium home-1 To whom correspondence should be addressed (email afshin.samali@nuigalway.ie).

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“…XBP1s has a diverse range of target genes which share the common aim of short term adaptation and ultimately restoration of ER function. Recent reports also suggest XBP1s signaling may be able to modulate apoptotic signaling by regulating Bcl-2 levels (Gomez et al, 2007; Kurata et al, 2011) but it remains currently unknown whether XBP1s can modulate Bcl-2 family member expression in response to ER stress. Overexpression of IRE1α in human embryonic kidney cells has been reported to induce death indicating that IRE1α could activate pro-apoptotic signaling components (Wang et al, 1998).…”

Section: Endoplasmic Reticulum Stress Apoptosis and Cell Deathmentioning

confidence: 99%

Endoplasmic reticulum stress in human skeletal muscle: any contribution to sarcopenia?

Deldicque¹

2013

Front. Physiol.

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Skeletal muscle is vital to life as it provides the mechanical power for locomotion, posture and breathing. Beyond these vital functions, skeletal muscle also plays an essential role in the regulation of whole body metabolism, e.g., glucose homeostasis. Although progressive loss of muscle mass with age seems unavoidable, it is critical for older people to keep the highest mass as possible. It is clear that the origin of sarcopenia is multifactorial but, in the present review, it was deliberately chosen to evaluate the likely contribution of one specific cellular stress, namely the endoplasmic reticulum (ER) stress. It is proposed that ER stress can: (1) directly impact muscle mass as one fate of prolonged and unresolved ER stress is cell death and; (2) indirectly create a state of anabolic resistance by inhibiting the mammalian target of rapamycin complex 1 (mTORC1) pathway. With age, many of the key components of the unfolded protein response, such as the chaperones and enzymes, display reduced expression and activity resulting in a dysfunctional ER, accelerating the rate of proteins discarded via the ER-associated degradation. In addition, ER stress can block the mTORC1 pathway which is essential in the response to the anabolic stimulus of nutrients and contractile activity thereby participating to the well-known anabolic resistance state in skeletal muscle during ageing. As exercise increases the expression of several chaperones, it could anticipate or restore the loss of unfolded protein response components with age and thereby reduce the level of ER stress. This hypothesis has not been tested yet but it could be a new mechanism behind the beneficial effects of exercise in the elderly not only for the preservation of muscle mass but also for the regulation of whole body metabolism.

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Anti-apoptotic function of Xbp1 as an IL-3 signaling molecule in hematopoietic cells

Cited by 69 publications

References 28 publications

IL‐17A promotes cell migration and invasion of glioblastoma cells via activation of PI3K/AKT signalling pathway

IL‐17A promotes cell migration and invasion of glioblastoma cells via activation of PI3K/AKT signalling pathway

The unfolded protein response at the crossroads of cellular life and death during endoplasmic reticulum stress

Endoplasmic reticulum stress in human skeletal muscle: any contribution to sarcopenia?

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