The anti-tumor effects of evodiamine on oral squamous cell carcinoma (OSCC) through regulating advanced glycation end products (AGE) / receptor for advanced glycation end products (RAGE) pathway

Ren, Liuyang; Lou, Ying; Sun, Mingyu

doi:10.1080/21655979.2021.1972082

Cited by 9 publications

(10 citation statements)

References 35 publications

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“…[43][44][45] Regarding OSCC, there have been several investigations that aimed to evaluate the role and expression of RAGE receptor. [46][47][48] In a study that evaluated 74 OSCC samples, the RAGE receptor was reported to be a prognostic factor, and was significantly associated with the depth of invasion and local recurrence. 46 Moreover, a particular role of RAGE in OSCC pathogenesis was confirmed in an in vitro study, where this receptor proved to be activated in a paracrine manner by the extracellular molecule high-mobility group box 1 (HMGB1) that was secreted by the OSCC cells.…”

Section: Discussionmentioning

confidence: 99%

“…47 Furthermore, RAGE proved to be significantly decreased by evodiamine, a novel anti-tumor drug, inhibiting proliferation, invasion and angiogenesis of OSCC both in vitro and in vivo. 48 Finally, the gene that encodes the RAGE receptor is predicted to be one of the hsa-miR-769-5p targets both in CDS and 5ʹUTR positions, according to the miRWalk v. 3.0 database. 19 Finally, for hsa-miR-4500, there is no evidence so far concerning its expression in OSCC.…”

Section: Discussionmentioning

confidence: 99%

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Gene network analysis of the transcriptome impact of methylated microRNAs on oral squamous cell carcinoma

et al. 2022

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Background. Oral squamous cell carcinoma (OSCC) is one of the most common head and neck squamous cell tumors. MicroRNAs and DNA methylation, as epigenetic mechanisms, regulate the expression of oncogenes and tumor suppressor genes, contributing to the carcinogenic development. However, the current knowledge on the genetic and epigenetic landscape of OSCC is still limited.Objectives. To assess the transcriptomic impact of microRNAs found to be methylated through Infinium genome-wide methylation profiling of archived OSCC tissues, and to analyze their biological role using gene network analysis.Materials and methods. We used the Infinium array-based methylation assay to assess the genome-wide methylation status at the single-CpG-site level of DNA purified from archived OSCC tissue samples. After quality control, filtering out poorly performing probes and normalization of data, we identified the differentially methylated microRNA loci. We performed a literature-based analysis of OSCC transcriptomic data to identify the predicted target genes for each microRNA, followed by individual network and pathway enrichment analyses.Results. The analysis of Infinium methylation array data revealed 1469 differentially hypomethylated loci, 4 of which were of interest, namely hsa-microRNA-124-3, hsa-microRNA-24-1, hsa-microRNA-769, and hsa-microRNA-4500. Network and pathway enrichment analyses revealed multiple pathways modulated through DNA methylation-microRNA expression axes.Conclusions. We describe the transcriptomic impact of 4 differentially methylated microRNAs in OSCC tissues samples and discuss their role in the pathology of OSCC. These results may contribute to a better understanding of how epigenetic mechanisms such as DNA methylation and microRNAs cooperate to impact the development of OSCC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Gene network analysis of the transcriptome impact of methylated microRNAs on oral squamous cell carcinoma

et al. 2022

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“…Angiogenesis was investigated by tube formation analysis according to a previous report [ 23 ]. In brief, HUVEC cells (1 × 10 4 /well) were added in Matrigel-coated 96-well plates overnight.…”

Section: Methodsmentioning

confidence: 99%

“…The interaction between IGF2BP2 and HPSE was analyzed by luciferase reporter analysis referring to a previous report with some modifications [ 23 ]. In brief, the WT or MUT sequence of HPSE 3ʹ untranslated region (UTR) with IGF2BP2 binding sites was inserted in the psi-CHECK2 vector (Promega), generating the WT and MUT HPSE luciferase reporter vectors.…”

Section: Methodsmentioning

confidence: 99%

Insulin-like growth factor 2 mRNA binding protein 2 regulates proliferation, migration, and angiogenesis of keratinocytes by modulating heparanase stability

