ArticlePloS one2011
Secretion of novel SEL1L endogenous variants is promoted by ER stress/UPR via endosomes and shed vesicles in human cancer cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- ER-associated degradation pathway protein SEL1L plays an evolutionarily conserved role in platelet adhesion.The Journal of clinical investigation · 2026Article
- Somatostatin and Somatostatin Receptors in Tumour Biology.International journal of molecular sciences · 2023Review
- Identification of novel genes for triple-negative breast cancer with semiparametric gene-based analysis.Journal of applied statistics · 2023Article
- Sourcing the immune system to induce immunogenic cell death in Kras-colorectal cancer cells.British journal of cancer · 2019Article
- Protein Expression Analysis in Uterine Cervical Cancer for Potential Targets in Treatment.Pathology oncology research : POR · 2019Article
- SEL1L SNP rs12435998, a predictor of glioblastoma survival and response to radio-chemotherapy.Oncotarget · 2015Article
- An integrative analysis of meningioma tumors reveals the determinant genes and pathways of malignant transformation.Frontiers in oncology · 2014Article
- Epithelial-mesenchymal transition induces endoplasmic-reticulum-stress response in human colorectal tumor cells.PloS one · 2014Article
- Cell and tissue microarray technologies for protein and nucleic acid expression profiling.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013Article
- A role for myocilin in receptor-mediated endocytosis.PloS one · 2013Article
- SEL1L, an UPR response protein, a potential marker of colonic cell transformation.Digestive diseases and sciences · 2012Article
- A SEL1L mutation links a canine progressive early-onset cerebellar ataxia to the endoplasmic reticulum-associated protein degradation (ERAD) machinery.PLoS genetics · 2012Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We describe here two novel endogenous variants of the human endoplasmic reticulum (ER) cargo receptor SEL1LA, designated p38 and p28. Biochemical and RNA interference studies in tumorigenic and non-tumorigenic cells indicate that p38 and p28 are N-terminal, ER-anchorless and more stable relative to the canonical transmembrane SEL1LA. P38 is expressed and constitutively secreted, with increase after ER stress, in the KMS11 myeloma line and in the breast cancer lines MCF7 and SKBr3, but not in the non-tumorigenic breast epithelial MCF10A line. P28 is detected only in the poorly differentiated SKBr3 cell line, where it is secreted after ER stress. Consistently with the presence of p38 and p28 in culture media, morphological studies of SKBr3 and KMS11 cells detect N-terminal SEL1L immunolabeling in secretory/degradative compartments and extracellularly-released membrane vesicles. Our findings suggest that the two new SEL1L variants are engaged in endosomal trafficking and secretion via vesicles, which could contribute to relieve ER stress in tumorigenic cells. P38 and p28 could therefore be relevant as diagnostic markers and/or therapeutic targets in cancer.
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