RPS27a enhances EBV-encoded LMP1-mediated proliferation and invasion by stabilizing of LMP1

Hong, Seung-Woo; Kim, Seung-Mi; Jin, Dong-Hoon; Kim, Yeong Seok; Hur, Dae Young

doi:10.1016/j.bbrc.2017.07.105

Cited by 25 publications

(14 citation statements)

References 30 publications

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“…UBA52 and RPS27A genes were found to be differently over-expressed during hepatoma cell apoptosis [58]. Furthermore, in several studies, RPS27A was found to be correlated with cell malignant transformation and enhanced chemoresistance [59,60]. Additionally, hub genes include RPS3, which is a ribosomal protein involved in DNA repair endonuclease.…”

Section: Discussionmentioning

confidence: 99%

Silver Nanoparticles Derived by Artemisia arborescens Reveal Anticancer and Apoptosis-Inducing Effects

Bordoni

Sanna

Lyu

et al. 2021

IJMS

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The fight against cancer is one of the main challenges for medical research. Recently, nanotechnology has made significant progress, providing possibilities for developing innovative nanomaterials to overcome the common limitations of current therapies. In this context, silver nanoparticles (AgNPs) represent a promising nano-tool able to offer interesting applications for cancer research. Following this path, we combined the silver proprieties with Artemisia arborescens characteristics, producing novel nanoparticles called Artemisia–AgNPs. A “green” synthesis method was performed to produce Artemisia–AgNPs, using Artemisia arborescens extracts. This kind of photosynthesis is an eco-friendly, inexpensive, and fast approach. Moreover, the bioorganic molecules of plant extracts improved the biocompatibility and efficacy of Artemisia–AgNPs. The Artemisia–AgNPs were fully characterized and tested to compare their effects on various cancer cell lines, in particular HeLa and MCF-7. Artemisia–AgNPs treatment showed dose-dependent growth inhibition of cancer cells. Moreover, we evaluated their impact on the cell cycle, observing a G1 arrest mediated by Artemisia–AgNPs treatment. Using a clonogenic assay after treatment, we observed a complete lack of cell colonies, which demonstrated cell reproducibility death. To have a broader overview on gene expression impact, we performed RNA-sequencing, which demonstrated the potential of Artemisia–AgNPs as a suitable candidate tool in cancer research.

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Section: Discussionmentioning

confidence: 99%

Silver Nanoparticles Derived by Artemisia arborescens Reveal Anticancer and Apoptosis-Inducing Effects

Bordoni

Sanna

Lyu

et al. 2021

IJMS

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“…RPS27A also performs extra-ribosomal functions when ribosome synthesis is perturbed. For example, RPS27A regulates LMP1 protein expression encoded by EBV in a proteasome-dependent pathway 38 . When shuttled from the nucleolus into the nucleoplasm, RPS27A enhanced p53 stability by suppressing MDM2-mediated p53 ubiquitination in response to ribosomal stress.…”

Section: Discussionmentioning

confidence: 99%

GYS1 induces glycogen accumulation and promotes tumor progression via the NF-κB pathway in Clear Cell Renal Carcinoma

