miR-145 improves metabolic inflammatory disease through multiple pathways

He, Min; Wu, Nan; Leong, Man Cheong; Zhang, Weiwei; Ye, Zi; Li, Rumei; Huang, Jinjing; Zhang, Zhaoyun; Li, Lianxi; Xiao, Yao; Zhou, Wenbai; Liu, Naijia; Yang, Zhihong; Dong, Xuehong; Li, Yintao; Chen, Lili; Qin, Li; Wang, Xuanchun; Wen, Jie; Zhao, Xiaolong; Lü, Bin; Yang, Yehong; Wang, Qinghua; Hu, Renming

doi:10.1093/jmcb/mjz015

Cited by 35 publications

(30 citation statements)

References 42 publications

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“…Studies reported the silencing of miR-145 associated with increased liver inflammation in mice. Likewise, the lentivirus-mediated miR-145 inhibited macrophage infiltration, ameliorated glucose metabolism, and weight loss ( 180 ). This target has been characterized as a tumor-suppressor miRNA, impacting cell growth ( 59 ), leading to Myc proto-oncogene downregulation ( 181 ).…”

Section: The Role Of Adipose Tissue Mirnas In Cancermentioning

confidence: 99%

The Impact of Adipose Tissue–Derived miRNAs in Metabolic Syndrome, Obesity, and Cancer

2020

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Obesity is a multifactorial and complex condition that is characterized by abnormal and excessive white adipose tissue accumulation, which can lead to the development of metabolic diseases, such as type 2 diabetes mellitus, nonalcoholic fatty liver disease, cardiovascular diseases, and several types of cancer. Obesity is characterized by excessive adipose tissue accumulation and associated with alterations in immunity, displaying a chronic low-grade inflammation profile. Adipose tissue is a dynamic and complex endocrine organ composed not only by adipocytes, but several immunological cells, which can secrete hormones, cytokines and many other factors capable of regulating metabolic homeostasis and several critical biological pathways. Remarkably, adipose tissue is a major source of circulating microRNAs (miRNAs), recently described as a novel form of adipokines. Several adipose tissue–derived miRNAs are deeply associated with adipocytes differentiation and have been identified with an essential role in obesity-associated inflammation, insulin resistance, and tumor microenvironment. During obesity, adipose tissue can completely change the profile of the secreted miRNAs, influencing circulating miRNAs and impacting the development of different pathological conditions, such as obesity, metabolic syndrome, and cancer. In this review, we discuss how miRNAs can act as epigenetic regulators affecting adipogenesis, adipocyte differentiation, lipid metabolism, browning of the white adipose tissue, glucose homeostasis, and insulin resistance, impacting deeply obesity and metabolic diseases. Moreover, we characterize how miRNAs can often act as oncogenic and tumor suppressor molecules, significantly modulating cancer establishment and progression. Furthermore, we highlight in this manuscript how adipose tissue–derived miRNAs can function as important new therapeutic targets.

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Section: The Role Of Adipose Tissue Mirnas In Cancermentioning

confidence: 99%

The Impact of Adipose Tissue–Derived miRNAs in Metabolic Syndrome, Obesity, and Cancer

2020

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“…For example, Liu et al [26] reported that miR-145 directed with CASC9, and the inhibition of miR-145 promoted cell migration and invasion but inhibited cell apoptosis in nasopharyngeal carcinoma cells, which provided a novel therapy for the treatment of nasopharyngeal carcinoma. Furthermore, there are various researches showing a robust association between miR-145 and inflammation [29][30][31]. However, the role of miR-145 in the treatment of tanshinone II A to cervical cancer have not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Tanshinone II A enhances pyroptosis and represses cell proliferation of HeLa cells by regulating miR-145/GSDMD signaling pathway

2020

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Cervical cancer is the fourth most common cancer in women globally. Lack of effective pharmacotherapies for cervical cancer mainly attributed to an elusive understanding of the mechanism underlying its pathogenesis. Pyroptosis plays a key role in inflammation and cancer. Our study identified microRNA (miR) 145 (miR-145)/gasdermin D (GSDMD) signaling pathway as critical mediators in the effect of tanshinone II A on HeLa cells. In the present study, we found that treatment of tanshinone II A led to an obvious repression of cell proliferation and an increase in apoptosis on HeLa cells, especially in high concentration. Compared with the controlled group, tanshinone II A enhanced the activity of caspase3 and caspase9. Notably, the results demonstrated that tanshinone II A regulated cell proliferation of HeLa cells by regulating miR-145/GSDMD signaling pathway. Treatment of tanshinone II A significantly up-regulated the expression of GSDMD and miR-145. After transfection of si-miR-145 plasmids, the effects of tanshinone II A on HeLa cells were converted, including cell proliferation, apoptosis and pyroptosis. In addition, the results showed that tanshinone II A treatment altered the expression level of PI3K, p-Akt, NF-kB p65 and Lc3-I. Collectively, our findings demonstrate that tanshinone II A exerts anticancer activity on HeLa cells by regulating miR-145/GSDMD signaling. The present study is the first time to identify miR-145 as a candidate target in cervical cancer and show an association between miR-145 and pyroptosis, which provides a novel therapy for the treatment of cervical cancer.

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“…Adding methyl groups (-CH 3 ) to DNA is the progress of DNA methylation, which usually leads to transcriptional silencing. 36 [40][41][42][43][44][45][46] MiR-145-5p can also target and inhibit KLF5 expression. 47 51 Moreover,…”

Section: Methylationmentioning

confidence: 99%

Roles of Krüppel‐like factor 5 in kidney disease

Liu

Zhou

et al. 2021

J Cellular Molecular Medi

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Transcription factor Krüppel‐like factor 5 (KLF5) is a member of the Krüppel‐like factors’ (KLFs) family. KLF5 regulates a number of cellular functions, such as apoptosis, proliferation and differentiation. Therefore, KLF5 can play a role in many diseases, including, cancer, cardiovascular disease and gastrointestinal disorders. An important role for KLF5 in the kidney was recently reported, such that KLF5 regulated podocyte apoptosis, renal cell proliferation, tubulointerstitial inflammation and renal fibrosis. In this review, we have summarized the available information in the literature with a brief description on how transcriptional, post‐transcriptional and post‐translational modifications of KLF5 modulate its function in a variety of organs including the kidney with a focus of its importance on the pathogenesis of various kidney diseases. Furthermore, we also have outlined the current and possible mechanisms of KLF5 activation in kidney diseases. These studies suggest a need for more systemic investigations, particularly for generation of animal models with renal cell‐specific deletion or overexpression of KLF5 gene to examine direct contributions of KLF5 to various kidney diseases. This will promote further experimentation in the development of therapies to prevent or treat various kidney diseases.

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miR-145 improves metabolic inflammatory disease through multiple pathways

Cited by 35 publications

References 42 publications

The Impact of Adipose Tissue–Derived miRNAs in Metabolic Syndrome, Obesity, and Cancer

The Impact of Adipose Tissue–Derived miRNAs in Metabolic Syndrome, Obesity, and Cancer

Tanshinone II A enhances pyroptosis and represses cell proliferation of HeLa cells by regulating miR-145/GSDMD signaling pathway

Roles of Krüppel‐like factor 5 in kidney disease

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