Abstract:Infection with the human papillomavirus (HPV) is a common occurrence among the global population, with millions of new cases emerging on an annual basis. Dysregulated microRNA (miRNA) expression is increasingly being identified to play a role in a number of different diseases, especially in the context of high-risk HPV infection. The present study investigated the miRNA expression profiles of warts induced by low-risk HPV. In warts, miR-27b, miR-24-1, miR-3654, miR-647, and miR-1914 were downregulated while mi… Show more
“…However, HPV infection is estimated to cause 22% of oropharyngeal cancer and 47% of tonsillar cancer cases [ 36 ]. A study by Al-Eitan et al demonstrated that three miRNAs (miR-27b, miR-1914-3p and miR-612) were up- and downregulated in warts (skin lesion due to low-risk HPV) compared to normal skin and, more importantly, that these three miRNAs interacted with the OLR1 gene coding for the Lox-1 receptor [ 37 ]. In this context, the effects of oxLDL on HPV-positive cells should be of great importance.…”
Cardiovascular disease (CVD) and cancer are two major causes of death worldwide. The question is, “Could there be a link between these two pathologies in addition to their shared, common risk factors?” To find some answers, we studied the effect of oxidized low-density lipoproteins (oxLDL) on head and neck cancer (HNC) cell lines, since oxLDL is a major contributor to atherosclerosis and the principal cause of CVD. In this study, we exposed three HNC cell lines (Detroit 562, UPCI-SCC-131 and FaDu) to oxLDL. We investigated two oxLDL receptors, CD36 and Lox-1, using immunofluorescence. Cancer cell migration was evaluated using Boyden chambers and the Wnt/β-catenin pathway was investigated using Western blotting. We demonstrated that the expression of CD36 and Lox-1 significantly increases after exposure to oxLDL. Moreover, we found that oxLDL reduces the migration of HNC cell lines, an observation that is in line with an increased degradation of β-catenin under oxLDL. Finally, the inhibition of CD36 with sulfosuccinimidyl oleate (SSO) reverses the inhibition of cell migration. In conclusion, we report that oxLDL seems to induce an increase in CD36 expression on HNC cell lines, enhancing the uptake of these lipids in cells to finally decrease cancer cell migration via the CD36/β-catenin pathway.
“…However, HPV infection is estimated to cause 22% of oropharyngeal cancer and 47% of tonsillar cancer cases [ 36 ]. A study by Al-Eitan et al demonstrated that three miRNAs (miR-27b, miR-1914-3p and miR-612) were up- and downregulated in warts (skin lesion due to low-risk HPV) compared to normal skin and, more importantly, that these three miRNAs interacted with the OLR1 gene coding for the Lox-1 receptor [ 37 ]. In this context, the effects of oxLDL on HPV-positive cells should be of great importance.…”
Cardiovascular disease (CVD) and cancer are two major causes of death worldwide. The question is, “Could there be a link between these two pathologies in addition to their shared, common risk factors?” To find some answers, we studied the effect of oxidized low-density lipoproteins (oxLDL) on head and neck cancer (HNC) cell lines, since oxLDL is a major contributor to atherosclerosis and the principal cause of CVD. In this study, we exposed three HNC cell lines (Detroit 562, UPCI-SCC-131 and FaDu) to oxLDL. We investigated two oxLDL receptors, CD36 and Lox-1, using immunofluorescence. Cancer cell migration was evaluated using Boyden chambers and the Wnt/β-catenin pathway was investigated using Western blotting. We demonstrated that the expression of CD36 and Lox-1 significantly increases after exposure to oxLDL. Moreover, we found that oxLDL reduces the migration of HNC cell lines, an observation that is in line with an increased degradation of β-catenin under oxLDL. Finally, the inhibition of CD36 with sulfosuccinimidyl oleate (SSO) reverses the inhibition of cell migration. In conclusion, we report that oxLDL seems to induce an increase in CD36 expression on HNC cell lines, enhancing the uptake of these lipids in cells to finally decrease cancer cell migration via the CD36/β-catenin pathway.
“…1 B. 15 Figure 1 Regulatory role and targets of miR-27b. Neuronally-enriched exosomes (NEEs) are shown to express miRNAs for intracellular communication and aberrant expression in various health conditions.…”
Section: Introductionmentioning
confidence: 99%
“…1B. 15 In comparison, miR-320b is also expressed in the brain and has been implicated in neuronal differentiation 16,17 , regulation of inflammatory processes via the nucleotide-binding oligomerization domain 18 , and regulation of endoplasmic reticulum stress 19 . miR-320b is robustly increased in anterior cingulate cortex and habenula of individuals with MDD 20 , regions of the brain thought to be important for pain affect and processing 21,22 .…”
This double-blind, randomized, within-subjects design evaluated whether acute administration of an anti-inflammatory drug modulates neuron-specific, inflammation-modulating microRNAs linked to macroscopic changes in reward processing. Twenty healthy subjects (10 females, 10 males) underwent a functional magnetic resonance imaging scan while performing a monetary incentive delay (MID) task and provided blood samples after administration of placebo, 200 mg, or 600 mg of ibuprofen. Neuronally-enriched exosomal microRNAs were extracted from serum and sequenced. Results showed that: (1) 600 mg of ibuprofen exhibited higher miR-27b-3p, miR-320b, miR-23b and miR-203a-3p expression than placebo; (2) higher mir-27b-3p was associated with lower insula activation during MID loss anticipation; and (3) there was an inverse relationship between miR-27b-3p and MID gain anticipation in bilateral putamen during placebo, a pattern attenuated by both 200 mg and 600 mg of ibuprofen. These findings are consistent with the hypothesis that miR-27b could be an important messaging molecule that is associated with regulating the processing of positive or negative valenced information.
“…In comparison, miR-320b is an intragenic miR on chromosome 1 that has been implicated in neuronal differentiation 30,31 , regulation of in ammatory processes via the nucleotide-binding oligomerization domain 32 , and regulation of endoplasmic reticulum stress 33 . miR-320b is robustly increased in anterior cingulate cortex and habenula of individuals with MDD 34 , regions of the brain thought to be important for pain affect and processing 35,36 .…”
This double-blind, randomized, repeated measures study evaluated whether acute administration of an anti-inflammatory drug modulates neuron-specific, inflammation-modulating microRNAs linked to macroscopic changes in reward processing. Twenty healthy subjects (10 females,10 males) completed a monetary incentive delay (MID) task and provided blood samples after administration of placebo, 200 mg, or 600 mg of ibuprofen. Neuronally-enriched exosomal microRNAs were extracted from plasma and sequenced. Results showed that: (1) 600 mg of ibuprofen exhibited higher miR-27b-3p, miR-320b, miR-23b and miR-203a-3p expression than placebo; (2) higher mir-27b-3p was associated with lower insula activation during MID loss anticipation; and (3) there was an inverse relationship between miR-27b-3p and MID gain anticipation in bilateral putamen during placebo, a pattern attenuated by both 200 mg and 600 mg of ibuprofen. Our findings indicate that miR-27b could be an important messaging molecule altered by anti-inflammatory drugs that relates to the processing of positive or negative valenced information.
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