Silencing protein kinase C ζ by microRNA-25-5p activates AMPK signaling and inhibits colorectal cancer cell proliferation

Zhang, Shihu; Zhang, Yiyang; Cheng, Qing; Ma, Zhaoqun; Gong, Guanwen; Deng, Zhangshuang; Xu, Kun; Wang, Gaoyuan; Wei, Yousong; Zou, Xiaoping

doi:10.18632/oncotarget.18649

Cited by 15 publications

(10 citation statements)

References 59 publications

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“…miR-574-5p also participates in the promotion of metastasis and invasion of lung cancer through PTPRU (protein tyrosine phosphatase, receptor type U) [ 35 , 36 ] and TLR9 signaling [ 37 ]. In addition, miR-25-5p has been shown to inhibit cell proliferation of colorectal cancer through activation of AMP-activated protein kinase (AMPK) signaling by silencing protein kinase C ζ [ 38 ], suggesting that sequestering of miR-25-5p activates cancer cell proliferation and affects regulation of energy metabolism and maintenance of glucose homeostasis mediated by AMPK signaling [ 39 ]. Further studies are needed to clarify the roles of sequestration of miRNAs such as miR-574-5p and miR-25-5p by the replication of HCV in the development of extrahepatic manifestations.…”

Section: Discussionmentioning

confidence: 99%

Various miRNAs compensate the role of miR-122 on HCV replication

Ono

Fukuhara

et al. 2020

PLoS Pathog

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One of the determinants for tissue tropism of hepatitis C virus (HCV) is miR-122, a liver-specific microRNA. Recently, it has been reported that interaction of miR-122 to HCV RNA induces a conformational change of the 5'UTR internal ribosome entry site (IRES) structure to form stem-loop II structure (SLII) and hijack of translating 80S ribosome through the binding of SLIII to 40S subunit, which leads to efficient translation. On the other hand, low levels of HCV-RNA replication have also been detected in some non-hepatic cells; however, the details of extrahepatic replication remain unknown. These observations suggest the possibility that miRNAs other than miR-122 can support efficient replication of HCV-RNA in nonhepatic cells. Here, we identified a number of such miRNAs and show that they could be divided into two groups: those that bind HCV-RNA at two locations (miR-122 binding sites I and II), in a manner similar to miR-122 (miR-122-like), and those that target a single site that bridges sites I and II and masking both G28 and C29 in the 5'UTR (non-miR-122-like). Although the enhancing activity of these non-hepatic miRNAs were lower than those of miR-122, substantial expression was detected in various normal tissues. Furthermore, structural modeling indicated that both miR-122-like and non-miR-122-like miRNAs not only can facilitate the formation of an HCV IRES SLII but also can stabilize IRES 3D structure in order to facilitate binding of SLIII to the ribosome. Together, these results suggest that HCV facilitates miR-122-independent replication in non-hepatic cells through recruitment of miRNAs other than miR-122. And our findings can provide a more detailed mechanism of miR-122dependent enhancement of HCV-RNA translation by focusing on IRES tertiary structure.

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Section: Discussionmentioning

confidence: 99%

Various miRNAs compensate the role of miR-122 on HCV replication

Ono

Fukuhara

et al. 2020

PLoS Pathog

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“…Another dysregulated miRNA found in our study was miR-25, which was found to be markedly upregulated in CHD patients with HF. MiR-25 belongs to the miR-106b-25 cluster; it is located on chromosome 7q22.1 and contributes to various pathological processes that are mostly related to cancers and diseases like diabetic nephropathy ( 25 - 27 ). Interestingly, miR-25 is also reported to be involved in the pathogenesis of HF.…”

Section: Discussionmentioning

confidence: 99%

Combination of PBMC miR-19b-5p, miR-221, miR-25-5p and hypertension correlates with increased risk of heart failure in coronary heart disease patients

