Mycoplasma fermentans deacetylase promotes mammalian cell stress tolerance

Cheng, Qunpeng; Wu, Lijuan; Tu, Rongfu; Wu, Jun; Kang, Wenqian; Su, Tong; Du, Ran; Liu, Wenbin

doi:10.1016/j.micres.2017.04.010

Cited by 4 publications

(5 citation statements)

References 55 publications

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“…Additionally, mycoplasma-derived p37 can promote metastasis through multiple mechanisms. In lung cancer mouse models, p37transfected cells showed an increased ability to degrade extracellular matrices and increase motility (41). This was accomplished through a p37-induced increase in matrix metallopeptidase-2 (MMP-2), and a subsequent increase in EGFR activation (41).…”

Section: Relevance To Cancermentioning

confidence: 99%

“…In lung cancer mouse models, p37transfected cells showed an increased ability to degrade extracellular matrices and increase motility (41). This was accomplished through a p37-induced increase in matrix metallopeptidase-2 (MMP-2), and a subsequent increase in EGFR activation (41). More recently, p37-transfected hepatocellular carcinoma cells (HCC) promoted metastasis via interactions with EpCAM, thereby promoting an epithelial-mesenchymal transition (EMT) phenotype in circulating HCC cells (42).…”

Section: Relevance To Cancermentioning

confidence: 99%

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The Role of the Microbiome in Cancer and Therapy Efficacy: Focus on Lung Cancer

et al. 2020

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The microbiome is extremely important for human health; more recently its role in the context of cancer became clear. Microbial effects range from enhancing cancer immunity and cancer therapy efficacy, to promoting cancer progression and inhibiting treatment efficacy. These broad implications led researchers to investigate these specific interactions, as well as how modification of the microbiome can improve cancer survival and treatment efficacy. While these interactions are better established for cancers such as gastric cancer, they are far less understood in others. As nonsmall cell lung cancer (NSCLC) makes up the majority of lung cancer cases, and is among the top causes of cancer deaths worldwide, understanding the mechanisms by which the microbiome may impact progression and treatment is crucial to improve patient survival and treatment response. A literature review was conducted to reveal the crosslink between human microbiome and lung cancer. This includes immune priming, induction of pro-or anti-tumor response, and the local effects of intra-tumoral microbiota. Overall, this is a complex multifactorial relationship, and there are broad implications as to how this knowledge can improve cancer treatment. Solutions include manipulation of the microbiome using probiotics, bacterial vaccines and antibiotics. Bacteria biomarkers may also be used as a diagnostic tool. The microbiome, defined as the collection of genomes from all the microorganisms found in a particular environment, is an emerging and widely studied factor in human health. Its implications in cancer are manifold (1). Specific microorganisms that are found within a specific environment (i.e., the microbiota) induce anti-tumor immunity through immune priming (1, 2). Dysbiosis, genotoxins, and inflammatory responses to microbiota are associated with cancer development (1). Additionally, cancer treatment efficacy can be enhanced or inhibited by intra-tumoral and gut microbiota (3-5). This knowledge leads to many questions regarding the interactions between the microbiome, cancer and cancer therapies. Most importantly, how can a better understanding of these interactions lead to improvement of current treatment efficacy? Compared to the gastrointestinal (GI) tract, the microbiota of the lung and other organs are far less understood (4, 6). Lung cancer is the first cause of death among oncologic patients and the second most common cancer worldwide (7). Investigating microbial-cancer relationships will aid in a better understanding of the role of microbes in mechanisms underlying tumorigenesis behind this as well as other cancers and hopefully improve treatment efficacy (4). These factors are poorly understood in lung cancer (3, 8, 9). Therefore, this review aims 4807 This article is freely accessible online.

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Section: Relevance To Cancermentioning

confidence: 99%

Section: Relevance To Cancermentioning

confidence: 99%

The Role of the Microbiome in Cancer and Therapy Efficacy: Focus on Lung Cancer

et al. 2020

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“…The hypothetical protein ADQ90530 was categorized as a sirtuin (also known as Sir2), which is responsible for NAD +dependent deacetylation. As the deacetylase of M. fermentans is expressed inside mammalian cells, it inhibits cell proliferation but promotes their antioxidation and antistarvation capacities, and alters gene expression, affecting physiological functions and the corresponding signal transduction pathways in host cells [74]. The long-held view is that M. hyopneumoniae is an extracellular pathogen, thus it remains unclear whether ADQ90530 in M. hyopneumoniae functions similarly with secreted deacetylase in intracellular pathogen M. fermentans.…”

