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4 results for “7-dehydrocholesterol”
7-Dehydrocholesterol-derived oxysterols cause neurogenic defects in Smith-Lemli-Opitz syndrome
<p>Defective 3beta-hydroxysterol-delta<sup>7 </sup>-reductase (DHCR7) in the developmental disorder, Smith-Lemli-Opitz syndrome (SLOS), results in deficiency in cholesterol and accumulation of its precursor, 7-dehydrocholesterol (7-DHC). Here, we show that loss of <i>DHCR7</i> causes accumulation of 7-DHC-derived oxysterol metabolites, premature neurogenesis, and perturbation of neuronal localization in developing murine or human cortical neural precursors, both <i>in vitro</i> and <i>in vivo</i>. We found that a major oxysterol, 3b,5a-dihydroxycholest-7-en-6-one (DHCEO), mediates these effects by initiating crosstalk between glucocorticoid receptor (GR) and neurotrophin receptor kinase TrkB. Either loss of <i>DHCR7</i> or direct exposure to DHCEO causes hyperactivation of GR and TrkB and their downstream MEK-ERK-C/EBP signaling pathway in cortical neural precursors. Moreover, direct inhibition of GR activation with an antagonist or inhibition of DHCEO accumulation with antioxidants rescues the premature neurogenesis phenotype caused by the loss of <i>DHCR7</i>. These results suggest that GR could be a new therapeutic target against the neurological defects observed in SLOS.</p>
7-Dehydrocholesterol-derived oxysterols cause neurogenic defects in Smith-Lemli-Opitz syndrome
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m6A-dependent 7-dehydrocholesterol reductase facilitates bladder cancer metastasis via cAMP/PKA/FAK axis
<p><span>Cholesterol homeostasis dysregulation </span><span>appears</span><span> in multiple tumors. However, the specific processes that cause abnormal cholesterol metabolism to affect the invasion and metastasis of bladder cancer (BC) are still unclear. In our investigation, we found a notable rise in the expression of 7-dehydrocholesterol reductase (DHCR7), a key enzyme involved in the synthesis of cholesterol, within BC tissues in comparison to normal tissues and correlated to the invasion and metastasis of BC. This elevated expression of DHCR7 in BC was attributed to the decreased degradation of mRNA mediated by YTHDF2. We discovered that DHCR7 </span><span>plays</span><span> a role in promoting bladder cancer invasion and metastasis </span><span>by</span><span> activating the cAMP-PKA-FAK pathway. Specifically, DHCR7 was found to increase the levels of cAMP by enhancing cholesterol content in lipid rafts, thereby facilitating the transduction of signaling pathways mediated by cAMP receptors. Additionally, DHCR7 was found to enhance the cAMP signaling pathway by reducing the concentration of 7-DHC and promoting the transcription of GIPR. Overall, our findings demonstrated that DHCR7 plays a crucial role in BC invasion and metastasis by modulating cholesterol synthesis and cAMP signaling pathways. Furthermore, AY9944, which acts as an inhibitor of DHCR7, shows promise as a viable therapeutic strategy for the suppression of invasion and metastasis in BC.</span></p>
The role of 7-dehydrocholesterol in inducing ER stress and apoptosis of head and neck squamous cell carcinoma
GEO Series GSE285603. Homo sapiens. 32 samples. Type: Expression profiling by high throughput sequencing.
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