Yao

Song

Xiong³

et al. 2018

Anatol J Cardiol

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Objective:The aim of this study was to explore the differences in microRNA (miRNA) profiles in peripheral blood mononuclear cells (PBMCs) between coronary heart disease (CHD) patients with and without heart failure (HF) and to assess the values of differentially expressed miRNAs (DEMs) regarding HF risk in CHD patients.Methods:Six CHD patients with HF and six age- and gender-matched CHD patients without HF were enrolled in the exploration stage, and 44 CHD patients with HF and 42 age- and gender-matched CHD patients without HF were recruited in the validation stage. Peripheral blood samples were collected from all the participants, and PBMCs were separated for miRNA detection. miRNA microarray and quantitative polymerase chain reaction were performed to assess the miRNA expression.Results:In the exploration stage, heat map analysis showed that CHD patients with HF could be distinguished from those without HF using PMBC miRNA expressions; 63 downregulated DEMs and 84 upregulated DEMs in PBMCs were identified in CHD patients with HF using volcano map, and top 8 DEMs were selected based on their p values. In the validation stage, PBMC miR-221, miR-19b-5p, and miR-25-5p were found to be markedly dysregulated in CHD patients with HF. Multiple logistic regression analysis showed PBMC miR-221, miR-19b-5p, miR-25-5p, and hypertension to be the independent predictive factors for HF in CHD patients. A receiver operating characteristic curve demonstrated that area under curve of the combination of miR-221, miR-19b-5p, miR-25-5p, and hypertension was 0.871 (95% CI: 0.794-0.944).Conclusion:CHD patients with and without HF could be differentiated according to PBMC miRNA profiles, and the combination of PBMC miR-19b-5p, miR-221, miR-25-5p, and hypertension correlates with an increased HF risk in CHD patients.

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“…Recent studies have revealed that some miRNAs are critically involved in MLT-induced apoptosis in several cancers, such as breast [31] and colon cancers [32]. Among them, though miR-25 was known to promote proliferation in several cancers, such as lung cancer [33], prostate cancer [34], ovarian cancer [35], and colorectal cancer [36] as an oncogene, miR-25-5p was reported to suppress PKCζ as a tumor suppressor [37,38]. Also, among several target molecules, neural precursor cell expressed developmentally downregulated 9 (NEDD9), so called Cas-L (Crk-associated substrate L) or human enhancer of filamentation1 (HEF1), promotes proliferation [39] and metastasis [19,39] in breast cancer, colorectal cancer, and head and neck cancer [40,41].…”

Section: Introductionmentioning

confidence: 99%

NEDD9 Inhibition by miR-25-5p Activation Is Critically Involved in Co-Treatment of Melatonin- and Pterostilbene-Induced Apoptosis in Colorectal Cancer Cells

Jung

Shin

Sim

et al. 2019

Cancers

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The underlying interaction between melatonin (MLT) and daily fruit intake still remains unclear to date, despite multibiological effects of MLT. Herein, the apoptotic mechanism by co-treatment of MLT and pterostilbene (Ptero) contained mainly in grape and blueberries was elucidated in colorectal cancers (CRCs). MLT and Ptero co-treatment (MLT+Ptero) showed synergistic cytotoxicity compared with MLT or Ptero alone, reduced the number of colonies and Ki67 expression, and also increased terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL) positive cells and reactive oxygen species (ROS) production in CRCs. Consistently, MLT+Ptero cleaved caspase 3 and poly (ADP-ribose) polymerase (PARP), activated sex-determining region Y-Box10 (SOX10), and also attenuated the expression of Bcl-xL, neural precursor cell expressed developmentally downregulated protein 9 (NEDD9), and SOX9 in CRCs. Additionally, MLT+Ptero induced differentially expressed microRNAs (upregulation: miR-25-5p, miR-542-5p, miR-711, miR-4725-3p, and miR-4484; downregulation: miR-4504, miR-668-3p, miR-3121-5p, miR-195-3p, and miR-5194) in HT29 cells. Consistently, MLT +Ptero upregulated miR-25-5p at mRNA level and conversely NEDD9 overexpression or miR-25-5p inhibitor reversed the ability of MLT+Ptero to increase cytotoxicity, suppress colony formation, and cleave PARP in CRCs. Furthermore, immunofluorescence confirmed miR-25-5p inhibitor reversed the reduced fluorescence of NEDD9 and increased SOX10 by MLT+Ptero in HT29 cells. Taken together, our findings provided evidence that MLT+Ptero enhances apoptosis via miR-25-5p mediated NEDD9 inhibition in colon cancer cells as a potent strategy for colorectal cancer therapy.

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Silencing protein kinase C ζ by microRNA-25-5p activates AMPK signaling and inhibits colorectal cancer cell proliferation

Cited by 15 publications

References 59 publications

Various miRNAs compensate the role of miR-122 on HCV replication

Various miRNAs compensate the role of miR-122 on HCV replication

Combination of PBMC miR-19b-5p, miR-221, miR-25-5p and hypertension correlates with increased risk of heart failure in coronary heart disease patients

NEDD9 Inhibition by miR-25-5p Activation Is Critically Involved in Co-Treatment of Melatonin- and Pterostilbene-Induced Apoptosis in Colorectal Cancer Cells

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