Inhibition of the Numb/Notch signaling pathway increases radiation sensitivity in human nasopharyngeal carcinoma cells

Shen, Erdong; Zeng, Qiang

doi:10.1002/kjm2.12087

Cited by 8 publications

(6 citation statements)

References 29 publications

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“…NUMB expression levels were also decreased in tongue cancer and its overexpression inhibited cell proliferation, migration and invasion via regulating Notch1 signaling (16). In nasopharyngeal carcinoma, the Notch signaling pathway was regulated by NUMB, which promoted cancer cell survival, migration and invasion, in addition to inhibiting colony formation and apoptosis (17). Moreover, NUMB expression has been reported to be regulated by miR-146a in oral carcinoma (18).…”

Section: Discussionmentioning

confidence: 99%

“…NUMB is an endocytic adaptor protein that is localized in the basement layer of polarized epithelial cells (14). In previous studies, NUMB has been found to serve crucial roles in human cancer (15)(16)(17)(18); for example, NUMB expression levels were decreased in ovarian cancer, which regulated cancer cell proliferation, invasion and epithelial-mesenchymal transition through regulating the p21 (RAC1) activated kinase 1/β-catenin signaling pathway (15). NUMB expression levels were also decreased in tongue cancer and its overexpression inhibited cell proliferation, migration and invasion via regulating Notch1 signaling (16).…”

Section: Discussionmentioning

confidence: 99%

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microRNA‑146b promotes neuroblastoma cell growth through targeting NUMB

Zhang

et al. 2020

Exp Ther Med

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Accumulating evidence has demonstrated that the abnormal expression of microRNA (miRNA/miR) serves a crucial role in the development of numerous types of human cancer, including neuroblastoma (NB). The present study aimed to investigate the expression levels and biological roles of miR-146b in NB. miR-146b expression levels in NB cell lines and human umbilical vein endothelial cells (HUVECs) were analyzed using reverse transcription-quantitative PCR, and the regulatory effects of miR-146b on NB cell proliferation, invasion and apoptosis in vitro were investigated using CCK-8 assay, transwell invasion assay and flow cytometry. In addition, bioinformatics analysis, western blotting and dual-luciferase reporter assays were used to determine whether NUMB was a target gene of miR-146b. miR-146b expression levels were increased in NB cell lines compared with HUVECs. The knockdown of miR-146b using a miR-146b inhibitor significantly inhibited NB cell proliferation and invasion, but promoted cell apoptosis in vitro. Furthermore, it was revealed that miR-146b promoted NB cell proliferation through targeting NUMB. In conclusion, miR-146b was suggested to serve as an oncogene, at least in part, through directly targeting NUMB, which indicated that miR-146b may be a potential therapeutic target for NB treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

microRNA‑146b promotes neuroblastoma cell growth through targeting NUMB

Zhang

et al. 2020

Exp Ther Med

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“…In addition, inhibition of the Numb/Notch signaling pathway increases radiation sensitivity in human nasopharyngeal carcinoma cells. 361 In this part, we primarily discuss the regulation of oxidative stress by EBV, the role of EBV lytic reactivation in EBVassociated diseases and the following radiation therapy. A better understanding of the relationship between them may lead to develop novel prevention and therapeutic strategies for EBVassociated diseases and facilitate the development of novel strategies against radiation-resistant tumors.…”

Section: Biomarkers Of Chemotherapy For Ebv-associated Tumorsmentioning

confidence: 99%

Targeting the signaling in Epstein–Barr virus-associated diseases: mechanism, regulation, and clinical study

Cao

Xie

Shi

et al. 2021

Sig Transduct Target Ther

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Epstein–Barr virus-associated diseases are important global health concerns. As a group I carcinogen, EBV accounts for 1.5% of human malignances, including both epithelial- and lymphatic-originated tumors. Moreover, EBV plays an etiological and pathogenic role in a number of non-neoplastic diseases, and is even involved in multiple autoimmune diseases (SADs). In this review, we summarize and discuss some recent exciting discoveries in EBV research area, which including DNA methylation alterations, metabolic reprogramming, the changes of mitochondria and ubiquitin-proteasome system (UPS), oxidative stress and EBV lytic reactivation, variations in non-coding RNA (ncRNA), radiochemotherapy and immunotherapy. Understanding and learning from this advancement will further confirm the far-reaching and future value of therapeutic strategies in EBV-associated diseases.

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“…NPC is considered a rare cancer in most parts of the world, but it has high morbidity and mortality rates due to its early metastasis and chemotherapy toxicity 21 , 22 . Radiation therapy is the main treatment for NPC, but radiation resistance can prevent effective treatment 23 . KDM4A has been found to contribute to the Warburg effect in the NPC process 8 , but the specific mechanism of KDM4A in NPC remains poorly defined.…”

Section: Discussionmentioning

confidence: 99%

Histone demethylase KDM4A plays an oncogenic role in nasopharyngeal carcinoma by promoting cell migration and invasion

Zhao

Ren

et al. 2021

Exp Mol Med

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Compelling evidence has indicated the vital role of lysine-specific demethylase 4 A (KDM4A), hypoxia-inducible factor-1α (HIF1α) and the mechanistic target of rapamycin (mTOR) signaling pathway in nasopharyngeal carcinoma (NPC). Therefore, we aimed to investigate whether KDM4A affects NPC progression by regulating the HIF1α/DDIT4/mTOR signaling pathway. First, NPC and adjacent tissue samples were collected, and KDM4A protein expression was examined by immunohistochemistry. Then, the interactions among KDM4A, HIF1α and DDIT4 were assessed. Gain- and loss-of-function approaches were used to alter KDM4A, HIF1α and DDIT4 expression in NPC cells. The mechanism of KDM4A in NPC was evaluated both in vivo and in vitro via RT-qPCR, Western blot analysis, MTT assay, Transwell assay, flow cytometry and tumor formation experiments. KDM4A, HIF1α, and DDIT4 were highly expressed in NPC tissues and cells. Mechanistically, KDM4A inhibited the enrichment of histone H3 lysine 9 trimethylation (H3K9me3) in the HIF1α promoter region and thus inhibited the methylation of HIF1α to promote HIF1α expression, thus upregulating DDIT4 and activating the mTOR signaling pathway. Overexpression of KDM4A, HIF1α, or DDIT4 or activation of the mTOR signaling pathway promoted SUNE1 cell proliferation, migration, and invasion but inhibited apoptosis. KDM4A silencing blocked the mTOR signaling pathway by inhibiting the HIF1α/DDIT4 axis to inhibit the growth of SUNE1 cells in vivo. Collectively, KDM4A silencing could inhibit NPC progression by blocking the activation of the HIF1α/DDIT4/mTOR signaling pathway by increasing H3K9me3, highlighting a promising therapeutic target for NPC.

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Inhibition of the Numb/Notch signaling pathway increases radiation sensitivity in human nasopharyngeal carcinoma cells

Cited by 8 publications

References 29 publications

microRNA‑146b promotes neuroblastoma cell growth through targeting NUMB

microRNA‑146b promotes neuroblastoma cell growth through targeting NUMB

Targeting the signaling in Epstein–Barr virus-associated diseases: mechanism, regulation, and clinical study

Histone demethylase KDM4A plays an oncogenic role in nasopharyngeal carcinoma by promoting cell migration and invasion

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