miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

Guo, Xiaofeng; Zhu, Yuekun; Hong, Xuemin; Zhang, Mukun; Qiu, Xingfeng; Wang, Zhenfa; Qi, Zhongquan; Hong, Xuehui

doi:10.1038/cddis.2017.300

Cited by 58 publications

(43 citation statements)

References 26 publications

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“…Our study provided evidence that CRY1 is indeed a target gene of miR-181a and that the elevation of miR-181a could lead to the direct down-regulation of CRY1. Moreover, miR-181d expression can also directly target the 3’-UTRs of CRY2 and FBXL3, providing information on its association with colorectal cancer (Guo et al 2017 ). Our results and others’ lead to the conclusion that an increased expression of miR-181a results in the down-regulation of CRY1, in turn promoting the GS and RTE injury in CKD.…”

Section: Discussionmentioning

confidence: 99%

Over-expressed microRNA-181a reduces glomerular sclerosis and renal tubular epithelial injury in rats with chronic kidney disease via down-regulation of the TLR/NF-κB pathway by binding to CRY1

Liu

Pang

Shang

et al. 2018

Mol Med

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BackgroundMicroRNAs (miRNAs) contribute to the progression of chronic kidney disease (CKD) by regulating renal homeostasis. This study explored the effects of miR-181a on CKD through the Toll-like receptor (TLR)/nuclear factor-kappa B (NF-κB) pathway by binding to CRY1.MethodsSeventy male rats were selected and assigned into specific groups: miR-181a mimic, miR-181a inhibitor, and siRNA against CRY1, with each group undergoing different treatments to investigate many different outcomes. First, 24-h urinary protein was measured. ELISA was used to determine the serum levels of SOD, ROS, MDA, IL-1β, IL-6, and TNF-α. Biochemical tests for renal function were performed to measure albumin, uric acid, and urea in urine and urea nitrogen and creatinine in serum. The glomerulosclerosis index (GSI) and renal tubular epithelial (RTE) cell apoptosis were detected using PASM staining and TUNEL staining, respectively. Finally, RT-qPCR and western blot were done to determine miR-181a, CRY1, TLR2, TLR4, and NF-κB expression.ResultsCRY1 is the target gene of miR-181a, according to a target prediction program and luciferase assay. Rats diagnosed with CKD presented increases in 24-h urinary protein; GSI; RTE cell apoptosis rate; serum ROS, MDA, IL-1β, IL-6, and TNF-α; and CRY1, TLR2, TLR4, and NF-κB expression, as well as decreases in SOD level and miR-181a expression. Following transfection with either the miR-181a mimic or si-CRY1, 24-h urinary protein, renal damage, GSI, and cell apoptosis rate were all decreased. In addition, the overexpression of miR-181a or inhibition of CRY1 alleviated the degree of kidney injury through suppression of the TLR/NF-κB pathway.ConclusionmiR-181a alleviates both GS and RTE injury in CKD via the down-regulation of the CRY1 gene and the TLR/NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

Over-expressed microRNA-181a reduces glomerular sclerosis and renal tubular epithelial injury in rats with chronic kidney disease via down-regulation of the TLR/NF-κB pathway by binding to CRY1

Liu

Pang

Shang

et al. 2018

Mol Med

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“…Na et al [83] demonstrated that miR-181d and miR-191 exhibited inversely correlated circadian rhythm by controlling the circadian initiators, clock and Bmal1 in mouse liver [83]. In colorectal cancer, miR-181d plays an oncogenic role by directly targeting the 3 -UTRs of CRY2 and FBXL3 and by promoting glycolysis which implies the notion that dysregulated expression of clock gene leads the formation of tumor [84,85]. Cancer progression is also influenced by the circadian system whose functioning is based on the rhythmic expression of clock genes.…”

