MiR-488 inhibits proliferation and cisplatin sensibility in non-small-cell lung cancer (NSCLC) cells by activating the eIF3a-mediated NER signaling pathway

Fang, Chao; Chen, Yixin; Wu, Na-Yi Yuan; Yin, Ji‐Ye; Li, Xiangping; Huang, Hsuan-Shun; Zhang, Wei; Zhou, Hong‐Hao; Liu, Zhao‐Qian

doi:10.1038/srep40384

Cited by 67 publications

(46 citation statements)

References 54 publications

(59 reference statements)

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“…Therefore, the knockdown of EIF3A interrupts DNA damage-induced cell death [71,72]. A recent study revealed that miR-488-3p levels are higher in cisplatin-resistant lung cancer cells than in parental cells, and NER is activated by miR-488-3p, which targets EIF3A [73] (Table 2).…”

Section: Mir-488-3pmentioning

confidence: 99%

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

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The susceptibility of cancer cells to different types of treatments can be restricted by intrinsic and acquired therapeutic resistance, leading to the failure of cancer regression and remission. To overcome this problem, a combination therapy has been proposed as a fundamental strategy to improve therapeutic responses; however, resistance is still unavoidable. MicroRNA (miRNAs) are associated with cancer therapeutic resistance. The modulation of dysregulated miRNA levels through miRNA-based therapy comprising a replacement or inhibition approach has been proposed to sensitize cancer cells to other anti-cancer therapies. The combination of miRNA-based therapy with other anti-cancer therapies (miRNA-based combinatorial cancer therapy) is attractive, due to the ability of miRNAs to target multiple genes associated with the signaling pathways controlling therapeutic resistance. In this article, we present an overview of recent findings on the role of therapeutic resistance-related miRNAs in different types of cancer. We review the feasibility of utilizing dysregulated miRNAs in cancer cells and extracellular vesicles as potential candidates for miRNA-based combinatorial cancer therapy. We also discuss innate properties of miRNAs that need to be considered for more effective combinatorial cancer therapy.Cells 2020, 9, 29 2 of 32 to confer the ability to acquire CSC properties onto cancer cells, thereby contributing to therapeutic resistance [7]. Moreover, cell-to-cell communication via extracellular vesicles among different types of cells within the cancer microenvironment could affect the efficacy of cancer therapies by delivering miRNAs that regulate various signaling pathways connected to therapeutic resistance [8,9].Combination therapies have been proposed to overcome therapeutic resistance via the combined inhibition of different mechanisms. For example, the combination of cobimetinib and pictilisib was reported to be beneficial for the treatment of colorectal cancer cells. However, resistance is unavoidable even after the combination treatment [10]. Similarly, the simultaneous inhibition of phosphoinositide 3-kinase (PI3K) and a mechanistic target of rapamycin kinase (mTOR) was reported to activate extracellular signal-regulated kinase (ERK), a pro-survival factor, in acute myeloid leukemia [11]. Therefore, it is still necessary to explore new combination strategies to defeat therapeutic resistance. An improved understanding of the cellular basis of cancer therapeutic resistance can further provide promising opportunities to design and develop novel cancer treatment strategies to manage cancers.MicroRNAs (miRNAs) are widely recognized, small, regulatory RNAs modulating numerous intracellular signaling pathways in several diseases, including cancers. Based on the expression levels and intracellular functions of miRNAs, they could act as tumor-suppressive or oncogenic factors in cancer cells [12][13][14]. The abnormal expression of miRNAs is associated with therapeutic resistance in cancer, and the modulation of m...

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Section: Mir-488-3pmentioning

confidence: 99%

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

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“…Lung cancer (LC), is characterized by unrestrained cell growth in lung tissues [1]. As one of the most common malignant tumors worldwide, the leading risk factors involved with the occurrence of LC include both smoking as well as exposure and environmental factors [2].…”

Section: Introductionmentioning

confidence: 99%

Endoplasmic Reticulum Stress Promotes Autophagy and Apoptosis and Reduces Chemotherapy Resistance in Mutant p53 Lung Cancer Cells

