We are analyzing https://link.springer.com/article/10.1186/s41065-022-00225-0.

Title:
SLC3A2 inhibits ferroptosis in laryngeal carcinoma via mTOR pathway | Hereditas
Description:
Objective This study aimed to explore the mRNA and protein expression of SLC3A2 in laryngeal carcinoma cells and tissues, and functional regulatory mechanism of SLC3A2 in cell ferroptosis of laryngeal carcinoma. Methods We chose the key gene-SLC3A2 of DEGs from TCGA by bioinformatics analysis, and then we constructed stable knockdown of SLC3A2 in laryngeal carcinoma cells. MTT assay and clonogenic assay were used to determine cell viability and cell growth, respectively. The mRNA and protein expression were determined by RT-qPCR and western blotting, respectively. Xenograft tumor model was used to determine the role of SLC3A2 in tumor growth. Results The results of limma analysis recovered that 92 genes were involved in both upregulated DEGs and high risk of poor prognosis, whereas 36 genes were involved in both downregulated DEGs and low risk of poor prognosis. Pathway enrichment analysis indicated that mTOR signaling pathway and ferroptosis exerted a role in regulating these intersection genes. Moreover, SLC3A2 is a key gene in ferroptosis in laryngeal carcinoma. SLC3A2 is highly expressed in laryngeal carcinoma tissues and cells. Patients with high SLC3A2 expression exerted poor survival. SLC3A2 deficiency inhibited cell proliferation and foci formation. Furthermore, knockdown of SLC3A2 expression induced the efficacy of ferroptosis and suppressed ferroptosis related proteins expression. Mechanically, SLC3A2 deficiency facilitated ferroptosis through upregulating the expression of mTOR and P70S6K, whereas inhibited p-mTOR and p-P70S6K expression in laryngeal carcinoma cells. SLC3A2 deficiency inhibited tumorigenesis in nude mice. Conclusion Our study suggests that SLC3A2 negatively regulates ferroptosis through mTOR pathway in laryngeal carcinoma.
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Keywords {🔍}

slca, cell, ferroptosis, laryngeal, cancer, article, expression, cells, google, scholar, carcinoma, data, cas, tumor, analysis, genes, pathway, mtor, gpx, fig, deficiency, assay, iron, death, tissues, related, analyzed, prognosis, normal, survival, lipid, degs, tcga, viability, signaling, lines, usa, liu, study, results, poor, gene, performed, protein, key, knockdown, growth, western, blotting, patients,

Topics {✒️}

quantitative real-time rt-pcr downstream pi3k/akt/mtor pathway slc3a2-nrg1-mediated lung cancer pi3k/akt signaling pathway mek/erk signaling pathways srebp1/scd1-mediated adipogenesis [27] autophagy-dependent ferroptosis induced regulate autophagy-dependent ferroptosis slc3a2-knockdown cell lines promoting ampk-mtor pathway pre-life information mining potential ferroptosis-related diagnostic sh-nc tumor tissues prevent hydroperoxide-induced ferroptosis article download pdf including download method anti-mouse p-mtor autophagy-dependent ferroptosis dysmorphic small mitochondria mtor signaling pathway anti-mouse p-p70s6k cystine/glutamate antiporter buffered salt solution mouse skeletal muscle hn8 cell lines yundan bai prepare privacy choices/manage cookies trends cell biol ampk/mtor pathway venn diagram tool full access oral pathol med 2 ml working solution promotes tumor growth cell death induced slc3a2-nrg1 fusion slc3a2 inhibits ferroptosis adhesion-induced phosphorylation neck cancer low-expression gene filtering lipoxygenases drives ferroptosis nrf2 inhibits ferroptosis intracellular redox balance srebp-mediated lipogenesis usp27-mediated cyclin nat chem biol inhibited p-mtor cell death subroutines cell death differ nonapoptotic cell death

