TNFAIP3 inhibits migration and invasion in nasopharyngeal carcinoma by suppressing epithelial mesenchymal transition

Huang, Teng; Yin, Lei; Wu, Jing; Gu, Juan; Ding, Kai; Zhang, N; Du, Mengnan; Qian, Lu‐Xi; Lu, Zhanwu; He, Xijing

doi:10.4149/neo_2017_309

Cited by 17 publications

(18 citation statements)

References 19 publications

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“…In addition to detecting gene expression, we found that GINS2 knockdown increased STAT1 and STAT2 protein expression and inhibited tumor migration and proliferation, which was consistent with a previous study. Furthermore, Huang et al reported that overexpression of TNFAIP3 inhibited migration and invasion in nasopharyngeal carcinoma [28]. Our results showed that GINS2 knockdown increased TNFAIP3 protein expression, suggesting that TNFAIP3 may be involved in the effects of GINS2 on NSCLC proliferation and migration.…”

Section: Discussionsupporting

confidence: 62%

GINS2 attenuates the development of lung cancer by inhibiting the STAT signaling pathway

Sun¹,

Zong²,

Cheng³

et al. 2021

J. Cancer

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GINS complex subunit 2 (GINS2) controls DNA replication. GINS2 expression is upregulated in several kinds of aggressive tumors. However, the effect of GINS2 in lung cancer remains unclear. We performed TCGA database analysis to confirm the clinical significance of GINS2 in lung cancer. After silencing GINS2 in A549 cells, we performed MTT assays, flow cytometry assays, colony formation assays, cell cycle analyses and RNA sequence analysis to elucidate the effect of GINS2 on lung cancer. Moreover, we assessed tumor growth and analyzed body fluorescence in mice as a measure of tumor burden. The TCGA database analysis demonstrated that GINS2 mRNA and protein was highly expressed in three kinds of lung cancer tissues. Subsequently, knockdown of GINS2 inhibited cell proliferation, colony formation, cell cycle arrest and apoptosis in A549 cells. On the other hand, we also investigated the effect of GINS2 on tumor formation in vivo. The analysis of nude mouse tumors showed that the tumor volume and weight of shGINS2 mice were significantly smaller than those of the control mice. To reveal the mechanism of GINS2 in lung cancer, we collected A549 cells with GINS2 knockdown to examine the downstream gene expression changes. The results showed that STAT1 and STAT2 mRNA and protein expression were significantly upregulated after GINS2 knockdown in A549 cells. Our results suggest that GINS2 inhibits the proliferation of lung cancer cells by inhibiting the STAT signaling pathway, which may be a potential biomarker for the diagnosis or prognosis of lung cancer.

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Section: Discussionsupporting

confidence: 62%

GINS2 attenuates the development of lung cancer by inhibiting the STAT signaling pathway

Sun¹,

Zong²,

Cheng³

et al. 2021

J. Cancer

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“…The correlation between these pathway and tumor progression, including NPC, has been proven in previous studies. Especially, focal adhesion (Liu et al, 2018;Yuan et al, 2019;Yu et al, 2019), apoptosis (Li M. et al, 2019;Liang et al, 2019;Wang et al, 2019;Xie et al, 2019), and the tumor necrosis factor (TNF) signaling pathway (Lu et al, 2011;Ou et al, 2015;Huang et al, 2017;Deng et al, 2018) have been reported to be closely related to NPC development.…”

Section: Discussionmentioning

confidence: 99%

Differential Expression and Alternative Splicing of Transcripts Associated With Cisplatin-Induced Chemoresistance in Nasopharyngeal Carcinoma

et al. 2020

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Radiotherapy and adjuvant cisplatin (DDP) chemotherapy are standard administrations applied to treat nasopharyngeal carcinoma (NPC). However, the molecular changes and functions of DDP in NPC chemo-resistance remain poorly understood. In the present study, transcriptomic sequencing between 5-8F and 5-8F/DDP cells was performed to identify differential expression and alternative splicing (AS) characteristics in DDP-resistant NPC cells. Transcriptomic profiling identified 1,757 upregulated genes and 1,473 downregulated differentially expressed genes (DEGs). Bioinformatic analysis revealed that these DEGs were associated with or participated in important biological regulatory functions in NPC. Validation of 20 significant DEGs using quantitative real-time reverse transcription PCR showed that the expression patterns of 17 mRNAs were in accordance with the sequencing data. Intron retention was identified as the major AS event in chemoresistant cells. Furthermore, the expression level of matrix metalloproteinase 1 (MMP1), which was one of the most upregulated mRNAs in the chemoresistant cell lines, was significantly associated with the migration, invasion, and proliferation of NPC cells in vitro. Our study revealed that dysregulated genes and AS-mediated DDP chemoresistance might play important roles in NPC development and progression. Targeting aberrantly expressed genes might clarify the pathogenesis of NPC and contribute to developing new therapeutic strategies for NPC.

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“…Using a mouse xenograft, Lee et al showed that with A20 knockdown lung metastasis of epithelial-like breast cancers could be inhibited, suggesting a role for A20 in TGFβ1-induced epithelial mesenchymal transition (EMT) (68). In nasopharyngeal carcinoma, however, A20 overexpression inhibited migration and invasion by suppressing EMT (48). These observations are of particular interest in chronic lung disease: Although EMT is a 'universal' and normal process during tissue repair, in many chronic respiratory diseases EMT appears deregulated leading to different degrees of fibrosis (reviewed in (107)).…”

Section: Role Of Snps / Mutations On A20 Expression and Functionmentioning

confidence: 99%

Regulators of A20 (TNFAIP3): new drug-able targets in inflammation

Momtazi

Lambrecht

Naranjo

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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Persistent activation of the transcription factor Nuclear factor-κB (NF-κB) is central to the pathogenesis of many inflammatory disorders, including those of the lung such as cystic fibrosis (CF), asthma, and chronic obstructive pulmonary disease (COPD). Despite recent advances in treatment, management of the inflammatory component of these diseases still remains suboptimal. A20 is an endogenous negative regulator of NF-κB signaling, which has been widely described in several autoimmune and inflammatory disorders and more recently in terms of chronic lung disorders. However, the underlying mechanism for the apparent lack of A20 in CF, COPD, and asthma has not been investigated. Transcriptional regulation of A20 is complex and requires coordination of different transcription factors. In this review we examine the existing body of research evidence on the regulation of A20, concentrating on pulmonary inflammation. Special focus is given to the repressor downstream regulatory element antagonist modulator (DREAM) and its nuclear and cytosolic action to regulate inflammation. We provide evidence that would suggest the A20-DREAM axis to be an important player in (airway) inflammatory responses and point to DREAM as a potential future therapeutic target for the modification of phenotypic changes in airway inflammatory disorders. A schematic summary describing the role of DREAM in inflammation with a focus on chronic lung diseases as well as the possible consequences of altered DREAM expression on immune responses is provided.

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TNFAIP3 inhibits migration and invasion in nasopharyngeal carcinoma by suppressing epithelial mesenchymal transition

Cited by 17 publications

References 19 publications

GINS2 attenuates the development of lung cancer by inhibiting the STAT signaling pathway

GINS2 attenuates the development of lung cancer by inhibiting the STAT signaling pathway

Differential Expression and Alternative Splicing of Transcripts Associated With Cisplatin-Induced Chemoresistance in Nasopharyngeal Carcinoma

Regulators of A20 (TNFAIP3): new drug-able targets in inflammation

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