Chen¹,

Huang²,

Huang³

et al. 2020

Theranostics

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Metabolism reprogramming is a hallmark of many cancer types. We focused on clear cell renal carcinoma (ccRCC) which is characterized by its clear and glycogen-enriched cytoplasm with unknown reasons. The aim of this study was to identify the clinical significance, biological function, and molecular regulation of glycogen synthase 1 (GYS1) in ccRCC glycogen accumulation and tumor progression. Methods: We determined the clinical relevance of GYS1 and glycogen in ccRCC by immunohistochemistry and periodic acid-schiff staining in fresh tissue and by tissue micro-array. Metabolic profiling with GYS1 depletion was performed by metabolomics analysis. In vitro and xenograft mouse models were used to evaluate the impact of GYS1 on cell proliferation. High-throughput RNA-Seq analyses and co-immunoprecipitation-linked mass spectrometry were used to investigate the downstream targets of GYS1. Flow cytometry and CCK8 assays were performed to determine the effect of GYS1 and sunitinib on cell viability. Results: We observed that GYS1 was significantly overexpressed and glycogen was accumulated in ccRCC tissues. These effects were correlated with unfavorable patient survival. Silencing of GYS1 induced metabolomic perturbation manifested by a carbohydrate metabolism shift. Overexpression of GYS1 promoted tumor growth whereas its silencing suppressed it by activating the canonical NF-κB pathway. The indirect interaction between GYS1 and NF-κB was intermediated by RPS27A, which facilitated the phosphorylation and nuclear import of p65. Moreover, silencing of GYS1 increased the synthetic lethality of ccRCC cells to sunitinib treatment by concomitantly suppressing p65. Conclusions: Our study findings reveal an oncogenic role for GYS1 in cell proliferation and glycogen metabolism in ccRCC. Re-sensitization of ccRCC cells to sunitinib suggests that GYS1 is a useful indicator of unfavorable prognosis as well as a therapeutic target for patients with ccRCC.

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“…41,42 Thus, the persistence and activation of LMP1 is also the premise of its biological function execution. 43 It can be seen that EV secretion is not only an important strategy for LMP1 to avoid degradation, but also an important mechanism for LMP1 to participate in intercellular signal exchange, and it continues to play a role in promoting tumor growth. Overall, this study offers new insights into the complex intersection of cellular secretory and degradative mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, it was reported that intracellular LMP1 is often degraded by ubiquitination in a proteasome‐dependent manner with a half‐life of 1.5‐7 hours, which is much shorter than the cell replication cycle (20‐24 hours), therefore, LMP1 is a short‐lived protein . Thus, the persistence and activation of LMP1 is also the premise of its biological function execution . It can be seen that EV secretion is not only an important strategy for LMP1 to avoid degradation, but also an important mechanism for LMP1 to participate in intercellular signal exchange, and it continues to play a role in promoting tumor growth.…”

Section: Discussionmentioning

confidence: 99%

Epstein‐Barr virus‐encoded latent membrane protein 1 promotes extracellular vesicle secretion through syndecan‐2 and synaptotagmin‐like‐4 in nasopharyngeal carcinoma cells

et al. 2020

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Increasing evidence indicates that extracellular vesicles (EVs) play an important role in cancer cell‐to‐cell communication. The Epstein‐Barr virus (EBV)‐encoded latent membrane protein 1 (LMP1), which is closely associated with nasopharyngeal carcinoma (NPC) pathogenesis, can trigger multiple cell signaling pathways that affect cell progression. Several reports have shown that LMP1 promotes EV secretion, and LMP1 trafficking by EVs can enhances cancer progression and metastasis. However, the molecular mechanism by which LMP1 promotes EV secretion is not well understood. In the present study, we found that LMP1 promotes EV secretion by upregulated syndecan‐2 (SDC2) and synaptotagmin‐like‐4 (SYTL4) through nuclear factor (NF)‐κB signaling in NPC cells. Further study indicated that SDC2 interacted with syntenin, which promoted the formation of the EVs, and SYTL4 is associated with the release of EVs. Moreover, we found that stimulation of EV secretion by LMP1 can enhance the proliferation and invasion ability of recipient NPC cells and tumor growth in vivo. In summary, we found a new mechanism by which LMP1 upregulates SDC2 and SYTL4 through NF‐κB signaling to promote EV secretion, and further enhance cancer progression of NPC.

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RPS27a enhances EBV-encoded LMP1-mediated proliferation and invasion by stabilizing of LMP1

Cited by 25 publications

References 30 publications

Silver Nanoparticles Derived by Artemisia arborescens Reveal Anticancer and Apoptosis-Inducing Effects

Silver Nanoparticles Derived by Artemisia arborescens Reveal Anticancer and Apoptosis-Inducing Effects

GYS1 induces glycogen accumulation and promotes tumor progression via the NF-κB pathway in Clear Cell Renal Carcinoma

Epstein‐Barr virus‐encoded latent membrane protein 1 promotes extracellular vesicle secretion through syndecan‐2 and synaptotagmin‐like‐4 in nasopharyngeal carcinoma cells

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