Deconvoluting the complexity of micro<scp>RNA</scp>s in autophagy to improve potential cancer therapy

Jiang, Yingnan; Gao, Suyu; Shang, L.; Zhao, Yuqian; Huang, Jian; Wang, Jinhui; Chen, Lixia

doi:10.1111/cpr.12277

Cited by 14 publications

(8 citation statements)

References 81 publications

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“…On the other hand, miR-27b-3p might prevent the autophagic degradation of impaired mitochondria 45 . The dual effect of miR-27b-3p is possibly tissue- or cellular context-dependent, which is consistent with other miRNAs 46 . Apart from many targets including PINK1, FOXO1, PPARγ and Apaf-1 investigated before, MKNK2, GREM1 and EEF1A1 that might be potential targets of miR-27b-3p were revealed in the regulatory network of MELAS pathogenesis.…”

Section: Discussionsupporting

confidence: 87%

Identification of miRNA, lncRNA and mRNA-associated ceRNA networks and potential biomarker for MELAS with mitochondrial DNA A3243G mutation

Wang

Zhuang

et al. 2017

Sci Rep

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Researchers in the field of mitochondrial biology are increasingly unveiling of the complex mechanisms between mitochondrial dysfunction and noncoding RNAs (ncRNAs). However, roles of ncRNAs underlying mitochondrial myopathy remain unexplored. The aim of this study was to elucidate the regulating networks of dysregulated ncRNAs in Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes (MELAS) with mitochondrial DNA (mtDNA) A3243G mutation, which might make contributions to the unveiling of the complex mechanisms underlying mitochondrial myopathy and, possibly, new tools applicable to clinical practice. Through high-throughput technology followed by quantitative real-time polymerase chain reaction (qRT-PCR) and bioinformatics analyses, for the first time, we found that the dysregulated muscle miRNAs and lncRNAs between 20 MELAS patients with mtDNA A3243G mutation and 20 controls formed complex regulation networks and participated in immune system, signal transduction, translation, muscle contraction and other pathways in discovery and training phase. Then, selected ncRNAs were validated in muscle and serum in independent validation cohorts by qRT-PCR. Finally, ROC curve analysis indicated reduced serum miR-27b-3p had the better diagnosis value than lactate and might serve as a novel, noninvasive biomarker for MELAS. Follow-up investigation is warranted to better understand roles of ncRNAs in mitochondrial myopathy pathogenesis.

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Section: Discussionsupporting

confidence: 87%

Identification of miRNA, lncRNA and mRNA-associated ceRNA networks and potential biomarker for MELAS with mitochondrial DNA A3243G mutation

Wang

Zhuang

et al. 2017

Sci Rep

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“…Because autophagy incidence is inside cells, the present study evaluates the expression of miRNAs in BC tissue samples. miRNAs have several roles in the regulation of autophagy processes such as recycling, degradation, fusion, vesicle nucleation, vesicle elongation, and induction ( 123 ).…”

Section: Mirnas Role In Autophagy and Bcg Therapymentioning

confidence: 99%

Optimization of BCG Therapy Targeting Neutrophil Extracellular Traps, Autophagy, and miRNAs in Bladder Cancer: Implications for Personalized Medicine

Mao

Ding

et al. 2021

Front. Med.

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Bladder cancer (BC) is the ninth most common cancer and the thirteenth most common cause of mortality worldwide. Bacillus Calmette Guerin (BCG) instillation is a common treatment option for BC. BCG therapy is associated with the less adversary effects, compared to chemotherapy, radiotherapy, and other conventional treatments. BCG could inhibit the progression and recurrence of BC by triggering apoptosis pathways, arrest cell cycle, autophagy, and neutrophil extracellular traps (NETs) formation. However, BCG therapy is not efficient for metastatic cancer. NETs and autophagy were induced by BCG and help to suppress the growth of tumor cells especially in the primary stages of BC. Activated neutrophils can stimulate autophagy pathway and release NETs in the presence of microbial pathogenesis, inflammatory agents, and tumor cells. Autophagy can also regulate NETs formation and induce production of reactive oxygen species (ROS) and NETs. Moreover, miRNAs are important regulator of gene expression. These small non-coding RNAs are also considered as an essential factor to control the levels of tumor development. However, the interaction between BCG and miRNAs has not been well-understood yet. Therefore, the present study discusses the roles of miRNAs in regulations of autophagy and NETs formation in BCG therapy in the treatment of BC. The roles of autophagy and NETs formation in BC treatment and efficiency of BCG are also discussed.

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“…We therefore also performed literature searches for links between autophagy and the other candidates from our list of predicted oxidative stress-modulated miRNAs shown in Table 3 . We found that several of these miRNAs have been implicated in autophagy regulation, that is, miR-15a, miR-20a/b, miR-23a/b, miR-29a, miR-106a/b, miR-195, and miR-590-3p [ 67 , 70 , 73 , 77 – 81 ]. For example, miR-29a targets the product of the essential autophagy-related gene ATG9A as well as that of the master transcriptional regulator of lysosomal biogenesis and autophagy, TFEB [ 77 ].…”

Section: Resultsmentioning

confidence: 99%

From Oxidative Stress Damage to Pathways, Networks, and Autophagy via MicroRNAs

Engedal

Žerovnik

Rudov

et al. 2018

Oxidative Medicine and Cellular Longevity

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Oxidative stress can alter the expression level of many microRNAs (miRNAs), but how these changes are integrated and related to oxidative stress responses is poorly understood. In this article, we addressed this question by using in silico tools. We reviewed the literature for miRNAs whose expression is altered upon oxidative stress damage and used them in combination with various databases and software to predict common gene targets of oxidative stress-modulated miRNAs and affected pathways. Furthermore, we identified miRNAs that simultaneously target the predicted oxidative stress-modulated miRNA gene targets. This generated a list of novel candidate miRNAs potentially involved in oxidative stress responses. By literature search and grouping of pathways and cellular responses, we could classify these candidate miRNAs and their targets into a larger scheme related to oxidative stress responses. To further exemplify the potential of our approach in free radical research, we used our explorative tools in combination with ingenuity pathway analysis to successfully identify new candidate miRNAs involved in the ubiquitination process, a master regulator of cellular responses to oxidative stress and proteostasis. Lastly, we demonstrate that our approach may also be useful to identify novel candidate connections between oxidative stress-related miRNAs and autophagy. In summary, our results indicate novel and important aspects with regard to the integrated biological roles of oxidative stress-modulated miRNAs and demonstrate how this type of in silico approach can be useful as a starting point to generate hypotheses and guide further research on the interrelation between miRNA-based gene regulation, oxidative stress signaling pathways, and autophagy.

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Deconvoluting the complexity of microRNAs in autophagy to improve potential cancer therapy

Cited by 14 publications

References 81 publications

Identification of miRNA, lncRNA and mRNA-associated ceRNA networks and potential biomarker for MELAS with mitochondrial DNA A3243G mutation

Identification of miRNA, lncRNA and mRNA-associated ceRNA networks and potential biomarker for MELAS with mitochondrial DNA A3243G mutation

Optimization of BCG Therapy Targeting Neutrophil Extracellular Traps, Autophagy, and miRNAs in Bladder Cancer: Implications for Personalized Medicine

From Oxidative Stress Damage to Pathways, Networks, and Autophagy via MicroRNAs

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