Zhi¹,

Li²,

Kong³

et al. 2021

Bioengineered

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Wound healing is related to proliferation, migration, and angiogenesis of keratinocytes. Insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) is an important N6-methyladenosine (m6A) reader, which is involved in multiple processes, including wound healing. However, the function and mechanism of IGF2BP2 in keratinocyte processes are largely uncertain. In the present study, expression levels of IGF2BP2 and heparanase (HPSE) were detected by quantitative reverse transcription polymerase chain reaction and western blotting assays. Cell proliferation was investigated by cell counting kit-8 (CCK-8) analysis. Cell migration was determined through wound healing assay. Angiogenesis was measured by tube formation assay and vascular endothelial growth factor (VEGF) level using enzyme linked immunosorbent assay (ELISA). The interaction between IGF2BP2 and HPSE was analyzed by RNA immunoprecipitation, pull-down and luciferase reporter analyses. The results showed that IGF2BP2 expression was enhanced in wound healing. IGF2BP2 downregulation constrained HaCaT cell proliferation, migration, and angiogenesis. IGF2BP2 knockdown decreased HPSE expression. IGF2BP2 could regulate HPSE stability by binding with 3ʹ untranslated region (UTR) of HPSE. HPSE upregulation attenuated silencing IGF2BP2-mediated suppression of proliferation, migration, and angiogenesis. As a conclusion, IGF2BP2 knockdown repressed proliferation, migration, and angiogenesis of HaCaT cells by decreasing HPSE stability.

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“…4 Evodiamine, a natural indole alkaloid extracted from the Evodia ruticarpa plant, has demonstrated potent anticancer activity against a range of tumors. 5 It exhibits topoisomerase inhibition 6 and has been shown to impact tumor characteristics like apoptosis, 7 cell proliferation, 8 invasion, migration, 9,10 and so forth. Metabolic reprogramming is a hallmark of tumorigenesis, 11 encompassing alterations in processes like aerobic glycolysis, the citric acid cycle, one-carbon metabolism, and lipid metabolism.…”

mentioning

confidence: 99%

Evodiamine inhibits EPRS expression to regulate glutamate metabolism and proliferation of oral squamous cell carcinoma cells

Lin,

Lv,

Ren

et al. 2024

The Kaohsiung J of Med Scie

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The effects of evodiamine (EVO) on oral squamous cell carcinoma (OSCC) are not yet understood. Based on our earlier findings, we hypothesized that evodiamine may affect OSCC cell proliferation and glutamate metabolism by modulating the expression of EPRS (glutamyl‐prolyl‐tRNA synthetase 1). From GEPIA, we obtained EPRS expression data in patients with OSCC as well as survival prognosis data. An animal model using Cal27 cells in BALB/c nude mice was established. The expression of EPRS was assessed by immunofluorescence, Western blotting, and quantitative PCR. Glutamate measurements were performed to evaluate the impact of evodiamine on glutamate metabolism of Cal27 and SAS tumor cells. transient transfection techniques were used to knock down and modulate EPRS in these cells. EPRS is expressed at higher levels in OSCC than in normal tissues, and it predicts poor prognosis in patients. In a nude mouse xenograft model, evodiamine inhibited tumor growth and the expression of EPRS. Evodiamine impacted cell proliferation, glutamine metabolism, and EPRS expression on Cal27 and SAS cell lines. In EPRS knockdown cell lines, both cell proliferation and glutamine metabolism are suppressed. EPRS's overexpression partially restores evodiamine's inhibitory effects on cell proliferation and glutamine metabolism. This study provides crucial experimental evidence supporting the potential therapeutic application of evodiamine in treating OSCC. Evodiamine exhibits promising anti‐tumor effects by targeting EPRS to regulate glutamate metabolism.

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The anti-tumor effects of evodiamine on oral squamous cell carcinoma (OSCC) through regulating advanced glycation end products (AGE) / receptor for advanced glycation end products (RAGE) pathway

Abstract: Sun (2021) The anti-tumor effects of evodiamine on oral squamous cell carcinoma (OSCC) through regulating advanced glycation end products (AGE) / receptor for advanced glycation end products (RAGE) pathway, Bioengineered, 12:1, 5985-5995,

Cited by 9 publications

References 35 publications

Gene network analysis of the transcriptome impact of methylated microRNAs on oral squamous cell carcinoma

Gene network analysis of the transcriptome impact of methylated microRNAs on oral squamous cell carcinoma

Insulin-like growth factor 2 mRNA binding protein 2 regulates proliferation, migration, and angiogenesis of keratinocytes by modulating heparanase stability

Evodiamine inhibits EPRS expression to regulate glutamate metabolism and proliferation of oral squamous cell carcinoma cells

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