Downregulation of miR-541 induced by heat stress contributes to malignant transformation of human bronchial epithelial cells via HSP27

Shen, Chengfeng; Liu, Weili; Zhang, Shuang; Pu, Lihui; Deng, Bingnan; Zeng, Qiang; Chen, Zhaoli; Wang, Xinxing

doi:10.1016/j.envres.2019.108954

“…Previous studies revealed the negative targeting relationship between miR-337-3p and JAK2/STAT3 and further demonstrated that STAT3 is directly targeted by miR-337-3p 21 , 22 . Additionally, accumulating evidence has validated that miRNAs expression is often dysregulated by stress in cancer, such as chronic stress 23 , heat stress 24 , and surgical stress 25 . The rapid development of sequencing technology enables the detection of genetic changes in mutated cells, which promote the understanding for cancer biology 26 , 27 .…”

Section: Introductionmentioning

confidence: 99%

Chronic stress promotes EMT-mediated metastasis through activation of STAT3 signaling pathway by miR-337-3p in breast cancer

Du

¹

,

Zeng

²

,

Xiao

³

et al. 2020

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Chronic stress could induce cancer metastasis by constant activation of the sympathetic nervous system, while cellular mechanism remains obscure. The aim of this research is to explore the metastasis associated negative effect of chronic stress. The analysis of transcriptome sequencing implied that activation of STAT3 signaling pathway by downregulated miR-337-3p might be a potential mechanism to induce epithelial to mesenchymal transition (EMT) of cancer cell and promote metastasis under chronic stress. We also verified this biological process in further experiments. Downregulation of miR-337-3p could downregulate E-cadherin expression and upregulate vimentin expression in vitro and in vivo. STAT3, related signal pathways of which are involved in metastasis regulation, was directly targeted by miR-337-3p. In conclusion, the above results denoted that activation of miR-337-3p/STAT3 axis might be a potential pathway for the increasing metastasis of breast cancer under chronic stress.

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“…In a recent study, HSP27 has been found to promote the epithelial-to-mesenchymal transition and proliferation in colorectal carcinoma cells [ 104 ]. HSP27 has also been found to inhibit apoptosis and promote malignant transformation of human bronchial epithelial cells [ 105 ]. These results highlight the important role of this mediator in proliferation and survival of epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Impact of Exosomes Released by Different Corneal Cell Types on the Wound Healing Properties of Human Corneal Epithelial Cells

Desjardins

¹

,

Berthiaume²,

Couture³

et al. 2022

IJMS

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Corneal wound healing involves communication between the different cell types that constitute the three cellular layers of the cornea (epithelium, stroma and endothelium), a process ensured in part by a category of extracellular vesicles called exosomes. In the present study, we isolated exosomes released by primary cultured human corneal epithelial cells (hCECs), corneal fibroblasts (hCFs) and corneal endothelial cells (hCEnCs) and determined whether they have wound healing characteristics of their own and to which point they modify the genetic and proteomic pattern of these cell types. Exosomes released by all three cell types significantly accelerated wound closure of scratch-wounded hCECs in vitro compared to controls (without exosomes). Profiling of activated kinases revealed that exosomes from human corneal cells caused the activation of signal transduction mediators that belong to the HSP27, STAT, β-catenin, GSK-3β and p38 pathways. Most of all, data from gene profiling analyses indicated that exosomes, irrespective of their cellular origin, alter a restricted subset of genes that are completely different between each targeted cell type (hCECs, hCFS, hCEnCs). Analysis of the genes specifically differentially regulated for a given cell-type in the microarray data using the Ingenuity Pathway Analysis (IPA) software revealed that the mean gene expression profile of hCECs cultured in the presence of exosomes would likely promote cell proliferation and migration whereas it would reduce differentiation when compared to control cells. Collectively, our findings represent a conceptual advance in understanding the mechanisms of corneal wound repair that may ultimately open new avenues for the development of novel therapeutic approaches to improve closure of corneal wounds.

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“…The above studies suggest that autophagy dysfunction plays a certain role in regulating the pathophysiology of atherosclerosis. Recently, some studies suggested that HSPB1 promotes autophagy [ 16 , 17 , 40 ]. Researchers have found that P2RX7 regulates autophagy by fine-tuning HSPB1 expression in astrocytes [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

HSPB1 Regulates Autophagy and Apoptosis in Vascular Smooth Muscle Cells in Arteriosclerosis Obliterans

Keqin

¹

,

Hou

²

,

Xu

³

et al. 2022

Cardiovascular Therapeutics

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Objective. Small heat shock protein-1 (HSPB1) is a small heat shock protein that participates in many cellular processes and alleviates stress-induced cell injury. Autophagy protects cells from many types of stress and plays a key role in preventing stress in arteriosclerosis obliterans (ASO). However, the roles of HSPB1 in autophagy and apoptosis in the context of ASO pathogenesis remain unclear. Methods. In vivo and in vitro studies were used to determine whether HSPB1 is associated with ASO progression. The expression of HSPB1 was measured in normal and sclerotic blood vessels. The role of HSPB1 and its potential downstream signaling pathway were determined in VSMCs by overexpressing and silencing HSPB1. Results. A total of 91 ASO patients admitted to and treated at our hospital from Sep. 2020 to Sep. 2021 were selected, and plasma HSPB1 expression was assessed. We divided the patients with ASO into the grade I ( n = 39 ), II ( n = 29 ), III ( n = 10 ), and IV ( n = 13 ) groups according to Fontaine’s classification. Plasma HSPB1 levels were markedly decreased in patients with grade III ( n = 10 ) and IV ( n = 13 ) ASO compared with patients with grade I ASO. Furthermore, HSPB1 expression was significantly decreased, and p62 and cleaved caspase-3 were increased in the sclerotic vasculature compared to the normal vasculature ( p < 0.05 ). Overexpression of HSPB1 promoted apoptosis of VSMCs following ox-LDL treatment. Knockdown of HSPB1 led to a marked increase in the expression of LC3II and Beclin-1 in ox-LDL-stimulated VSMCs, whereas knockdown of HSPB1 attenuated these changes ( p < 0.05 ). Importantly, overexpression of HSPB1 promoted the dephosphorylation of JNK in ox-LDL-stimulated VSMCs. Conversely, downregulation of HSPB1 induced the opposite change. Conclusion. Loss of HSPB1 promotes VSMC autophagy and inhibits VSMC apoptosis, which are associated with ASO. HSPB1 and its downstream signaling pathways could be potential therapeutic targets for ASO treatment.

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Downregulation of miR-541 induced by heat stress contributes to malignant transformation of human bronchial epithelial cells via HSP27

Cited by 10 publications

References 44 publications

Chronic stress promotes EMT-mediated metastasis through activation of STAT3 signaling pathway by miR-337-3p in breast cancer

Chronic stress promotes EMT-mediated metastasis through activation of STAT3 signaling pathway by miR-337-3p in breast cancer

Impact of Exosomes Released by Different Corneal Cell Types on the Wound Healing Properties of Human Corneal Epithelial Cells

HSPB1 Regulates Autophagy and Apoptosis in Vascular Smooth Muscle Cells in Arteriosclerosis Obliterans

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