Tumor cells induce LAMP2a expression in tumor-associated macrophage for cancer progression

Wang, Ruibo; Liu, Yantong; Liu, Li; Chen, Mei; Wang, Xiuxuan; Yang, Jingyun; Gong, Yanqiu; Ding, Bi Sen; Wei, Yuquan; Wei, Xiawei

doi:10.1016/j.ebiom.2019.01.045

Cited by 53 publications

(41 citation statements)

References 73 publications

(125 reference statements)

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“…A recent study in TAMs shows that LAMP2A expression is up-regulated by tumor cells in several mouse tumor models and cancer patients' samples. Suppression of Lamp2a gene expression by either shRNA or CRISPR/Cas9 prevents TAMs activation and tumor growth, whereas substrates degradation by CMA seems to promote macrophage pro-tumorigenic activation [148] (Figure 2).…”

Section: Cma In Innate Immune Responsementioning

confidence: 99%

Autophagy in the Immunosuppressive Perivascular Microenvironment of Glioblastoma

Molina

García‐Bernal

Valdor

2019

Cancers

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Glioblastoma (GB) has been shown to up-regulate autophagy with anti- or pro-oncogenic effects. Recently, our group has shown how GB cells aberrantly up-regulate chaperone-mediated autophagy (CMA) in pericytes of peritumoral areas to modulate their immune function through cell-cell interaction and in the tumor’s own benefit. Thus, to understand GB progression, the effect that GB cells could have on autophagy of immune cells that surround the tumor needs to be deeply explored. In this review, we summarize all the latest evidence of several molecular and cellular immunosuppressive mechanisms in the perivascular tumor microenvironment. This immunosuppression has been reported to facilitate GB progression and may be differently modulated by several types of autophagy as a critical point to be considered for therapeutic interventions.

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Section: Cma In Innate Immune Responsementioning

confidence: 99%

Autophagy in the Immunosuppressive Perivascular Microenvironment of Glioblastoma

Molina

García‐Bernal

Valdor

2019

Cancers

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“…It is capable of promoting the proliferation and differentiation of tumor cells through the regulation of H 2 O 2 levels,55 and the repression of PRDX1 expression causes the elevated levels of ROS-stimulated phosphorylation of p38 MAPKα, together with promoting the H 2 O 2 -stimulated senescence in breast cancer cells 56. Other studies have figured out that PRDX1 has the potential to suppresses tumor cell death50 and promote tumor growth 57. In addition, it was explored that the drug resistance formation accompanies a substantial rise in the expression of PRDX1 gene in the breast cancer cell strains 58…”

Section: Discussionmentioning

confidence: 99%

<p>The Prognosis Of Peroxiredoxin Family In Breast Cancer</p>

Wang¹,

Zhong²,

Bi³

et al. 2019

CMAR

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PurposePRDX (Peroxiredoxin) family has involved in breast cancer tumorigenesis from the evidence obtained from cell lines, human tissues and mouse models. Nonetheless, the diversified expression patterns, coupled with the prognostic values of PRDX family, still require explanation. This study aimed at investigating the clinical importance and biological of PRDXs in breast cancer.Patients and methodsSpecimens of paraffin sections used for immunohistochemistry were collected from the hospital and the remaining patient information was retrieved from online databases. The expression and survival data of PRDXs in patients with breast cancer were from ONCOMINE, GEPIA, Kaplan–Meier Plotter. cBioPortal, Metascape, String, Cytoscape and DAVID were used to predict functions and pathways of the changes in PRDXs and their frequently altered neighbor genes. Immunohistochemistry was used to detect the expression of PRDXs in breast cancer.ResultsWe discovered the expression levels of PRDX1-5 were higher in breast cancer tissues than in normal tissues, whereas the expression level of PRDX6 was observed as lower in the former one in comparison with that of the latter one. There existed a correlation between the expression levels of PRDX4, 5 and the advanced tumor stage. Survival analysis revealed that the expression of PRDXs were all associated with relapse-free survival (RFS) in all of the patients with breast cancer. Eventually, we discovered significant regulation of the cellular oxidant detoxification and detoxification of ROS by the PRDX changes, together with obtaining the core modules of genes (TXN, TXN2, TXNRD1, TXNRD2, GPX1 and GPX2) linked to the PRDX family of genes in breast cancer.ConclusionThe PRDX family is widely involved in the development of breast cancer and affects the prognosis of patients. The functions and pathways of the changes in PRDXs and their frequently altered neighbor genes can be further verified by wet experiments.

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“…The first evidence that linked CMA to the immune system was that LAMP2A participates in the display of cytoplasmic epitopes via class II molecules in antigen-presenting cells (Zhou et al, 2005 ). Further research has shown a positive association between CMA and activation of T cells (Valdor et al, 2014 ) and tumor-associated macrophages in hepatocellular carcinoma (Guo et al, 2017 ) and breast cancer (Wang et al, 2019b ). However, very little is known regarding the physiological role of CMA in this organ, although several studies have described the role of other types of autophagy in the brain’s immune system (Plaza-Zabala et al, 2017 ; Molina et al, 2019 ).…”

Section: Physiological Roles Of Cma In the Brainmentioning

confidence: 99%

Impact of Chaperone-Mediated Autophagy in Brain Aging: Neurodegenerative Diseases and Glioblastoma

Auzmendi-Iriarte

Matheu

2021

Front. Aging Neurosci.

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Brain aging is characterized by a time-dependent decline of tissue integrity and function, and it is a major risk for neurodegenerative diseases and brain cancer. Chaperone-mediated autophagy (CMA) is a selective form of autophagy specialized in protein degradation, which is based on the individual translocation of a cargo protein through the lysosomal membrane. Regulation of processes such as proteostasis, cellular energetics, or immune system activity has been associated with CMA, indicating its pivotal role in tissue homeostasis. Since first studies associating Parkinson’s disease (PD) to CMA dysfunction, increasing evidence points out that CMA is altered in both physiological and pathological brain aging. In this review article, we summarize the current knowledge regarding the impact of CMA during aging in brain physiopathology, highlighting the role of CMA in neurodegenerative diseases and glioblastoma, the most common and aggressive brain tumor in adults.

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Tumor cells induce LAMP2a expression in tumor-associated macrophage for cancer progression

Cited by 53 publications

References 73 publications

Autophagy in the Immunosuppressive Perivascular Microenvironment of Glioblastoma

Autophagy in the Immunosuppressive Perivascular Microenvironment of Glioblastoma

<p>The Prognosis Of Peroxiredoxin Family In Breast Cancer</p>

Impact of Chaperone-Mediated Autophagy in Brain Aging: Neurodegenerative Diseases and Glioblastoma

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