scholarly journals Ultraviolet Radiation and Chronic Inflammation—Molecules and Mechanisms Involved in Skin Carcinogenesis: A Narrative Review

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 326
Author(s):  
Magdalena Ciążyńska ◽  
Irmina Olejniczak-Staruch ◽  
Dorota Sobolewska-Sztychny ◽  
Joanna Narbutt ◽  
Małgorzata Skibińska ◽  
...  
Keyword(s):  
Ultraviolet Radiation ◽  
Chronic Inflammation ◽  
Potential Role ◽  
Tumor Formation ◽  
Skin Carcinogenesis ◽  
Molecular Networks ◽  
Cancer Therapies ◽  
Inflammatory Microenvironment ◽  
Skin Cancers

The process of skin carcinogenesis is still not fully understood. Both experimental and epidemiological evidence indicate that chronic inflammation is one of the hallmarks of microenvironmental-agent-mediated skin cancers and contributes to its development. Maintaining an inflammatory microenvironment is a condition leading to tumor formation. Multiple studies focus on the molecular pathways activating tumorigenesis by inflammation and indicate several biomarkers and factors that can improve diagnostic and prognostic processes in oncology and dermatology. Reactive oxygen species produced by ultraviolet radiation, oxidizers, or metabolic processes can damage cells and initiate pro-inflammatory cascades. Considering the potential role of inflammation in cancer development and metastasis, the identification of early mechanisms involved in carcinogenesis is crucial for clinical practice and scientific research. Moreover, it could lead to the progress of advanced skin cancer therapies. We focus on a comprehensive analysis of available evidence and on understanding how chronic inflammation and ultraviolet radiation can result in skin carcinogenesis. We present the inflammatory environment as complex molecular networks triggering tumorigenesis and constituting therapeutic targets.

Potential of Mesenchymal Stem Cells in Anti-Cancer Therapies

2020 ◽  
Vol 15 (6) ◽  
pp. 482-491 ◽  
Author(s):  
Milena Kostadinova ◽  
Milena Mourdjeva
Keyword(s):  
Cancer Cells ◽  
Small Population ◽  
Tumor Formation ◽  
Bioactive Molecules ◽  
Cancer Therapies ◽  
New Methods ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Blocking Mechanisms

Mesenchymal stem/stromal cells (MSCs) are localized throughout the adult body as a small population in the stroma of the tissue concerned. In injury, tissue damage, or tumor formation, they are activated and leave their niche to migrate to the site of injury, where they release a plethora of growth factors, cytokines, and other bioactive molecules. With the accumulation of data about the interaction between MSCs and tumor cells, the dualistic role of MSCs remains unclear. However, a large number of studies have demonstrated the natural anti-tumor properties inherent in MSCs, so this is the basis for intensive research for new methods using MSCs as a tool to suppress cancer cell development. This review focuses specifically on advanced approaches in modifying MSCs to become a powerful, precision- targeted tool for killing cancer cells, but not normal healthy cells. Suppression of tumor growth by MSCs can be accomplished by inducing apoptosis or cell cycle arrest, suppressing tumor angiogenesis, or blocking mechanisms mediating metastasis. In addition, the chemosensitivity of cancer cells may be increased so that the dose of the chemotherapeutic agent used could be significantly reduced.

scholarly journals Targeting the Interleukin-6/Jak/Stat Pathway in Human Malignancies

2012 ◽  
Vol 30 (9) ◽  
pp. 1005-1014 ◽  
Author(s):  
Pasquale Sansone ◽  
Jacqueline Bromberg
Keyword(s):  
Interleukin 6 ◽  
Potential Role ◽  
Tumor Formation ◽  
Janus Kinase ◽  
Cytokine Signaling ◽  
Metastatic Progression ◽  
And Function ◽  
Principal Pathway ◽  
Stat Pathway

The Janus kinase/signal transducer and activator of transcription (Jak/Stat) pathway was discovered 20 years ago as a mediator of cytokine signaling. Since this time, more than 2,500 articles have been published demonstrating the importance of this pathway in virtually all malignancies. Although there are dozens of cytokines and cytokine receptors, four Jaks, and seven Stats, it seems that interleukin-6–mediated activation of Stat3 is a principal pathway implicated in promoting tumorigenesis. This transcription factor regulates the expression of numerous critical mediators of tumor formation and metastatic progression. This review will examine the relative importance and function of this pathway in nonmalignant conditions as well as malignancies (including tumor intrinsic and extrinsic), the influence of other Stats, the development of inhibitors to this pathway, and the potential role of inhibitors in controlling or eradicating cancers.

