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Biomedicines, Volume 6, Issue 2 (June 2018)

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Cover Story (view full-size image) Normal mammary stem cells (red cells in the upper-right mammary gland) interplay with immune system [...] Read more.
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Open AccessArticle Human Depotentiation following Induction of Spike Timing Dependent Plasticity
Biomedicines 2018, 6(2), 71; https://doi.org/10.3390/biomedicines6020071
Received: 15 March 2018 / Revised: 17 May 2018 / Accepted: 4 June 2018 / Published: 18 June 2018
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Abstract
Depotentiation (DP) is a crucial mechanism for the tuning of memory traces once LTP (Long Term Potentiation) has been induced via learning, artificial procedures, or other activities. Putative unuseful LTP might be abolished via this process. Its deficiency is thought to play a
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Depotentiation (DP) is a crucial mechanism for the tuning of memory traces once LTP (Long Term Potentiation) has been induced via learning, artificial procedures, or other activities. Putative unuseful LTP might be abolished via this process. Its deficiency is thought to play a role in pathologies, such as drug induced dyskinesia. However, since it is thought that it represents a mechanism that is linked to the susceptibility to interference during consolidation of a memory trace, it is an important process to consider when therapeutic interventions, such as psychotherapy, are administered. Perhaps a person with an abnormal depotentiation is prone to lose learned effects very easily or on the other end of the spectrum is prone to overload with previously generated unuseful LTP. Perhaps this process partly explains why some disorders and patients are extremely resistant to therapy. The present study seeks to quantify the relationship between LTP and depotentiation in the human brain by using transcranial magnetic stimulation (TMS) over the cortex of healthy participants. The results provide further evidence that depotentiation can be quantified in humans by use of noninvasive brain stimulation techniques. They provide evidence that a nonfocal rhythmic on its own inefficient stimulation, such as a modified thetaburst stimulation, can depotentiate an associative, focal spike timing-dependent PAS (paired associative stimulation)-induced LTP. Therefore, the depotentiation-like process does not seem to be restricted to specific subgroups of synapses that have undergone LTP before. Most importantly, the induced LTP seems highly correlated with the amount of generated depotentiation in healthy individuals. This might be a phenomenon typical of health and might be distorted in brain pathologies, such as dystonia, or dyskinesias. The ratio of LTP/DP might be a valuable marker for potential distortions of persistence versus deletion of memory traces represented by LTP-like plasticity. Full article
(This article belongs to the Special Issue Neural Mechanisms of Learning)
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Open AccessArticle Antimicrobial and Antibiofilm Activities of Citrus Water-Extracts Obtained by Microwave-Assisted and Conventional Methods
Biomedicines 2018, 6(2), 70; https://doi.org/10.3390/biomedicines6020070
Received: 31 May 2018 / Revised: 14 June 2018 / Accepted: 15 June 2018 / Published: 17 June 2018
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Abstract
Citrus pomace is a huge agro-food industrial waste mostly composed of peels and traditionally used as compost or animal feed. Owing to its high content of compounds beneficial to humans (e.g., flavonoids, phenol-like acids, and terpenoids), citrus waste is increasingly used to produce
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Citrus pomace is a huge agro-food industrial waste mostly composed of peels and traditionally used as compost or animal feed. Owing to its high content of compounds beneficial to humans (e.g., flavonoids, phenol-like acids, and terpenoids), citrus waste is increasingly used to produce valuable supplements, fragrance, or antimicrobials. However, such processes require sustainable and efficient extraction strategies by solvent-free techniques for environmentally-friendly good practices. In this work, we evaluated the antimicrobial and antibiofilm activity of water extracts of three citrus peels (orange, lemon, and citron) against ten different sanitary relevant bacteria. Both conventional extraction methods using hot water (HWE) and microwave-assisted extraction (MAE) were used. Even though no extract fully inhibited the growth of the target bacteria, these latter (mostly pseudomonads) showed a significant reduction in biofilm biomass. The most active extracts were obtained from orange and lemon peel by using MAE at 100 °C for 8 min. These results showed that citrus peel water infusions by MAE may reduce biofilm formation possibly enhancing the susceptibility of sanitary-related bacteria to disinfection procedures. Full article
(This article belongs to the Special Issue Plant Derived Biomedicines)
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Open AccessArticle Assessing Clinical Outcomes in Colorectal Cancer with Assays for Invasive Circulating Tumor Cells
Biomedicines 2018, 6(2), 69; https://doi.org/10.3390/biomedicines6020069
Received: 10 April 2018 / Revised: 17 May 2018 / Accepted: 1 June 2018 / Published: 6 June 2018
