Down-modulation of SEL1L, an Unfolded Protein Response and Endoplasmic Reticulum-associated Degradation Protein, Sensitizes Glioma Stem Cells to the Cytotoxic Effect of Valproic Acid

Cattaneo, Monica; Baronchelli, Simona; Schiffer, Davide; Mellai, Marta; Caldera, Valentina; Saccani, Gloria; Dalprà, Leda; Daga, Antonio; Orlandi, Rosaria; Blasio, Pasquale De; Biunno, Ida

doi:10.1074/jbc.m113.527754

Cited by 25 publications

(19 citation statements)

References 45 publications

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“…Within GBM cell lines, the SNP rs12435998 down-regulates SEL1L expression only in NS and, at the same time, it increases the sensitivity to VPA, confirming a previous observation [ 21 ]. In fact, compared to wild type NS, the cell viability after VPA was significantly lower in NS with the TC/CC variant genotype.…”

Section: Discussionsupporting

confidence: 86%

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SEL1L SNP rs12435998, a predictor of glioblastoma survival and response to radio-chemotherapy

Mellai¹,

Cattaneo

Storaci

et al. 2015

Oncotarget

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The suppressor of Lin-12-like (C. elegans) (SEL1L) is involved in the endoplasmic reticulum (ER)-associated degradation pathway, malignant transformation and stem cells.In 412 formalin-fixed and paraffin-embedded brain tumors and 39 Glioblastoma multiforme (GBM) cell lines, we determined the frequency of five SEL1L single nucleotide genetic variants with regulatory and coding functions by a SNaPShot™ assay. We tested their possible association with brain tumor risk, prognosis and therapy.We studied the in vitro cytotoxicity of valproic acid (VPA), temozolomide (TMZ), doxorubicin (DOX) and paclitaxel (PTX), alone or in combination, on 11 GBM cell lines, with respect to the SNP rs12435998 genotype.The SNP rs12435998 was prevalent in anaplastic and malignant gliomas, and in meningiomas of all histologic grades, but unrelated to brain tumor risks. In GBM patients, the SNP rs12435998 was associated with prolonged overall survival (OS) and better response to TMZ-based radio-chemotherapy. GBM stem cells with this SNP showed lower levels of SEL1L expression and enhanced sensitivity to VPA.

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Section: Discussionsupporting

confidence: 86%

“…SEL1L is involved in several other neoplasia [ 16 – 20 ]. Its reduced protein expression by RNA interference increases GBM stem cell sensitivity to valproic acid (VPA) treatments [ 21 ]. SEL1L also plays a role in the neural stem cell self-renewal [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

SEL1L SNP rs12435998, a predictor of glioblastoma survival and response to radio-chemotherapy

Mellai¹,

Cattaneo

Storaci

et al. 2015

Oncotarget

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“…mSEL‐1L was well expressed during CNS development (Donoviel, Donoviel, Fan, Hadjantonakis, & Bernstein, ) and its deficiency led to severe defects in brain, in addition to general organogenesis and maintenance (Francisco et al, ). Previously was shown the essential function of mSEL‐1L in guaranteeing the balance between self‐renewal and differentiation in neural progenitors (Cardano et al, ), possibly by controlling the fine tuning levels of self‐renewal and fate determinant regulators (Cardano et al, ; Cattaneo et al, ).…”

Section: Introductionmentioning

confidence: 99%

mSEL‐1L deficiency affects vasculogenesis and neural stem cell lineage commitment

Cardano¹,

Diaferia²,

Conti

et al. 2017

Journal Cellular Physiology

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mSEL-1L is a highly conserved ER-resident type I protein, involved in the degradation of misfolded peptides through the ubiquitin-proteasome system (UPS), a pathway known to control the plasticity of the vascular smooth muscle cells (VSMC) phenotype and survival. In this article, we demonstrate that mSEL-1L deficiency interferes with the murine embryonic vascular network, showing particular irregularities in the intracranic and intersomitic neurovascular units and in the cerebral capillary microcirculation. During murine embryogenesis, mSEL-1L is expressed in cerebral areas known to harbor progenitor neural cells, while in the adult brain the protein is specifically restricted to the stem cell niches, co-localizing with Sox2 and Nestin. Null mice are characterized by important defects in the development of telenchephalic regions, revealing conspicuous aberration in neural stem cell lineage commitment. Moreover, mSEL-1L depletion in vitro and in vivo appears to affect the harmonic differentiation of the NSCs, by negatively influencing the corticogenesis processes. Overall, the data presented suggests that the drastic phenotypic characteristics exhibited in mSEL-1L null mice can, in part, be explained by the negative influence it plays on Notch1 signaling pathway.

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“…Mellai et al [2020] reported that overexpression of SEL1L in malignant gliomas is associated significantly with TERT promoter mutation, EGFR gene amplification, and other well-known negative prognostic markers for gliomas, leading the authors to suggest a role for SEL1L in glioma progression. Furthermore, downregulation of SEL1L conferred positive sensitivity to valproic acid treatment [Cattaneo et al, 2014] which may suggest a role of SEL1L in gene-target therapy.…”

Section: Discussionmentioning

confidence: 93%

Narrowing down the Common Cytogenetic Deletion 14q to a 5.6-Mb Critical Region in 1p/19q Codeletion Oligodendroglioma-Relapsed Patients Points to Two Potential Relapse-Related Genes: SEL1L and STON2

Zhang

Guzmán

Batanian

2020

Cytogenet Genome Res

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abnormalities including a 14q deletion of 16.5 Mb at 14q24.2q31.3. This region overlaps with 2 previously iden tified minimal regions, 14q21.2q24.3 and 14q31.3q32.1, based on 142 cases of glioma. The authors reported no cor relation between these 2 regions and survival. By extracting these 2 regions from our patient's deletion and comparing it to 12 other cases of 1p/19q codeletion oligodendroglio mas reported in the literature, we narrowed down the 14q loss possible critical region to 5.6 Mb mapping at 14q31.1q31.2. This region contains 2 potential relapserelat ed genes: SEL1L and STON2.

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Down-modulation of SEL1L, an Unfolded Protein Response and Endoplasmic Reticulum-associated Degradation Protein, Sensitizes Glioma Stem Cells to the Cytotoxic Effect of Valproic Acid

Cited by 25 publications

References 45 publications

SEL1L SNP rs12435998, a predictor of glioblastoma survival and response to radio-chemotherapy

SEL1L SNP rs12435998, a predictor of glioblastoma survival and response to radio-chemotherapy

mSEL‐1L deficiency affects vasculogenesis and neural stem cell lineage commitment

Narrowing down the Common Cytogenetic Deletion 14q to a 5.6-Mb Critical Region in 1p/19q Codeletion Oligodendroglioma-Relapsed Patients Points to Two Potential Relapse-Related Genes: <b><i>SEL1L</i></b> and <b><i>STON2</i></b>

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