scholarly journals The system of nitrogen oxide generation of small intestine in experimental gastroenterocolitis

2014 ◽  
Vol 18 (2 (70)) ◽  
Author(s):  
A. S. Tkachenko ◽  
V. H. Hopkalov ◽  
M. A. Orlova
Keyword(s):  
Small Intestine ◽  
Nitrogen Oxide ◽  
Chronic Inflammation ◽  
Potential Role ◽  
Food Additive ◽  
Enos Activity ◽  
Microcirculatory Disorders

The activity of endothelial and inducible NO-synthases and the content of S-nitrosothiols were studied in the small intestine homogenates of rats with chronic experimental gastroenterocolitis caused by food additive carrageenan intake during 2 and 4 weeks. It was established that carrageenan intake during 2 weeks led to a decrease of eNOS activity and increased the activity of iNOS in small intestine homogenate, causing increased production of NO and, therefore of Snitrosothiols. A decreased NO synthesis in four-week use of carrageenan indicated a potential role of NO deficiency in the development of microcirculatory disorders and chronic inflammation.

scholarly journals Effect of lncRNA PVT1/miR186/KLF5 Axis on the Occurrence and Progression of Cholangiocarcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Qiang Sun ◽  
Xueyi Gong ◽  
Jianlong Wu ◽  
Zhipeng Hu ◽  
Qiao Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Cell Invasion ◽  
Noncoding Rna ◽  
Potential Role ◽  
Bioinformatic Analysis ◽  
Tumor Formation ◽  
Invasion Assay ◽  
Transwell Invasion Assay

This study primarily focused on the effect of the long noncoding RNA (lncRNA) PVT1/miR186/KLF5 axis on the occurrence and progression of cholangiocarcinoma (CCA). miR186 was found both in the lncRNA PVT1 targeting miRNAs and KLF5 targeting miRNAs using bioinformatic analysis. The expression of lncRNA PVT1 and KLF5 in the TFK-1, QBC939, and HuCCT1 cell lines and normal biliary epithelial HIBEpiC cells was detected by RT-qPCR. The significance of lncRNA PVT1 and KLF5 on cell proliferation was analyzed using the MTT assay and clone formation assay in lncRNA PVT1 and KLF5 silencing HuCCT1 cell lines and lncRNA PVT1and KLF5 overexpressing TFK-1 and QBC939 cell lines, respectively. The potential role of lncRNA PVT1 and KLF5 in cell migration was detected using the transwell invasion assay in CCA cell lines and tumor formation assay. Additionally, lncRNA PVT1 and KLF5 were proved to be highly expressed in CCA tissues and cell lines. Silencing and overexpressing of lncRNA PVT1 or KLF5 markedly inhibited or increased the cell proliferation and cell invasion in CCA cell lines, respectively. Silencing and overexpressing of lncRNA PVT1 significantly inhibited and increased the expression of KLF5 in CCA cell lines, respectively. Silencing of lncRNA PVT1 increased the expression of miR186, and silencing of miR186 increased the expression of KLF5 in CCA cell lines. Cotransfection of lncRNA PVT1 and miR186 increased the expression of KLF5 compared with controls. Overall, these results demonstrated that the lncRNA PVT1/miR186/KLF5 axis might exert a key role in the occurrence and progression of CCA, and this axis might provide a new target for treating CCA.

Association between Cataract and Keratinocytic Skin Cancers or Melanoma: Speculating on the Common Role of Sun and Ultraviolet Radiation Exposures

2017 ◽  
Vol 24 (5) ◽  
pp. 336-340 ◽  
Author(s):  
David Varssano ◽  
Mira Friedman ◽  
Michaella Goldstein ◽  
Shai Bar-Sela ◽  
Tal Sella ◽  
...  
Keyword(s):  
Ultraviolet Radiation ◽  
Skin Cancers ◽  
The Common

scholarly journals Interaction of Muc2 and Apc on Wnt Signaling and in Intestinal Tumorigenesis: Potential Role of Chronic Inflammation

2008 ◽  
Vol 68 (18) ◽  
pp. 7313-7322 ◽  
Author(s):  
Kan Yang ◽  
Natalia V. Popova ◽  
Wan Cai Yang ◽  
Ioanna Lozonschi ◽  
Selam Tadesse ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Chronic Inflammation ◽  
Potential Role ◽  
Intestinal Tumorigenesis

scholarly journals Suppression of in vivo tumor formation induced by simian virus 40-transformed cells in mice receiving antiidiotypic antibodies.

