microRNA‐96 protects pancreatic β‐cell function by targeting PAK1 in gestational diabetes mellitus

Li, Lei; Li, Hongyan; Wan, Jipeng; Zhou, Qian; Zhou, Yu; Zhang, Chunhua

doi:10.1002/biof.1461

Cited by 43 publications

(32 citation statements)

References 35 publications

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“…Similarly, Li et al evaluated microRNA expression in placental tissue from three GDM and three CTRLs [90]. A significant downregulation of miR-96 was reported in GDM compared to CTRLs and an inverse correlation between miR-96 expression and blood glucose emerged.…”

Section: β-Cell Dysfunctionmentioning

confidence: 99%

Non-Coding RNA: Role in Gestational Diabetes Pathophysiology and Complications

Filardi

Catanzaro

Mardente

et al. 2020

IJMS

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Gestational Diabetes Mellitus (GDM) is defined as glucose intolerance that develops in the second or third trimester of pregnancy. GDM can lead to short-term and long-term complications both in the mother and in the offspring. Diagnosing and treating this condition is therefore of great importance to avoid poor pregnancy outcomes. There is increasing interest in finding new markers with potential diagnostic, prognostic and therapeutic utility in GDM. Non-coding RNAs (ncRNAs), including microRNAs, long non-coding RNAs and circular RNAs, are critically involved in metabolic processes and their dysregulated expression has been reported in several pathological contexts. The aberrant expression of several circulating or placenta-related ncRNAs has been linked to insulin resistance and β-cell dysfunction, the key pathophysiological features of GDM. Furthermore, significant associations between altered ncRNA profiles and GDM-related complications, such as macrosomia or trophoblast dysfunction, have been observed. Remarkably, the deregulation of ncRNAs, which might be linked to a detrimental intrauterine environment, can lead to changes in the expression of target genes in the offspring, possibly contributing to the development of long-term GDM-related complications, such as metabolic and cardiovascular diseases. In this review, all the recent findings on ncRNAs and GDM are summarized, particularly focusing on the molecular aspects and the pathophysiological implications of this complex relationship.

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Section: β-Cell Dysfunctionmentioning

confidence: 99%

Non-Coding RNA: Role in Gestational Diabetes Pathophysiology and Complications

Filardi

Catanzaro

Mardente

et al. 2020

IJMS

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“…Accumulating studies have suggested miRNAs are closely related to glycometabolic disorders including GDM by regulating placental immunity, pancreatic β cell functions, insulin sensitivity, and insulin resistance [14][15][16]. Circulating miRNAs contributing to tissue cross-talk have also been identified as potential biomarkers for GDM [17].…”

Section: Mediators Of Inflammationmentioning

confidence: 99%

miR-657 Promotes Macrophage Polarization toward M1 by Targeting FAM46C in Gestational Diabetes Mellitus

Wang

Liu

et al. 2019

Mediators of Inflammation

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MicroRNA (miRNA) has been widely suggested to play a vital role of in the pathogenesis of gestational diabetes mellitus (GDM). We have previously demonstrated that miR-657 can regulate macrophage inflammatory response in GDM. However, the role of miR-657 on M1/M2 macrophage polarization in GDM pathogenesis is not clear yet. This study is aimed at elucidating this issue and identifying novel potential GDM therapeutic targets based on miRNA network. miR-657 is found to be upregulated in placental macrophages demonstrated by real-time PCR, which can enhance macrophage proliferation and migration in vitro. Luciferase reporter assay shows the evidence that FAM46C is a target of miR-657. In addition, miR-657 can promote macrophage polarization toward the M1 phenotype by downregulating FAM46C in macrophages. The present study strongly suggests miR-657 is involved in GDM pathogenesis by regulating macrophage proliferation, migration, and polarization via targeting FAM46C. miR-657/FAM46C may serve as promising targets for GDM diagnosis and treatment.

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“…The regulation of miRNAs on target genes is also a hot spot in oncology. Studies have revealed that miR-485-5p 79 , miR-140-5p 80 , miR-96 81 , miR-7 82 , miR-494 83 , miR-34b 84 , and miR-145 85 can directly target and degrade the mRNA of PAK1 in order to block the translation of PAK1. In addition, PAK1 can be directly activated by interaction with Rho-related GTPases CDC42 and RAC1 86 .…”

Section: Endogenous Upstream Regulators Of Pak1mentioning

confidence: 99%

P21-Activated Kinase 1: Emerging biological functions and potential therapeutic targets in Cancer

Yao

Rajoka

et al. 2020

Theranostics

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The p21-Activated kinase 1 (PAK1), a member of serine-threonine kinases family, was initially identified as an interactor of the Rho GTPases RAC1 and CDC42, which affect a wide range of processes associated with cell motility, survival, metabolism, cell cycle, proliferation, transformation, stress, inflammation, and gene expression. Recently, the PAK1 has emerged as a potential therapeutic target in cancer due to its role in many oncogenic signaling pathways. Many PAK1 inhibitors have been developed as potential preclinical agents for cancer therapy. Here, we provide an overview of essential roles that PAK1 plays in cancer, including its structure and autoactivation mechanism, its crucial function from onset to progression to metastasis, metabolism, immune escape and even drug resistance in cancer; endogenous regulators; and cancer-related pathways. We also summarize the reported PAK1 small-molecule inhibitors based on their structure types and their potential application in cancer. In addition, we provide overviews on current progress and future challenges of PAK1 in cancer, hoping to provide new ideas for the diagnosis and treatment of cancer.

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microRNA‐96 protects pancreatic β‐cell function by targeting PAK1 in gestational diabetes mellitus

Cited by 43 publications

References 35 publications

Non-Coding RNA: Role in Gestational Diabetes Pathophysiology and Complications

Non-Coding RNA: Role in Gestational Diabetes Pathophysiology and Complications

miR-657 Promotes Macrophage Polarization toward M1 by Targeting FAM46C in Gestational Diabetes Mellitus

P21-Activated Kinase 1: Emerging biological functions and potential therapeutic targets in Cancer

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