<i>Helicobacter pylori</i>‐induced exosomal MET educates tumour‐associated macrophages to promote gastric cancer progression

Che, Ying; Geng, Biao; Xu, Yue; Miao, Xin; Chen, Ling; Mu, Xiaoli; Pan, Jinshun; Zhang, Chen; Zhao, Ting; Wang, Chao; Li, Xiang; Wen, Hao; Zheng, Liduan; Qin, You

doi:10.1111/jcmm.13847

Cited by 49 publications

(33 citation statements)

References 35 publications

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“…Pan et al found association between H.pylori-infected GC cells and macrophages through exosome. They also demonstrated that H.pylori-induced exosomal MET educated tumor-associated macrophages to promote gastric cancer progression [62]. Human T cell responses was inhibited by H.pylori outer membrane vesicles via induction of monocyte cyclo-oxygenase-2 (COX-2) expression has been proved.…”

Section: Roles Of H Pylori Derived Evs In Gcmentioning

confidence: 94%

The roles of extracellular vesicles in gastric cancer development, microenvironment, anti-cancer drug resistance, and therapy

et al. 2019

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Gastric cancer (GC) is one of the leading causes of cancer-related death in both men and women due to delayed diagnosis and high metastatic frequency. Extracellular vesicles (EVs) are membrane-bound nanovesicles which are released by cells into body fluids such as plasma, saliva, breast milk, cerebrospinal fluid, semen, urine, lymphatic fluid, amniotic fluid, sputum and synovial fluid. EVs deliver almost all types of biomolecules such as proteins, nucleic acids, metabolites, and even pharmacological compounds. These bioactive molecules can be delivered to recipient cells to influence their biological properties, modify surrounding microenvironment and distant targets. The extensive exploration of EVs enhances our comprehension of GC biology referring to tumor growth, metastasis, immune response and evasion, chemoresistance and treatment. In this review, we will sum up the effects of GC-derived EVs to the tumor microenvironment. Moreover, we will also summarize the function of microenvironment-derived EVs in GC and discuss how the bidirectional communication between tumor and microenvironment affect GC growth, metastatic behavior, immune response, and drug resistance. At last, we prospect the clinical application viewpoint of EVs in GC.

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Section: Roles Of H Pylori Derived Evs In Gcmentioning

confidence: 94%

The roles of extracellular vesicles in gastric cancer development, microenvironment, anti-cancer drug resistance, and therapy

et al. 2019

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“…HP infection is the single most important factor for GC and recent research has implied that the exosome is implicated in the initiation of HP -related diseases. For instance, HP -induced exosomal mesenchymal-epithelial transition factor (MET) can exert a pro-tumorigenic effect on tumor-associated macrophages to promote GC progression [ 42 ]. Another study indicated that exosomes from conditioned media of human gastric epithelial cells are involved in the endothelial function impairment in HP infection [ 43 ].…”

Section: Role Of Exosomal Rna In the Initiation And Development Ofmentioning

confidence: 99%

The Significance of Exosomal RNAs in the Development, Diagnosis, and Treatment of Gastric Cancer

Zhao

Zhou

et al. 2021

Genes

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Gastric cancer (GC) is one of the most common malignancies in the world. Exosomes, a subset of extracellular vesicles with an average diameter of 100 nm, contain and transfer a variety of functional macromolecules such as proteins, lipids, and nucleic acids. A large number of studies indicated that exosomes can play a significant role in the initiation and development of GC via facilitating intercellular communication between gastric cancer cells and microenvironment. Exosomal RNAs, one of the key functional cargos, are involved in the pathogenesis, development, and metastasis of GC. In addition, recent studies elucidated that exosomal RNAs may serve as diagnostic and prognostic biomarkers or therapeutic targets for GC. In this review, we summarized the function of exosomal RNA in the tumorigenesis, progression, diagnosis, and treatment of GC, which may further unveil the functions of exosome and promote the potentially diagnostic and therapeutic application of exosomes in GC.

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“…However, the role of M2 macrophages in EMT is unclear. In GC tissues (H. pylori-positive), tumor-infiltrating macrophages express activated mesenchymal-epithelial transition factor (MET) [153]. A 2017 study by Fu et al has shown a significant correlation between the expression of the CD68 marker characteristic to TAMs and losing expression of the epithelial marker E-cadherin, as well the presence of the mesenchymal marker vimentin [146].…”

Section: Tumor-associated Macrophages In Gastric Cancermentioning

confidence: 99%

Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

Baj

Brzozowska

Forma

et al. 2020

IJMS

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Infection with Helicobacter pylori, a Gram-negative, microaerophilic pathogen often results in gastric cancer in a subset of affected individuals. This explains why H. pylori is the only bacterium classified as a class I carcinogen by the World Health Organization. Several studies have pinpointed mechanisms by which H. pylori alters signaling pathways in the host cell to cause diseases. In this article, the authors have reviewed 234 studies conducted over a span of 18 years (2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016)(2017)(2018)(2019)(2020). The studies investigated the various mechanisms associated with gastric cancer induction. For the past 1.5 years, researchers have discovered new mechanisms contributing to gastric cancer linked to H. pylori etiology. Alongside alteration of the host signaling pathways using oncogenic CagA pathways, H. pylori induce DNA damage in the host and alter the methylation of DNA as a means of perturbing downstream signaling. Also, with H. pylori, several pathways in the host cell are activated, resulting in epithelial-to-mesenchymal transition (EMT), together with the induction of cell proliferation and survival. Studies have shown that H. pylori enhances gastric carcinogenesis via a multifactorial approach. What is intriguing is that most of the targeted mechanisms and pathways appear common with various forms of cancer.EMT refers to the process by which the mesenchymal phenotype is acquired by epithelial cells (ECs) mainly via the reduction of their intracellular adhesions and proliferative capacity (Figure 1.) [47].

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Helicobacter pylori‐induced exosomal MET educates tumour‐associated macrophages to promote gastric cancer progression

Cited by 49 publications

References 35 publications

The roles of extracellular vesicles in gastric cancer development, microenvironment, anti-cancer drug resistance, and therapy

The roles of extracellular vesicles in gastric cancer development, microenvironment, anti-cancer drug resistance, and therapy

The Significance of Exosomal RNAs in the Development, Diagnosis, and Treatment of Gastric Cancer

Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

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