Downregulation of lncRNA FOXD2-AS1 Confers Radiosensitivity to Gastric Cancer Cells via miR-1913/SETD1A Axis

Guo, Fengying; Guo, Ruixiang; Zhang, Licheng

doi:10.1159/000522653

Cited by 10 publications

(7 citation statements)

References 45 publications

(41 reference statements)

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“…Furthermore, the reductions of ACSL4, ROS, and MDA levels and increases in iron, GPX4, SOD, and GSH levels were indicative of reinforced NSCLC cell ferroptosis. In gastric cancer, the upregulation of SETD1A reverses lncRNA FOXD2‐AS1 silencing‐produced effects on cell proliferation, apoptosis, and radio‐sensitivity 30 . Taken together, HOXC‐AS3 upregulation counteracted silencing SETD1A‐exerted promotional action on NSCLC cell ferroptosis.…”

Section: Discussionmentioning

confidence: 90%

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SETD1A‐mediated H3K4me3 methylation upregulates lncRNA HOXC‐AS3 and the binding of HOXC‐AS3 to EP300 and increases EP300 stability to suppress the ferroptosis of NSCLC cells

Shi,

Zhang,

Shen

et al. 2023

Thoracic Cancer

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BackgroundHistone methyltransferases are crucial regulators in non‐small cell lung cancer (NSCLC) development. This study explored the mechanism of histone methyltransferase SET domain containing 1A (SETD1A)‐mediated H3K4me2 methylation in NSCLC cell ferroptosis and provides novel targets for NSCLC treatment.MethodsUpon downregulation of SETD1A in NSCLC cell lines, cell proliferation potential, malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) activities, iron content, and SETD1A, long noncoding RNA HOXC cluster antisense RNA 3 (lncRNA HOXC‐AS3), E1A binding protein p300 (EP300), glutathione peroxidase 4 (GPX4) expressions were determined via cell counting kit‐8, ELISA, iron assay kits, RT‐qPCR, and western blot. Enrichment levels of SETD1A and H3K4me3 in the HOXC‐AS3 promotor were measured via chromatin immunoprecipitation, and the binding of HOXC‐AS3 and EP300 was analyzed via RNA immunoprecipitation. Rescue experiments were performed to confirm their roles in NSCLC cell ferroptosis. Xenograft tumor models were established to validate the role of SETD1A in vivo.ResultsSETD1A, H3K4me3, HOXC‐AS3, and EP300 were highly‐expressed in NSCLC cells. Silencing SETD1A inhibited NSCLC cell proliferation, increased MDA and iron levels, and decreased SOD, GSH, and GPX4 levels. SETD1A downregulation reduced H3K4me3 level, HOXC‐AS3 expression, the binding of HOXC‐AS3 to EP300, and EP300 stability. Overexpression of HOXC‐AS3 or EP300 reversed the promotion of silencing SETD1A on NSCLC cell ferroptosis. Silencing SETD1A reduced tumor volume and weight and positive rate of ki67 and increased ferroptosis through the HOXC‐AS3/EP300 axis.ConclusionSETD1A‐mediated H3K4me2 methylation promoted HOXC‐AS3 expression, binding of HOXC‐AS3 to EP300, and EP300 stability, thereby suppressing NSCLC cell ferroptosis.

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Section: Discussionmentioning

confidence: 90%

“…In gastric cancer, the upregulation of SETD1A reverses lncRNA FOXD2‐AS1 silencing‐produced effects on cell proliferation, apoptosis, and radio‐sensitivity. 30 Taken together, HOXC‐AS3 upregulation counteracted silencing SETD1A‐exerted promotional action on NSCLC cell ferroptosis.…”

Section: Discussionmentioning

confidence: 99%

SETD1A‐mediated H3K4me3 methylation upregulates lncRNA HOXC‐AS3 and the binding of HOXC‐AS3 to EP300 and increases EP300 stability to suppress the ferroptosis of NSCLC cells

Shi,

Zhang,

Shen

et al. 2023

Thoracic Cancer

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“…FOXD2-AS1 emerges as a critical regulator in tumorigenesis. Studies have demonstrated that dysregulated FOXD2-AS1 renders gastric cancer cells more sensitive to radiation through modulation of the miR-1913/SET binding protein 1 (SETD1A) axis [10]. Suppression of FOXD2-AS1 attenuates cell proliferation, while its upregulation increased miR-31 expression and consequent dysregulation of Paired box 9 (PAX9) expression in retinoblastoma [11].…”

Section: What New Results Were Revealed?mentioning

confidence: 99%

FOXD2-AS1 inhibits the proliferation and migration in prostate cancer: an in vitro and in vivo study

