miR-141-3p promotes proliferation and metastasis of nasopharyngeal carcinoma by targeting NME1

Li, Manyi; Huang, Haiping; Cheng, Fuwei; Hu, Xiaoqing; Liu, Jisheng

doi:10.1016/j.advms.2020.03.005

Cited by 16 publications

(8 citation statements)

References 20 publications

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“…However, the role of miR-141-3p was inconsistent on the metastasis of different cancers. miR-141-3p promoted metastasis by targeting NME1in nasopharyngeal carcinoma [ 37 ], and also regulated osteoblast activity to increase the metastasis of prostate cancer [ 38 ]. While other researchers found that miR-141-3p suppressed metastasis of papillary thyroid cancer by targeting Yin Yang 1 [ 39 ] and the decreased miR-141-3p-promoted metastasis of prostate cancer by activating NF-kB pathway [ 40 ].…”

Section: Necroptosis and Cancer Metastasismentioning

confidence: 99%

Non-coding RNAs in necroptosis, pyroptosis and ferroptosis in cancer metastasis

et al. 2021

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Distant metastasis is the main cause of death for cancer patients. Recently, the newly discovered programmed cell death includes necroptosis, pyroptosis, and ferroptosis, which possesses an important role in the process of tumor metastasis. At the same time, it is widely reported that non-coding RNA precisely regulates programmed death and tumor metastasis. In the present review, we summarize the function and role of necroptosis, pyrolysis, and ferroptosis involving in cancer metastasis, as well as the regulatory factors, including non-coding RNAs, of necroptosis, pyroptosis, and ferroptosis in the process of tumor metastasis.

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Section: Necroptosis and Cancer Metastasismentioning

confidence: 99%

Non-coding RNAs in necroptosis, pyroptosis and ferroptosis in cancer metastasis

et al. 2021

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“…Human nasopharyngeal epithelial NP69 cells (Biobw, Beijing, China) and NPC cells C666-1, 5–8 F, 6–10B (Meisen, Hangzhou, China), and SUNE-1 (EK-Bioscience, Shanghai, China) were cultured in RPMI-1640 (Gibco; Thermo Fisher Scientific) supplemented with 10% FBS (Gibco) and 1% P/S in an incubator set at 37°C and 5% CO 2 [ 17 ].…”

Section: Methodsmentioning

confidence: 99%

Cullin 4A/protein arginine methyltransferase 5 (CUL4A/PRMT5) promotes cell malignant phenotypes and tumor growth in nasopharyngeal carcinoma

2022

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Targeted therapy is an important therapeutic strategy currently, however, the development of targeted therapy for nasopharyngeal carcinoma (NPC) is relatively lagging. Cullin 4A (CUL4A) was reported to be overexpressed in NPC; nevertheless, the specific role of CUL4A remains unrevealed. NPC cells and tumor-bearing mice were cultivated to explore the role and mechanism of CUL4A in NPC. After evaluating CUL4A levels in NPC cells, functional experiments were carried out to investigate the effects of CUL4A knockdown and overexpression on cell proliferative, invasive and migratory aptitude as well as NF-κB signaling. Following the GeneMANIA database predicted that protein arginine methyltransferase 5 (PRMT5) was downstream of CUL4A, the mediated role of PRMT5 in the regulation of CUL4A on cells was then determined. Moreover, the tumor volumes and weights of tumor-bearing mice were recorded, and the levels of proliferation-, migration-, and NF-κB signaling-related proteins in the tumor were determined. Herein, CUL4A was enhanced in NPC cells, and its knockdown and overexpression separately suppressed and promoted cell proliferative, invasive, and migratory aptitude as well as NF-κB signal activation. Novelty, PRMT5 knockdown reversed the influences of CUL4A overexpression on these aspects. In addition, its knockdown likewise reversed the facilitating impact of CUL4A expression on tumor growth and declined the expression levels of proliferation-, migration-, and NF-κB signaling-related protein in the tumor. Together, this paper indicated that CUL4A promoted the proliferative, invasive, and migratory aptitude of NPC cells as well as tumor growth by promoting PRMT5 to activate NF-κB signaling.