1985 ◽  
Vol 161 (6) ◽  
pp. 1432-1449 ◽  
Author(s):  
R C Kennedy ◽  
G R Dreesman ◽  
J S Butel ◽  
R E Lanford
Keyword(s):  
Potential Role ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Cellular Protein ◽  
Tumor Formation ◽  
Transformed Cells ◽  
Antiidiotypic Antibodies ◽  
Carboxyl Terminal

This study characterizes four private idiotypes (Id) associated with monoclonal antibodies (mAb) to simian virus 40 (SV40) tumor antigen (T-Ag), and to a cellular protein, p53. Anti-Id recognized Id determinants associated with the antibody-combining site. BALB/c mice receiving a pool of anti-Id directed against mAb recognizing distinct amino and carboxyl terminal epitopes of T-Ag before receiving a tumorigenic dose of SV40-transformed cells showed suppression of tumor formation. Serum obtained from these mice before tumor challenge contained anti-anti-Id that failed to bind T-Ag. These data support the potential role of regulatory idiotopes in tumor immunity.

scholarly journals The role of the bacterial microbiome in the treatment of cancer

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zi-Kun Yu ◽  
Rui-Ling Xie ◽  
Rui You ◽  
You-Ping Liu ◽  
Xu-Yin Chen ◽  
...  
Keyword(s):  
Potential Role ◽  
Human Microbiome ◽  
Cancer Therapeutics ◽  
Future Research ◽  
Host Immune System ◽  
Cancer Therapies ◽  
Cancer Treatments ◽  
Bacterial Microbiota ◽  
Bacterial Microbiome

AbstractThe human microbiome is defined as the microorganisms that reside in or on the human body, such as bacteria, viruses, fungi, and protozoa, and their genomes. The human microbiome participates in the modulation of human metabolism by influencing several intricate pathways. The association between specific bacteria or viruses and the efficacy of cancer treatments and the occurrence of treatment-related toxicity in cancer patients has been reported. However, the understanding of the interaction between the host microbiome and the cancer treatment response is limited, and the microbiome potentially plays a greater role in the treatment of cancer than reported to date. Here, we provide a thorough review of the potential role of the gut and locally resident bacterial microbiota in modulating responses to different cancer therapeutics to demonstrate the association between the gut or locally resident bacterial microbiota and cancer therapy. Probable mechanisms, such as metabolism, the immune response and the translocation of microbiome constituents, are discussed to promote future research into the association between the microbiome and other types of cancer. We conclude that the interaction between the host immune system and the microbiome may be the basis of the role of the microbiome in cancer therapies. Future research on the association between host immunity and the microbiome may improve the efficacy of several cancer treatments and provide insights into the cause of treatment-related side effects.

Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice

2007 ◽  
Vol 293 (4) ◽  
pp. E1118-E1128 ◽  
Author(s):  
Jianping Ye ◽  
Zhanguo Gao ◽  
Jun Yin ◽  
Qing He
Keyword(s):  
Adipose Tissue ◽  
Chronic Inflammation ◽  
Potential Role ◽  
Gene Promoter ◽  
Obese Mice ◽  
Probe Signal ◽  
Hypoxia Response ◽  
Tnf Α ◽  
Partial Oxygen

Chronic inflammation and reduced adiponectin are widely observed in the white adipose tissue in obesity. However, the cause of the changes remains to be identified. In this study, we provide experimental evidence that hypoxia occurs in adipose tissue in obese mice and that adipose hypoxia may contribute to the endocrine alterations. The adipose hypoxia was demonstrated by a reduction in the interstitial partial oxygen pressure (Po2), an increase in the hypoxia probe signal, and an elevation in expression of the hypoxia response genes in ob/ ob mice. The adipose hypoxia was confirmed in dietary obese mice by expression of hypoxia response genes. In the adipose tissue, hypoxia was associated with an increased expression of inflammatory genes and decreased expression of adiponectin. In dietary obese mice, reduction in body weight by calorie restriction was associated with an improvement of oxygenation and a reduction in inflammation. In cell culture, inflammatory cytokines were induced by hypoxia in primary adipocytes and primary macrophages of lean mice. The transcription factor NF-κB and the TNF-α gene promoter were activated by hypoxia in 3T3-L1 adipocytes and NIH3T3 fibroblasts. In addition, adiponectin expression was reduced by hypoxia, and the reduction was observed in the gene promoter in adipocytes. These data suggest a potential role of hypoxia in the induction of chronic inflammation and inhibition of adiponectin in the adipose tissue in obesity.

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