2023

Journal of Men's Health

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FOXD2 Adjacent Opposite Strand RNA 1 (FOXD2-AS1), a long noncoding RNA (lncRNA), exhibits specifically elevated in numerous cancerous cells. Numerous studies have shown that FOXD2-AS1 encourages cellular proliferation, migration and invasion. Nevertheless, the exact mechanism through which FOXD2-AS1 contributes to prostate cancer (PCa) remains unclear. Consequently, we aimed to explore the implications of FOXD2-AS1 on the growth of PCa. Initially, an elevation of FOXD2-AS1 observed in PCa cells (PC-3, DU145 and Lncap) than the prostate normal cell line RWPE2. Then, PC-3 cells were tranafected with shFOXD2-AS1, sh-Numerical Control (shNC) or FOXD2-AS1 to assess the implications of FOXD2-AS. Cell growth was measured with cell counting kit-8 (CCK8) and 5-ethynyl-2′-deoxyuridine (EDU) assays, and cell invasion and migration were assessed by Transwell assays, which demonstrated that FOXD2-AS1 silence impeded proliferation, migration and invasion of PC-3 cells. Additionally, we discovered that FOXD2-AS1 bonded with miR-206/programmed cell death protein 10 (PDCD10) trough analyzing the interaction sites of lncRNA, miRNA and protein. Then, these interaction abilities were confirmed by dual-luciferase reporter assays and RT-qPCR, suggesting FOXD2-AS1 could upregulate the amount of PDCD10 through suppressing miR-206. Furthermore, the role of FOXD2-AS1 silencing on PCa carcinogenesis were assessed. In vivo experiment, shFOXD2-AS1 led to a notable reduction in both the size and weight of PCa. These findings indicated that FOXD2-AS1 silencing effectively hindered the progression of prostate cancer. In conclusion, the upregulation of FOXD2-AS1 was observed in PCa, and the knockdown of FOXD2-AS1 could alleviated tumor development by targeting miR-206 to upregulate PDCD10 expression.

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“…The overexpression of hsa-miR-1913 was also associated with multiple forms of cancer [44][45][46][47][48][49], similar to hsa-miR-7704 [50][51][52]. However, the role of these miRNAs in HMPV infection warrants additional research.…”

Section: Discussionmentioning

confidence: 99%

Human Metapneumovirus-Induced Host microRNA Expression Impairs the Interferon Response in Macrophages and Epithelial Cells

Martínez-Espinoza,

Bungwon,

Guerrero-Plata

2023

Viruses

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Human metapneumovirus (HMPV) is a nonsegmented, single-stranded negative RNA virus and a member of the Pneumoviridae family. During HMPV infection, macrophages play a critical role in defending the respiratory epithelium by secreting large amounts of type I interferon (IFN). MicroRNAs (miRNAs) are small, noncoding, single-stranded RNAs that play an essential role in regulating gene expression during normal cellular homeostasis and disease by binding to specific mRNAs, thereby regulating at the transcriptional and post-transcriptional levels with a direct impact on the immune response and other cellular processes. However, the role of miRNAs in macrophages and respiratory viral infections remains largely unknown. Here, we characterized the susceptibility of THP-1-derived macrophages to HMPV infection and the effect of hsa-miR-4634 on these cells. Transfection of an miRNA mimic and inhibitor demonstrated that hsa-miR-4634 regulates the IFN response in HMPV-infected macrophages, suggesting that HMPV induces the expression of the miRNA as a subversion mechanism of the antiviral response. This effect was not limited to macrophages, as a similar effect was also observed in epithelial cells. Overall, our results demonstrate that hsa-miR-4634 is an important factor in regulating the IFN response in macrophages and epithelial cells during HMPV infection.

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Downregulation of lncRNA FOXD2-AS1 Confers Radiosensitivity to Gastric Cancer Cells via miR-1913/SETD1A Axis

Cited by 10 publications

References 45 publications

SETD1A‐mediated H3K4me3 methylation upregulates lncRNA HOXC‐AS3 and the binding of HOXC‐AS3 to EP300 and increases EP300 stability to suppress the ferroptosis of NSCLC cells

SETD1A‐mediated H3K4me3 methylation upregulates lncRNA HOXC‐AS3 and the binding of HOXC‐AS3 to EP300 and increases EP300 stability to suppress the ferroptosis of NSCLC cells

FOXD2-AS1 inhibits the proliferation and migration in prostate cancer: an in vitro and in vivo study

Human Metapneumovirus-Induced Host microRNA Expression Impairs the Interferon Response in Macrophages and Epithelial Cells

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