DDX19A Promotes Metastasis of Cervical Squamous Cell Carcinoma by Inducing NOX1-Mediated ROS Production

Jiang, Yanjun; Wang, Baibin; Li, Yongliang; Shen, Jian; Wei, Yongzhong; Li, Hanjie; Chen, Shangqiu; Yang, Hua; Zeng, Fa‐Min; Liu, Changqing; Wang, Feng; He, Huanhuan; Chen, Yong; Liu, Jihong

doi:10.3389/fonc.2021.629974

Cited by 5 publications

(5 citation statements)

References 42 publications

(43 reference statements)

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“…RT-PCR and IHC analyses confirmed the significant overexpression of NOX1 in cervical cancer compared with adjacent normal tissues. Similar results based on tissue microarray immunohistochemical staining were reported by Jiang et al [ 6 ]. Data from Transwell and scratch experiments showed a strong association of NOX1 overexpression with enhanced invasion and migration of HeLa cells, consistent with earlier findings by Jiang et al [ 6 ] that NOX1 promotes the invasion and migration of SiHa and HCC94 cell lines.…”

Section: Discussionsupporting

confidence: 90%

“…Similar results based on tissue microarray immunohistochemical staining were reported by Jiang et al [ 6 ]. Data from Transwell and scratch experiments showed a strong association of NOX1 overexpression with enhanced invasion and migration of HeLa cells, consistent with earlier findings by Jiang et al [ 6 ] that NOX1 promotes the invasion and migration of SiHa and HCC94 cell lines. Furthermore, overexpression of NOX1 promoted HeLa cell growth in vivo, supporting its carcinogenic role in cervical cancer.…”

Section: Discussionsupporting

confidence: 90%

“…Recently, overexpression of DEAD-box helicase 19A (DDX19A) was reported to increase NOX-1-mediated production of reactive oxygen species (ROS) to induce migration and invasion of cervical squamous cell carcinoma cells. Additionally, high expression of NOX1 was associated with significantly decreased overall patient survival [ 6 ]. However, expression patterns of the NOX1 gene in cervical cancer and adjacent tissues and its tumor-promoting mechanisms remain to be established.…”

Section: Introductionmentioning

confidence: 99%

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Exosomal NOX1 promotes tumor-associated macrophage M2 polarization-mediated cancer progression by stimulating ROS production in cervical cancer: a preliminary study

Gu,

Feng,

et al. 2023

Eur J Med Res

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Background Cervical cancer the fourth most frequently diagnosed cancer and the fourth leading cause of cancer death in women, with an estimated 604,000 new cases and 342,000 deaths worldwide in 2020 for high rates of recurrence and metastasis. Identification of novel targets could aid in the prediction and treatment of cervical cancer. NADPH oxidase 1 (NOX1) gene-mediated production of reactive oxygen species (ROS) could induce migration and invasion of cervical cancer cells. Tumor-associated macrophages (TAMs) play important roles in cervical cancer. Tumor cell-derived exosomes mediate signal transduction between the tumor and tumor microenvironment. Elucidation of the mechanisms of NOX1-carrying exosomes involved in the regulation of TAMs may provide valuable insights into the progression of cervical cancer. Methods Uniformly standardized mRNA data of pan-carcinoma from the UCSC database were downloaded. Expression of NOX1 in tumor and adjacent normal tissues for each tumor type was calculated using R language software and significant differences were analyzed. SNP data set were downloaded for all TCGA samples processed using MuTect2 software from GDC. Cell experiment and animal tumor formation experiment were used to evaluate whether exosomal NOX1 stimulating ROS production to promote M2 polarization of TAM in cervical cancer. Results NOX1 is highly expressed with a low mutational frequency in pan-carcinoma. Upregulation of NOX1 may be associated with infiltration of M2-type macrophages in cervical cancer tissues, and NOX1 promotes malignant features of cervical cancer cells by stimulating ROS production. Exosomal NOX1 promotes M2 polarization of by stimulating ROS production. Exosomal NOX1 enhances progression of cervical cancer and M2 polarization in vivo by stimulating ROS production. Conclusion Exosomal NOX1 promotes TAM M2 polarization-mediated cancer progression through stimulating ROS production in cervical cancer.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

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Exosomal NOX1 promotes tumor-associated macrophage M2 polarization-mediated cancer progression by stimulating ROS production in cervical cancer: a preliminary study