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WebPage:
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         headline:SLC3A2 inhibits ferroptosis in laryngeal carcinoma via mTOR pathway
         description:This study aimed to explore the mRNA and protein expression of SLC3A2 in laryngeal carcinoma cells and tissues, and functional regulatory mechanism of SLC3A2 in cell ferroptosis of laryngeal carcinoma. We chose the key gene-SLC3A2 of DEGs from TCGA by bioinformatics analysis, and then we constructed stable knockdown of SLC3A2 in laryngeal carcinoma cells. MTT assay and clonogenic assay were used to determine cell viability and cell growth, respectively. The mRNA and protein expression were determined by RT-qPCR and western blotting, respectively. Xenograft tumor model was used to determine the role of SLC3A2 in tumor growth. The results of limma analysis recovered that 92 genes were involved in both upregulated DEGs and high risk of poor prognosis, whereas 36 genes were involved in both downregulated DEGs and low risk of poor prognosis. Pathway enrichment analysis indicated that mTOR signaling pathway and ferroptosis exerted a role in regulating these intersection genes. Moreover, SLC3A2 is a key gene in ferroptosis in laryngeal carcinoma. SLC3A2 is highly expressed in laryngeal carcinoma tissues and cells. Patients with high SLC3A2 expression exerted poor survival. SLC3A2 deficiency inhibited cell proliferation and foci formation. Furthermore, knockdown of SLC3A2 expression induced the efficacy of ferroptosis and suppressed ferroptosis related proteins expression. Mechanically, SLC3A2 deficiency facilitated ferroptosis through upregulating the expression of mTOR and P70S6K, whereas inhibited p-mTOR and p-P70S6K expression in laryngeal carcinoma cells. SLC3A2 deficiency inhibited tumorigenesis in nude mice. Our study suggests that SLC3A2 negatively regulates ferroptosis through mTOR pathway in laryngeal carcinoma.
         datePublished:2022-01-20T00:00:00Z
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            Evolutionary Biology
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      headline:SLC3A2 inhibits ferroptosis in laryngeal carcinoma via mTOR pathway
      description:This study aimed to explore the mRNA and protein expression of SLC3A2 in laryngeal carcinoma cells and tissues, and functional regulatory mechanism of SLC3A2 in cell ferroptosis of laryngeal carcinoma. We chose the key gene-SLC3A2 of DEGs from TCGA by bioinformatics analysis, and then we constructed stable knockdown of SLC3A2 in laryngeal carcinoma cells. MTT assay and clonogenic assay were used to determine cell viability and cell growth, respectively. The mRNA and protein expression were determined by RT-qPCR and western blotting, respectively. Xenograft tumor model was used to determine the role of SLC3A2 in tumor growth. The results of limma analysis recovered that 92 genes were involved in both upregulated DEGs and high risk of poor prognosis, whereas 36 genes were involved in both downregulated DEGs and low risk of poor prognosis. Pathway enrichment analysis indicated that mTOR signaling pathway and ferroptosis exerted a role in regulating these intersection genes. Moreover, SLC3A2 is a key gene in ferroptosis in laryngeal carcinoma. SLC3A2 is highly expressed in laryngeal carcinoma tissues and cells. Patients with high SLC3A2 expression exerted poor survival. SLC3A2 deficiency inhibited cell proliferation and foci formation. Furthermore, knockdown of SLC3A2 expression induced the efficacy of ferroptosis and suppressed ferroptosis related proteins expression. Mechanically, SLC3A2 deficiency facilitated ferroptosis through upregulating the expression of mTOR and P70S6K, whereas inhibited p-mTOR and p-P70S6K expression in laryngeal carcinoma cells. SLC3A2 deficiency inhibited tumorigenesis in nude mice. Our study suggests that SLC3A2 negatively regulates ferroptosis through mTOR pathway in laryngeal carcinoma.
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      dateModified:2022-01-20T00:00:00Z
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         Evolutionary Biology
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