Section: Uncharacterized/hypothetical Virulence-related Proteinsmentioning

confidence: 99%

Quantitative Proteomic Analyses of a Pathogenic Strain and Its Highly Passaged Attenuated Strain ofMycoplasma hyopneumoniae

Fang

Liu

et al. 2019

BioMed Research International

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Mycoplasma hyopneumoniae is the causative agent of porcine enzootic pneumonia, a chronic respiratory disease in swine resulting in enormous economic losses. To identify the components that contribute to virulence and unveil those biological processes potentially related to attenuation, we used isobaric tags for relative and absolute quantification technology (iTRAQ) to compare the protein profiles of the virulent M. hyopneumoniae strain 168 and its attenuated highly passaged strain 168L. We identified 489 proteins in total, 70 of which showing significant differences in level of expression between the two strains. Remarkably, proteins participating in inositol phosphate metabolism were significantly downregulated in the virulent strain, while some proteins involved in nucleoside metabolism were upregulated. We also mined a series of novel promising virulence-associated factors in our study compared with those in previous reports, such as some moonlighting adhesins, transporters, lipoate-protein ligase, and ribonuclease and several hypothetical proteins with conserved functional domains, deserving further research. Our survey constitutes an iTRAQ-based comparative proteomic analysis of a virulent M. hyopneumoniae strain and its attenuated strain originating from a single parent with a well-characterized genetic background and lays the groundwork for future work to mine for potential virulence factors and identify candidate vaccine proteins.

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“…However, the interaction of DnaK and cancer is not just dependent on p53 dysregulation which reveals that focusing on signaling pathways in carcinogenesis is not enough. Mycoplasma infection induces MMP-1 and MMP-9 [145], 5-lipoxygenase (5-LOX, ALOX5, 15-LO-1, 15-LOX-1) and cyclooxygenase 2 (Cox-2) [146], cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) and interleukin 6 (IL-6) [147], plasmin [148], fibroblasts [149], p107 [150], IL-6, interleukin 1 beta (IL-1b), TGF-b and fibrosis [151], epidermal growth factor receptor (EGFR), phosphatidylinositide 3-kinase (PI3K), Akt, tumor suppressor phosphatase and tensin homolog (PTEN) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) [152][153][154], deacetylates forkhead box protein O3a (FOXO3a) [155], and downregulates E-cadherin [156].…”

Section: Fibronectin and Decorinmentioning

confidence: 99%

Undervalued ubiquitous proteins

Brücher

Jamall

2019

4open

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The role of ubiquitous proteins (UPs) and their corresponding enzymes have been underestimated in carcinogenesis as the focus of much research revolved around measuring mutations and/or other genetic epiphenomena as surrogate markers of cancer and cancer progression. Over the past three decades, the scientific community has come to realize that the concentration on microdissection of cancer cells without accounting for the neighborhood in which these cells reside, i.e., the stroma, fails to reflect the true nature of cancer biology. UPs are fundamental for cellular homeostasis and phylogenetic development as well as for the integrity of the cytoskeleton and for the stability of cells and tissues in regards to intercellular signaling, cell shape and mobility, apoptosis, wound healing, and cell polarity. Corresponding enzymes are used by microorganisms to gain entry into the host by degradation of UPs and play a role to cleave peptide bonds for killing disease-causing life forms along for the creation of the precancerous niche (PCN) during carcinogenesis, cancer invasion, and in metastasis. The language used by such proteins as well as their complementary enzymes with its influence on multiple pathways and the cross-linked extracellular matrix is incompletely understood. The role of UPs in the disruption of signaling homeostasis and resulting interference with crosstalk in carcinogenesis appears sufficiently delineated to warrant a much more refined examination of their qualitative and quantitative contribution to the development of cancer and cancer therapy.

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Mycoplasma fermentans deacetylase promotes mammalian cell stress tolerance

Cited by 4 publications

References 55 publications

The Role of the Microbiome in Cancer and Therapy Efficacy: Focus on Lung Cancer

The Role of the Microbiome in Cancer and Therapy Efficacy: Focus on Lung Cancer

Quantitative Proteomic Analyses of a Pathogenic Strain and Its Highly Passaged Attenuated Strain ofMycoplasma hyopneumoniae

Undervalued ubiquitous proteins

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