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“…In NPC, miR-138 and miR-184, suppress tumor progression by targeting CCDN1 and Notch2, respectively [26,27]. In contrast, miR-214 and miR-141-3p, which are known as oncogenic miRNAs, have been shown to promote cell proliferation and facilitate tumor progression of NPC [25,28]. Recent studies have demonstrated that miR-874-3p is an important negative regulator of cancers such as epithelial ovarian, esophageal squamous cell carcinoma and hepatocellular carcinoma [29][30][31], indicating that miR-874-3p plays a significant role in modulating tumor progression.…”

Section: Introductionmentioning

confidence: 99%

Aberrant miR-874-3p/leptin/EGFR/c-Myc signaling contributes to nasopharyngeal carcinoma pathogenesis

Luo

Tsai

Hwang

et al. 2022

J Exp Clin Cancer Res

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Background Leptin is important in physiological and pathological functions in various cancers, however, the significance and mechanisms of leptin in nasopharyngeal carcinoma remain ambiguous. Methods Leptin expression was analyzed by QPCR, immunohistochemistry, Western blotting, and TCGA database. The impact of gain- or loss-of-function of leptin were determined by MTT, colony formation, wound healing, and Transwell assays in NPC cells, and by a xenograft tumor model. Leptin-modulated glucose consumption and lactate production were assessed by ELISA. Furthermore, leptin-regulated signaling pathways were examined by QPCR and Western blotting assays. The immunoprecipitation assay was conducted to determine interaction between leptin and EGFR. In addition, miR-874-3p-regulated leptin expression was evaluated using bioinformatics, QPCR, luciferase assay, AGO2-RIP assay, and Western blotting. Results In this study, we found that leptin was highly expressed in the sera and tumor tissues of patients with NPC, and elevated leptin expression was associated with advanced clinical features and poor prognosis. Functional assays demonstrated that leptin remarkably promoted NPC cell growth, motility, and glycolysis in vitro and in vivo. Mechanistically, leptin associated with EGFR, resulting in enhanced cell growth through the regulation of cell-cycle related markers, glycolysis-related genes, and EGFR/AKT/c-Myc signaling. Moreover, leptin potentiated the invasive capacity of NPC cells by promoting EMT. We further explored that miR-874-3p influenced leptin-mediated NPC progression. Overexpression of miR-874-3p prevented cell growth, motility, glucose consumption, and lactate production in NPC cells, whereas miR-874-3p inhibition had the opposite effects. AGO-RIP assays confirmed that Argonaute 2 (AGO2), a protein associated with miR-874-3p, regulated leptin expression in NPC cells. The rescue assays indicated that inhibition of leptin suppressed the effects of miR-874-3p inhibitor. In clinical specimens, miR-874-3p was negatively correlated with leptin. Conclusions Leptin may serve as a novel prognostic factor and potential therapeutic target for patients with NPC. In addition, a newly discovered regulatory axis of leptin/EGFR/AKT/c-Myc can provide a novel therapeutic strategy for NPC.

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miR-141-3p promotes proliferation and metastasis of nasopharyngeal carcinoma by targeting NME1

Cited by 16 publications

References 20 publications

Non-coding RNAs in necroptosis, pyroptosis and ferroptosis in cancer metastasis

Non-coding RNAs in necroptosis, pyroptosis and ferroptosis in cancer metastasis

Cullin 4A/protein arginine methyltransferase 5 (CUL4A/PRMT5) promotes cell malignant phenotypes and tumor growth in nasopharyngeal carcinoma

Aberrant miR-874-3p/leptin/EGFR/c-Myc signaling contributes to nasopharyngeal carcinoma pathogenesis

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