miR-34a inhibits progression of neuroblastoma by targeting autophagy-related gene 5

Cheng, Xinru; Xu, Qiao; Zhang, Yixia; Shen, Min; Zhang, Shanshan; Mao, Fengxia; Li, Bing; Yan, Xiaomin; Shi, Zhang; Wang, Li; Sheng, Guang-Yao; Zhang, Qian

doi:10.1016/j.ejphar.2019.01.071

Cited by 30 publications

(19 citation statements)

References 23 publications

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“…For example, in a previous study, miR-144-3p expression levels were reported to be downregulated in NB cell lines, which subsequently suppressed NB cell proliferation, cell cycle progression and migration through regulating homeobox protein A7 (11). Similarly, another previous study discovered that miR-34a expression levels were reduced in NB tissues and cell lines (12), and miR-34a overexpression was found to inhibit cell metastasis and autophagy, but promote apoptosis through targeting autophagy-related gene 5 (12). In addition, miR-129 expression levels were decreased, whereas myosin X expression levels were increased in NB tissues, and this axis was found to regulate NB cell growth and chemosensitivity (13).…”

Section: Discussionmentioning

confidence: 82%

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: 82%

microRNA‑146b promotes neuroblastoma cell growth through targeting NUMB

Zhang

et al. 2020

Exp Ther Med

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“…It is to be noted that in vitro studies have given direct evidence that curcumin induced G2/M arrest and DNA damage in tumor cells [64,65,66,67,68,69,70,71,72], but it acts as a protective agent for normal cells [73]. Moreover, curcumin modulates autophagy in NB cells [74]: the role of autophagy in NB is an emerging field of great interest in both biological and therapeutic aspects [75,76,77,78].…”

Section: Discussionmentioning

confidence: 99%

Role of GOLPH3 and TPX2 in Neuroblastoma DNA Damage Response and Cell Resistance to Chemotherapy

Ognibene

Podestà

Garaventa

et al. 2019

IJMS

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Neuroblastoma (NB) is an aggressive, relapse-prone infancy tumor of the sympathetic nervous system and is the leading cause of death among preschool age diseases, so the search for novel therapeutic targets is crucial. Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in the development, and in the DNA damage response, of various human cancers. Golgi dispersal is a common feature of DNA damage response in mammalian cells. Understanding how cells react to DNA damage is essential in order to recognize the systems used to escape from elimination. We induced DNA damage in two human neuroblastoma cell lines by curcumin. The exposure of neuroblastoma cells to curcumin induced: (a) up-regulation of GOLPH3+ cells; (b) augmentation of double-strand breaks; (c) Golgi fragmentation and dispersal throughout the cytoplasm; (d) increase of apoptosis and autophagy; (e) increased expression of TPX2 oncoprotein, able to repair DNA damage. Primary neuroblastoma samples analysis confirmed these observations. Our findings suggest that GOLPH3 expression levels may represent a clinical marker of neuroblastoma patients’ responsiveness to DNA damaging therapies—and of possible resistance to them. Novel molecules able to interfere with GOLPH3 and TPX2 pathways may have therapeutic benefits when used in combination with standard DNA damaging therapeutic agents in neuroblastoma

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“…Cheng et al revealed that ATG5 was elevated in NB tissues and cells, and overexpression of ATG5 overturned the effects on proliferation, migration, invasion and autophagy of NB cells by miR−34a addition, our results were in line with them. 26 Therefore, we concluded that SNHG16 upregulated ATG5 via sponging miR-542-3p to boost cell proliferation, migration, invasion and autophagy in NB cells (Figure 9).…”

Section: Discussionmentioning

confidence: 92%

“…22 Cumulating data indicated that ATG5 was a common target of different miRNAs for regulating autophagy. [23][24][25][26] For example, Cheng et al revealed that miR-34a could repress the progression of NB via downregulating ATG5 expression. 26 However, the exact role of ATG5 and its related mechanism in NB are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non Coding RNA SNHG16 Facilitates Proliferation, Migration, Invasion and Autophagy of Neuroblastoma Cells via Sponging miR-542-3p and Upregulating ATG5 Expression</p>

Wen¹,

Gong²,

Dong³

et al. 2020

OTT

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Background: Neuroblastoma (NB) is a heterogeneous pediatric malignant tumor with many biological and clinical characteristics. Long non-coding RNA small nucleolar RNA host gene 16 (SNHG16) plays vital role in the development of NB. However, the potential mechanism of SNHG16 in the progression of NB is rarely reported. Methods: The expression levels of SNHG16, miR-542-3p and autophagy-related gene 5 (ATG5) were measured with quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, migration and invasion of NB cells were determined using 3-(4, 5-dimethylthiazol-2-YI)-2, 5-diphenyltetrazolium bromide (MTT) or transwell assay. Protein levels of ATG5, microtubule-associated protein A1/1B-light chain3 (LC3-I/II) and p62 were detected by Western blot analysis. The interaction between miR-542-3p and SNHG16 or ATG5 was predicted by starBase and confirmed by dual luciferase reporter assay. Xenograft mice models were constructed to confirm the role of SNHG16 in vivo. Results: SNHG16 was upregulated in NB tissues and cells and associated with clinical stage and poor prognosis of NB. Knockdown of SNHG16 impeded proliferation, migration, invasion and autophagy of NB cells in vitro, and suppressed tumor growth in vivo. Interestingly, SNHG16 mediated ATG5 expression through sponging miR-542-3p in NB cells. Moreover, miR-542-3p downregulation reversed the inhibitory effects of SNHG16 silencing on proliferation, migration, invasion and autophagy of NB cells. Besides, ATG5 overturned the regulatory effects on proliferation, migration, invasion and autophagy of NB cells induced by SNHG16 or miR-542-3p knockdown. Conclusion: SNHG16 facilitated proliferation, migration, invasion and autophagy of NB cells via sponging miR-542-3p and upregulating ATG5 expression in NB.

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miR-34a inhibits progression of neuroblastoma by targeting autophagy-related gene 5

Cited by 30 publications

References 23 publications

microRNA‑146b promotes neuroblastoma cell growth through targeting NUMB

microRNA‑146b promotes neuroblastoma cell growth through targeting NUMB

Role of GOLPH3 and TPX2 in Neuroblastoma DNA Damage Response and Cell Resistance to Chemotherapy

<p>Long Non Coding RNA SNHG16 Facilitates Proliferation, Migration, Invasion and Autophagy of Neuroblastoma Cells via Sponging miR-542-3p and Upregulating ATG5 Expression</p>

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