2017
DOI: 10.18632/oncotarget.23618
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TrkAIII signals endoplasmic reticulum stress to the mitochondria in neuroblastoma cells, resulting in glycolytic metabolic adaptation

Abstract: Alternative TrkAIII splicing characterises advanced stage metastatic disease and post-therapeutic relapse in neuroblastoma (NB), and in NB models TrkAIII exhibits oncogenic activity. In this study, we report a novel role for TrkAIII in signaling ER stress to the mitochondria in SH-SY5Y NB cells that results in glycolytic metabolic adaptation. The ER stress-inducing agents DTT, A23187 and thapsigargin activated the ER stress-response in control pcDNA SH-SY5Y and TrkAIII expressing SH-SY5Y cells and in TrkAIII S… Show more

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Cited by 10 publications
(47 citation statements)
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“…TrkAIII intracellular re-localisation and oncogenic behaviour supports the growing concept that mislocalization of TrkA-derived oncogenes underpins oncogenic signaling [ 3 , 7 , 19 , 26 , 32 , 40 , 50 ]. In contrast to fully-spliced cell surface TrkA receptors that associate with caveolin in low density membrane fractions [ 23 ] and exhibit tumour suppressing activity in NB [ 1 , 19 ], TrkAIII receptors do not associate with caveolin in low density membrane fractions [ 23 ] and re-localise to intracellular pre-Golgi membranes, in which they exhibits spontaneous activation and self-perpetual recycling between the ER and ERGIC-COPI compartments [ 19 , 40 , 50 ].…”
Section: Trkaiii Triggers a Variety Of Pro-tumorigenic Mechanismsmentioning
confidence: 61%
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“…TrkAIII intracellular re-localisation and oncogenic behaviour supports the growing concept that mislocalization of TrkA-derived oncogenes underpins oncogenic signaling [ 3 , 7 , 19 , 26 , 32 , 40 , 50 ]. In contrast to fully-spliced cell surface TrkA receptors that associate with caveolin in low density membrane fractions [ 23 ] and exhibit tumour suppressing activity in NB [ 1 , 19 ], TrkAIII receptors do not associate with caveolin in low density membrane fractions [ 23 ] and re-localise to intracellular pre-Golgi membranes, in which they exhibits spontaneous activation and self-perpetual recycling between the ER and ERGIC-COPI compartments [ 19 , 40 , 50 ].…”
Section: Trkaiii Triggers a Variety Of Pro-tumorigenic Mechanismsmentioning
confidence: 61%
“…2 ) (manuscript in preparation). Spontaneous TrkAIII activation could also result from down-regulating the expression and activity of TrkA de-phosphorylating PTPases, such as Shp1 and PTP1B [ 19 , 32 ], in a manner analogous to PTP1B regulation of the NB-associated oncogene Alk [ 33 , 34 ], which may also influence potential interactions between Alk and TrkAIII [ 35 ].…”
Section: Oncogenic Alternative Trkaiii Splicing: a De-regulated Physimentioning
confidence: 99%
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