Lung cancer-derived extracellular vesicles induced myotube atrophy and adipocyte lipolysis via the extracellular IL-6-mediated STAT3 pathway

Hu, Wenjun; Ru, Zeyuan; Zhou, Yali; Xiao, Wen; Sun, Rulin; Zhang, Santao; Gao, Yingying; Li, Xiang; Zhang, Xiaoping; Yang, Hongmei

doi:10.1016/j.bbalip.2019.04.006

Cited by 65 publications

(59 citation statements)

References 37 publications

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“…Critically, the results obtained in vivo for miR-21-5p lend strong support to the in vitro observations and to the notion that cellular senescence is, at least partly, fractal of the ageing process; they also indicate that circulating factors derived from senescent cells can be used as biomarkers to depict and track ageing trajectories [84]. Even though senescence has been described as a terminal process, mounting evidence supports the view that the adverse effects of the senescence program can be attenuated or delayed [85] and that sEVs could play a critical anti-senescence role [86][87][88].…”

Section: Discussionmentioning

confidence: 85%

Small extracellular vesicles deliver miR‐21 and miR‐217 as pro‐senescence effectors to endothelial cells

Mensà¹,

Guescini

Giuliani³

et al. 2020

J of Extracellular Vesicle

129

106

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The role of epigenetics in endothelial cell senescence is a cutting-edge topic in ageing research. However, little is known of the relative contribution to pro-senescence signal propagation provided by microRNAs shuttled by extracellular vesicles (EVs) released from senescent cells. Analysis of microRNA and DNA methylation profiles in non-senescent (control) and senescent (SEN) human umbilical vein endothelial cells (HUVECs), and microRNA profiling of their cognate small EVs (sEVs) and large EVs demonstrated that SEN cells released a significantly greater sEV number than control cells. sEVs were enriched in miR-21-5p and miR-217, which target DNMT1 and SIRT1. Treatment of control cells with SEN sEVs induced a miR-21/miR-217-related impairment of DNMT1-SIRT1 expression, the reduction of proliferation markers, the acquisition of a senescent phenotype and a partial demethylation of the locus encoding for miR-21. MicroRNA profiling of sEVs from plasma of healthy subjects aged 40-100 years showed an inverse U-shaped age-related trend for miR-21-5p, consistent with senescence-associated biomarker profiles. Our findings suggest that miR-21-5p/miR-217 carried by SEN sEVs spread pro-senescence signals, affecting DNA methylation and cell replication.

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Section: Discussionmentioning

confidence: 85%

Small extracellular vesicles deliver miR‐21 and miR‐217 as pro‐senescence effectors to endothelial cells

Mensà¹,

Guescini

Giuliani³

et al. 2020

J of Extracellular Vesicle

129

106

View full text Add to dashboard Cite

show abstract

“…These adipocytes are part of a vicious circle where cancer cells induce the secretion of lipids and adipokines by adipocytes to promote tumour growth (see later for the effects of adipocytes on cancer cells). The demonstration of adipose tissue modifications by tumours has been made initially in breast [12] and ovarian [13] cancers but the molecular mechanisms have been demonstrated in several other tumour types such as prostate [14] , pancreas [15], lung [16], hepatocarcinoma [17] and leukaemia [18]. It has been demonstrated in mammary adipose tissue that cancer proximity decreases adipogenesis-related genes and increases the expression of secretion-related genes [12,19].…”

Section: ) Modification Of Adipose Tissue By Cancer Cells : Cancer-amentioning

confidence: 99%

“…Among the mechanisms involved in the induction of the activated phenotype of adipocytes by cancer cells, extracellular vesicles and miRNA have been recently described to promote adipocyte lipolysis and inflammation. In lung cancer, extracellular vesicles transfer IL-6 to induce adipocyte lipolysis through STAT3 pathway [16]. In hepatocarcinoma exosomes released by cancer cells activate NFκB signalling and induce an inflammatory phenotype in adipocytes with the secretion of IL-6, IL-8 and macrophage chemoattractant protein (MCP-1) [17].…”

Section: ) Modification Of Adipose Tissue By Cancer Cells : Cancer-amentioning

confidence: 99%

Interaction between adipose tissue and cancer cells: role for cancer progression

Dumas

Brisson

2020

Cancer Metastasis Rev

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Environment surrounding tumours are now recognised to play an important role in tumour development and progression. Among the cells found in the tumour environment, adipocytes from adipose tissue establish a vicious cycle with cancer cells to promote cancer survival, proliferation, metastasis and treatment resistance. This cycle is particularly of interest in the context of obesity which has been found as cancer risk factor. Cancers cells can reprogram adipocyte physiology leading to an "activated" phenotype characterized by delipidation and secretion of inflammatory adipokines. The adipocyte secretions then influence tumour growth and metastasis which has been mainly attributed to interleukin 6 (IL-6) or leptin but also to the release of fatty acids which are able to change cancer cell metabolism and signalling pathways.The aim of this review is to report recent advances in the understanding of the molecular mechanisms linking adipose tissue with cancer progression in order to propose new therapeutic strategies based on pharmacological or nutritional intervention.

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“…16,17 The neutralization of extracellular IL-6 prevents adipose tissue lipolysis, because in cachectic mice that are administered an anti-IL-6 receptor antibody, white adipose tissue (WAT) lipolysis and browning are inhibited. 18,19 However, we were unable to determine whether the high IL-6 concentration played a role in the insulin-induced lipoatrophy in the present case.…”

Section: Discussionmentioning

confidence: 58%

Multifocal lipoatrophy secondary to insulin injection in a patient with type 2 diabetes, hepatitis B virus infection, and liver cirrhosis

Lou

2021

J Int Med Res

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Lipoatrophy secondary to insulin injection is a rare complication of insulin use. Localized lipoatrophy is recognized by a loss of subcutaneous fat caused by insulin injection. We report the case of a 69-year-old non-obese female patient with type 2 diabetes mellitus, decompensated liver cirrhosis, and hepatitis B virus (HBV) infection who developed multifocal lipoatrophy during the administration of human insulin and an insulin analog.

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Lung cancer-derived extracellular vesicles induced myotube atrophy and adipocyte lipolysis via the extracellular IL-6-mediated STAT3 pathway

Cited by 65 publications

References 37 publications

Small extracellular vesicles deliver miR‐21 and miR‐217 as pro‐senescence effectors to endothelial cells

Small extracellular vesicles deliver miR‐21 and miR‐217 as pro‐senescence effectors to endothelial cells

Interaction between adipose tissue and cancer cells: role for cancer progression

Multifocal lipoatrophy secondary to insulin injection in a patient with type 2 diabetes, hepatitis B virus infection, and liver cirrhosis

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