Gan

Zhou

Zhong

et al. 2017

Cell Physiol Biochem

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Background/Aims: Lung cancer (LC) continues to be one of the most prevalent cancers around the world. During this study we aimed to investigate the involvement of endoplasmic reticulum stress (ERS) in autophagy, apoptosis, and chemotherapy resistance of mutant p53 LC cells. Methods: Immunohistochemistry was employed to help determine the p53 mutation status of cancer cells from 92 primary LC patients, who were subsequently assigned to either the mutant p53 (n = 39) or wild-type p53 group (n = 53). Results: Mutant p53 cells exhibited increased expression of the C/EBP homologous protein (CHOP), glucose-regulated protein 78 (GRP78), and inositol-requiring enzyme-1α (IRE1α). The Mutant p53 cells were also found to be sensitive to chemotherapy and displayed decreased expression of PI3K, Akt, and mTOR. The mutant p53 cell lines were treated with tunicamycin to induce ERS and rapamycin in order to inhibit mTOR. Both agents increased the expression of CHOP, GRP78, IRE1α, LC3-II/LC3-I, Atg5, Atg7, caspase-3, caspase-12, cleaved caspase-3, cleaved caspase-12, as well as decreases in cell proliferation as well as the expression levels of PI3K, Akt, and mTOR. Enhanced levels of cell apoptosis and reduced chemotherapy resistance were also detected. Conclusion: The findings of our study suggest that ERS promotes autophagy and apoptosis, while acting to reduce chemotherapy resistance in mutant p53 LC cells by downregulating the PI3K/Akt/mTOR signaling pathway.

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“…It is generally recognized that the MyD88/NF-κB signaling pathway participated in the lipopolysaccharide (LPS)-induced inflammatory response [21,22] . A novel document reported that the MyD88/NF-κB signaling pathway was associated with a pyrin domain containing 3 (NLRP3) inflammasome activities and an IL-1β secretion, which were believed to be important for innate immunity [12] . Furthermore, Jang et al found that the MyD88/NF-κB signaling pathway was closely related to the occurrence and development of inflammatory diseases [23] .…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, current evidence supports the assertion that MyD88 acts as a Toll-like receptor (TLR) adapter protein crucial for innate inflammation responses via the activation of downstream signaling pathways. Some of these pathways include NF-κB and mitogen-activated protein kinase signaling pathways, driving robust synthesis, and the gene expression of cytokines and pro-inflammatory mediators [11,12] . MicroRNAs (miRNAs), which are small noncoding RNAs consisting of endogenous 21-23 nucleotides, were bound to 3'-untranslated regions (UTR) of the target gene in order to post-transcriptionally regulate the eukaryotic gene expression.…”

Section: Introductionmentioning

confidence: 99%

MiR-539 Inhibits Inﬂammation in Renal Transplant Iscemia-Reperfusion Injury Via Blocking the MyD88/NF-κB Pathway

Ge¹

2018

Clin Surg Res Commun

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Objective: This study was conducted in order to investigate the anti-inflammatory effects of miR-539 on renal transplant ischemia-reperfusion (I/R) injury. Methods: A mouse model replicating renal transplant I/R injury and a cellular model of oxygen-glucose deprivation (OGD) treatment were established. The blood urea nitrogen (BUN) levels were determined for all models. The miR-539 expressions were detected in the kidney tissues and HK-2 cells following the different transfections using qRT-PCR. Western blotting was used to analyze myeloid differentiation factor 88 (MyD88), as well as the unphosphorylated and phosphorylated Nuclear factor-κB (NF-κB) protein expressions. The interactions between miR-539 and MyD88 were examined through a luciferase reporter assay. Moreover, proinflammatory cytokines levels, including the tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8, were measured using an enzyme-linked immunosorbent assay (ELISA). A renal tubular necrosis score (TNS) was employed as a means of assessing the renal function of mouse model. Results: miR-539 was downregulated during renal I/R injury. In vitro, miR-539 relieved the secretion of proinflammatory cytokines. A luciferase reporter assay demonstrated that MyD88 was a direct target of miR-539. Further investigation revealed that miR-539 inhibited I/R injury-induced inflammation by downregulating the MyD88/NF-κB pathway. It was shown that miR-539 exerted anti-inflammatory effects in the mice that underwent renal transplant I/R injury. Conclusion: MiR-539 alleviated inflammation in renal transplant I/R injury through the MyD88/NF-κB pathway.

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MiR-488 inhibits proliferation and cisplatin sensibility in non-small-cell lung cancer (NSCLC) cells by activating the eIF3a-mediated NER signaling pathway

Cited by 67 publications

References 54 publications

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Endoplasmic Reticulum Stress Promotes Autophagy and Apoptosis and Reduces Chemotherapy Resistance in Mutant p53 Lung Cancer Cells

MiR-539 Inhibits Inﬂammation in Renal Transplant Iscemia-Reperfusion Injury Via Blocking the MyD88/NF-κB Pathway

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