M2 tumor-associated macrophages produce interleukin-17 to suppress oxaliplatin-induced apoptosis in hepatocellular carcinoma

Guo, Bin; Li, Leilei; Guo, Jiapei; Liu, Aidong; Wu, Jinghua; Wang, Haixin; Shi, Jun; Pang, Dequan; Cao, Qing

doi:10.18632/oncotarget.17973

Cited by 51 publications

(42 citation statements)

References 37 publications

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“…Moreover, CMA confers resistance to cancer treatment through cell type–specific mechanisms. For instance, CMA prevents apoptosis and contributes to resistance to oxaliplatin in hepatocellular carcinoma by degrading the apoptosis trigger cyclin D1, 19 and to irradiation by degrading HMGB1 20 . Furthermore, active degradation of the acetyltransferase p300/CBP by CMA confers resistance to 5‐fluorouracil in colorectal cancer 21 .…”

Section: Discussionmentioning

confidence: 99%

Chaperone‐mediated autophagy receptor modulates tumor growth and chemoresistance in non–small cell lung cancer

et al. 2020

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Chaperone‐mediated autophagy (CMA) is a lysosomal degradation pathway of selective soluble proteins. Lysosome‐associated membrane protein type 2a (LAMP2A) is the key receptor protein of CMA; downregulation of LAMP2A leads to CMA blockade. Although CMA activation has been involved in cancer growth, CMA status and functions in non–small cell lung cancer (NSCLC) by focusing on the roles in regulating chemosensitivity remain to be clarified. In this study, we found that LAMP2A expression is elevated in NSCLC cell lines and patient's tumors, conferring poor survival and platinum resistance in NSCLC patients. LAMP2A knockdown in NSCLC cells suppressed cell proliferation and colony formation and increased the sensitivity to chemotherapeutic drugs in vitro. Furthermore, we found that intrinsic apoptosis signaling is the mechanism of cell death involved with CMA blockade. Remarkably, LAMP2A knockdown repressed tumorigenicity and sensitized the tumors to cisplatin treatment in NSCLC‐bearing mice. Our discoveries suggest that LAMP2A is involved in the regulation of cancer malignant phenotypes and represents a promising new target against chemoresistant NSCLC.

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Section: Discussionmentioning

confidence: 99%

Chaperone‐mediated autophagy receptor modulates tumor growth and chemoresistance in non–small cell lung cancer

et al. 2020

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“…Finally, there is an inverse correlation between cyclin D1 expression levels and CMA activity [ 83 ]. There is still a long way to go to actually prove that cyclin D1 is a CMA substrate, but whether this modulation occurs through a direct or indirect mechanism, the fact is that CMA affects cyclin D1 levels.…”

Section: Cma Control Of Cell Cycle In Distinct Cellular Contextsmentioning

confidence: 99%

The Role of Chaperone-Mediated Autophagy in Cell Cycle Control and Its Implications in Cancer

Andrade-Tomaz

Souza

Rocha

et al. 2020

Cells

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The cell cycle involves a network of proteins that modulate the sequence and timing of proliferation events. Unregulated proliferation is the most fundamental hallmark of cancer; thus, changes in cell cycle control are at the heart of malignant transformation processes. Several cellular processes can interfere with the cell cycle, including autophagy, the catabolic pathway involved in degradation of intracellular constituents in lysosomes. According to the mechanism used to deliver cargo to the lysosome, autophagy can be classified as macroautophagy (MA), microautophagy (MI), or chaperone-mediated autophagy (CMA). Distinct from other autophagy types, CMA substrates are selectively recognized by a cytosolic chaperone, one-by-one, and then addressed for degradation in lysosomes. The function of MA in cell cycle control, and its influence in cancer progression, are already well-established. However, regulation of the cell cycle by CMA, in the context of tumorigenesis, has not been fully addressed. This review aims to present and debate the molecular mechanisms by which CMA can interfere in the cell cycle, in the context of cancer. Thus, cell cycle modulators, such as MYC, hypoxia-inducible factor-1 subunit alpha (HIF-1α), and checkpoint kinase 1 (CHK1), regulated by CMA activity will be discussed. Finally, the review will focus on how CMA dysfunction may impact the cell cycle, and as consequence promote tumorigenesis.

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“…Tumor-associated macrophages are the major components of tumor inflammatory infiltration and are key mediators between tumors and inflammation (Mantovani et al, 1992). Guo et al found that M2 macrophages in the HCC microenvironment can secrete large amounts of IL-17 and inhibit oxaliplatin-induced apoptosis by activating chaperone-mediated autophagy (Guo B. et al, 2017). Tumor-associated neutrophils are also an important part of the tumor microenvironment and can promote various biological activities of tumors (Galdiero et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Establishment of a Prognostic Model Using Immune-Related Genes in Patients With Hepatocellular Carcinoma

Wang

Wang²,

Hua

et al. 2020

Front. Genet.

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Hepatocellular carcinoma (HCC) is one of the most prevalent neoplasms worldwide, particularly in China. Immune-related genes (IRGs) and immune infiltrating lymphocytes play specific roles in tumor growth. Considering how important immunotherapy has become for HCC treatment in the past decade, our objective was to establish a prognostic model by screening survival-related IRGs in patients with HCC. Using edgeR, we identified differentially expressed IRGs (DEIRGs), DEmiRNAs, and DElncRNAs. Functional enrichment analysis of DEIRGs was performed to investigate the biological functions of IRGs via gene ontology annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Protein-protein interaction and competing endogenous RNA networks were established using Cytoscape. Survival-associated IRGs were selected via univariate COX regression analysis, a The Cancer Genome Atlas (TCGA) prognostic model and GSE76427 validation model were developed using multivariate COX regression analysis test by AIC (Akaike Information Criterion). We identified 116 DEIRGs in patients with HCC; the "cytokine-cytokine receptor interaction" pathway was found to be the most enriched pathway. Via the prognostic model helped us classify patients into high-and low-risk score groups based on overall survival (OS); high risk score was associated with worse OS, and a positive correlation was observed between the prognostic model and immune cell infiltration. To summarize, we established a prognostic model using survival-related IRGs that provides sufficient information for prognosis prediction and immunotherapy of patients with HCC.

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M2 tumor-associated macrophages produce interleukin-17 to suppress oxaliplatin-induced apoptosis in hepatocellular carcinoma

Cited by 51 publications

References 37 publications

Chaperone‐mediated autophagy receptor modulates tumor growth and chemoresistance in non–small cell lung cancer

Chaperone‐mediated autophagy receptor modulates tumor growth and chemoresistance in non–small cell lung cancer

The Role of Chaperone-Mediated Autophagy in Cell Cycle Control and Its Implications in Cancer

Establishment of a Prognostic Model Using Immune-Related Genes in Patients With Hepatocellular Carcinoma

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