Section: Role Of Micrornas In Molecular Clock Regulation: Implicationmentioning

confidence: 99%

Role of Non-Coding RNAs in Lung Circadian Clock Related Diseases

Chinnapaiyan

Dutta

Devadoss

et al. 2020

IJMS

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Circadian oscillations are regulated at both central and peripheral levels to maintain physiological homeostasis. The central circadian clock consists of a central pacemaker in the suprachiasmatic nucleus that is entrained by light dark cycles and this, in turn, synchronizes the peripheral clock inherent in other organs. Circadian dysregulation has been attributed to dysregulation of peripheral clock and also associated with several diseases. Components of the molecular clock are disrupted in lung diseases like chronic obstructive pulmonary disease (COPD), asthma and IPF. Airway epithelial cells play an important role in temporally organizing magnitude of immune response, DNA damage response and acute airway inflammation. Non-coding RNAs play an important role in regulation of molecular clock and in turn are also regulated by clock components. Dysregulation of these non-coding RNAs have been shown to impact the expression of core clock genes as well as clock output genes in many organs. However, no studies have currently looked at the potential impact of these non-coding RNAs on lung molecular clock. This review focuses on the ways how these non-coding RNAs regulate and in turn are regulated by the lung molecular clock and its potential impact on lung diseases.

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“…The majority of the remaining previously reported genes in pCRC are the MIR-15 family member, Mir-29-P2a/b ( miR-29b ), two MIR-96 family members, Mir-135-P3, Mir-130-P2a ( miR-301a ) [41,42] , Mir-181-P1c [43] , and Mir-224 [18,39] . Mir-95-P2…”

Section: Pcrc Signature Mirnasmentioning

confidence: 99%

A microRNA Signature of Metastatic Colorectal Cancer

Høye

Fromm

Böttger

et al. 2020

Preprint

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BackgroundAlthough microRNAs (miRNAs) are involved in all hallmarks of cancer, miRNA dysregulation in the metastatic process remains poorly understood. We investigated the role of miRNAs in metastatic evolution of colorectal cancer (CRC) by analyzing smallRNA-seq datasets from primary CRC, metastatic locations (liver, lung and peritoneum), and corresponding adjacent tissues. Addressing main challenges of miRNA analysis, a bioinformatics pipeline was developed that contains bona fide miRNA annotations from MirGeneDB, utilizes the quality control software miRTrace, applies physiologically meaningful cutoffs and accounts for contribution of cell-type specific miRNAs and host tissue effects. ResultsTwo hundred-and-seventy-five miRNA sequencing datasets were analyzed, and after adjusting for the contribution of heterogeneity in cellular composition, strong signatures for primary and metastatic CRC were identified. The signature for primary CRC contained many previously known miRNAs with known functions. Deregulation of specific miRNAs was associated with individual metastatic sites, but the metastatic signatures contained overlapping miRNAs involved in key elements of the metastatic process, such as epithelial-to-mesenchymal transition and hypoxia. Notably, four of these miRNAs (MIR-8, MIR-10, MIR-375, MIR-210) belong to deeply conserved families present in many other organisms, triggering questions about their evolutionary functions and opportunities for experimental validation. Conclusion:Applying a meticulous pipeline for the analysis of smallRNA-seq data, miRNA signatures for primary and metastatic CRC were identified, contributing novel insights into miRNA involvement in CRC metastatic evolution and site-specific metastatic adaptations. New datasets can easily be included in this publicly available pipeline to continuously improve the knowledge in the field.

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miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

Cited by 58 publications

References 26 publications

Over-expressed microRNA-181a reduces glomerular sclerosis and renal tubular epithelial injury in rats with chronic kidney disease via down-regulation of the TLR/NF-κB pathway by binding to CRY1

Over-expressed microRNA-181a reduces glomerular sclerosis and renal tubular epithelial injury in rats with chronic kidney disease via down-regulation of the TLR/NF-κB pathway by binding to CRY1

Role of Non-Coding RNAs in Lung Circadian Clock Related Diseases

A microRNA Signature of Metastatic Colorectal Cancer

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