Gu,

Feng,

et al. 2023

Eur J Med Res

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“…DDX19A (chr16: 70,390,764–70,407,281 at a length of 16,518 bp) is a member of the DEAD-box family. A previous study has shown that DDX19A is overexpressed in cervical squamous cell carcinoma and promotes cell invasion and migration by inducing productions of reactive oxygen species [ 40 ]. DDX19A is identified as a prognostic factor of breast cancer disease progression [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Silencing of let-7b-5p inhibits ovarian cancer cell proliferation and stemness characteristics by Asp-Glu-Ala-Asp-box helicase 19A

et al. 2021

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The emergence and recurrence of ovarian cancer are associated with ovarian cancer stem cells. For cancer treatment, gene delivery of microbubbles (MB)-mediated microRNA (miRNA) is considered as a promising approach. In this study, our aim is to investigate the effects of MBmediated let-7b-5p inhibitor on the proliferation and stemness characteristics of ovarian cancer (OVCA) cells. Let-7b-5p inhibitor mediated by MB was prepared (termed MB-let-7b-5p inhibitor), and the effects of MB-let-7b-5p inhibitor and let-7b-5p inhibitor on OVCA cell viability, proliferation and stemness characteristics were investigated. We found that MB-let-7b-5p inhibitor presented a higher transfection efficiency than let-7b-5p inhibitor alone. The inhibitory effect of MBlet-7b-5p inhibitor on OVCA cells was more significant than let-7b-5p inhibitor. Let-7b-5p targeted DEAD (Asp-Glu-Ala-Asp)-box helicase 19A (DDX19A), which was downregulated in OVCA cells. The downregulation of DDX19A reversed the inhibitory effects of MB-let-7b-5p inhibitor on OVCA cells. To sum up, we found that MB-let-7b-5p suppressed OVCA cell malignant behaviors by targeting DDX19A.

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“…RNA helicases involved in RNA metabolic process including transcription, RNA transport, RNA degradation [60] overexpressed in CSCC [60], BC cell lines [61] PT induces EMT [60] promotes cell migration, invasion, metastasis, NOX1 expression and ROS production [60] GPI Glucose-6-phosphate isomerase/neuroleukin cytoplasmic glycolytic-related enzyme, secreted in ECM of cancer cells it is called autocrine motility factor (AMF) [62] and functions as a cytokine or growth factor [63] overexpressed in BC [63], LUAD/NSCLC, glioblastoma, ccRCC [64], GC [62] PT REACTOME_GLUCONEOGENESIS;…”

Section: Ptbp1/hnrnp1mentioning

confidence: 99%

Two-Dimensional-PAGE Coupled with nLC-MS/MS-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in MCF7 Breast Cancer Cells Transfected for JTB Protein Silencing

Jayathirtha,

Jayaweera,

Whitham

et al. 2023

Molecules

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The identification of new cancer-associated genes/proteins, the characterization of their expression variation, the interactomics-based assessment of differentially expressed genes/proteins (DEGs/DEPs), and understanding the tumorigenic pathways and biological processes involved in BC genesis and progression are necessary and possible by the rapid and recent advances in bioinformatics and molecular profiling strategies. Taking into account the opinion of other authors, as well as based on our own team’s in vitro studies, we suggest that the human jumping translocation breakpoint (hJTB) protein might be considered as a tumor biomarker for BC and should be studied as a target for BC therapy. In this study, we identify DEPs, carcinogenic pathways, and biological processes associated with JTB silencing, using 2D-PAGE coupled with nano-liquid chromatography tandem mass spectrometry (nLC-MS/MS) proteomics applied to a MCF7 breast cancer cell line, for complementing and completing our previous results based on SDS-PAGE, as well as in-solution proteomics of MCF7 cells transfected for JTB downregulation. The functions of significant DEPs are analyzed using GSEA and KEGG analyses. Almost all DEPs exert pro-tumorigenic effects in the JTBlow condition, sustaining the tumor suppressive function of JTB. Thus, the identified DEPs are involved in several signaling and metabolic pathways that play pro-tumorigenic roles: EMT, ERK/MAPK, PI3K/AKT, Wnt/β-catenin, mTOR, C-MYC, NF-κB, IFN-γ and IFN-α responses, UPR, and glycolysis/gluconeogenesis. These pathways sustain cancer cell growth, adhesion, survival, proliferation, invasion, metastasis, resistance to apoptosis, tight junctions and cytoskeleton reorganization, the maintenance of stemness, metabolic reprogramming, survival in a hostile environment, and sustain a poor clinical outcome. In conclusion, JTB silencing might increase the neoplastic phenotype and behavior of the MCF7 BC cell line. The data is available via ProteomeXchange with the identifier PXD046265.

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DDX19A Promotes Metastasis of Cervical Squamous Cell Carcinoma by Inducing NOX1-Mediated ROS Production

Cited by 5 publications

References 42 publications

Exosomal NOX1 promotes tumor-associated macrophage M2 polarization-mediated cancer progression by stimulating ROS production in cervical cancer: a preliminary study

Exosomal NOX1 promotes tumor-associated macrophage M2 polarization-mediated cancer progression by stimulating ROS production in cervical cancer: a preliminary study

Silencing of let-7b-5p inhibits ovarian cancer cell proliferation and stemness characteristics by Asp-Glu-Ala-Asp-box helicase 19A

Two-Dimensional-PAGE Coupled with nLC-MS/MS-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in MCF7 Breast Cancer Cells Transfected for JTB Protein Silencing

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