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Abstract
Colorectal carcinoma (CRC) is the second leading cause of cancer-related mortality. The goals of this study are to evaluate the association between levels of invasive circulating tumor cells (iCTCs) with CRC outcomes and to explore the molecular characteristics of iCTCs. Peripheral blood from
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Colorectal carcinoma (CRC) is the second leading cause of cancer-related mortality. The goals of this study are to evaluate the association between levels of invasive circulating tumor cells (iCTCs) with CRC outcomes and to explore the molecular characteristics of iCTCs. Peripheral blood from 93 patients with Stage I–IV CRC was obtained and assessed for the detection and characterization of iCTCs using a functional collagen-based adhesion matrix (CAM) invasion assay. Patients were followed and assessed for overall survival. Tumor cells isolated by CAM were characterized using cell culture and microarray analyses. Of 93 patients, 88 (95%) had detectable iCTCs, ranging over 0–470 iCTCs/mL. Patients with Stage I–IV disease exhibited median counts of 0.0 iCTCs/mL (n = 6), 13.0 iCTCs/mL (n = 12), 41.0 iCTCs/mL (n = 12), and 133.0 iCTCs/mL (n = 58), respectively (p < 0.001). Kaplan–Meier curve analysis demonstrated a significant survival benefit in patients with low iCTC counts compared with in patients with high iCTC counts (log-rank p < 0.001). Multivariable Cox model analysis revealed that iCTC count was an independent prognostic factor of overall survival (p = 0.009). Disease stage (p = 0.01, hazard ratio 1.66; 95% confidence interval: 1.12–2.47) and surgical intervention (p = 0.03, HR 0.37; 95% CI: 0.15–0.92) were also independent prognostic factors. Gene expression analysis demonstrated the expression of both endothelial and tumor progenitor cell biomarkers in iCTCs. CAM-based invasion assay shows a high detection sensitivity of iCTCs that inversely correlated with overall survival in CRC patients. Functional and gene expression analyses showed the phenotypic mosaics of iCTCs, mimicking the survival capability of circulating endothelial cells in the blood stream. Full article
(This article belongs to the Special Issue Cancer Biomarkers and Targets in Digestive Organs)
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Open AccessReview HIF Oxygen Sensing Pathways in Lung Biology
Biomedicines 2018, 6(2), 68; https://doi.org/10.3390/biomedicines6020068
Received: 8 May 2018 / Revised: 28 May 2018 / Accepted: 30 May 2018 / Published: 6 June 2018
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Abstract
Cellular responses to oxygen fluctuations are largely mediated by hypoxia-inducible factors (HIFs). Upon inhalation, the first organ inspired oxygen comes into contact with is the lungs, but the understanding of the pulmonary HIF oxygen-sensing pathway is still limited. In this review we will
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Cellular responses to oxygen fluctuations are largely mediated by hypoxia-inducible factors (HIFs). Upon inhalation, the first organ inspired oxygen comes into contact with is the lungs, but the understanding of the pulmonary HIF oxygen-sensing pathway is still limited. In this review we will focus on the role of HIF1α and HIF2α isoforms in lung responses to oxygen insufficiency. In particular, we will discuss novel findings regarding their role in the biology of smooth muscle cells and endothelial cells in the context of hypoxia-induced pulmonary vasoconstriction. Moreover, we will also discuss recent studies into HIF-dependent responses in the airway epithelium, which have been even less studied than the HIF-dependent vascular responses in the lungs. In summary, we will review the biological functions executed by HIF1 or HIF2 in the pulmonary vessels and epithelium to control lung responses to oxygen fluctuations as well as their pathological consequences in the hypoxic lung. Full article
(This article belongs to the Special Issue Hypoxia)
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Open AccessReview Learning and Unlearning of Pain
Biomedicines 2018, 6(2), 67; https://doi.org/10.3390/biomedicines6020067
Received: 17 April 2018 / Revised: 23 May 2018 / Accepted: 1 June 2018 / Published: 5 June 2018
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Abstract
This review provides an overview of learning mechanisms and memory aspects for the development of chronic pain. Pain can be influenced in important ways by an individual’s personality, by family, and by the sociocultural environment in which they live. Therefore, learning mechanisms can
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This review provides an overview of learning mechanisms and memory aspects for the development of chronic pain. Pain can be influenced in important ways by an individual’s personality, by family, and by the sociocultural environment in which they live. Therefore, learning mechanisms can explain why pain experience and pain behavior can increase or decrease. Linking pain with positive consequences or removing negative consequences can contribute significantly to the chronification of pain. We will provide an overview of treatment options that use the characteristics of extinction. Operant extinction training and cognitive behavioral approaches show promising results for the treatment of chronic pain. Full article
(This article belongs to the Special Issue Neural Mechanisms of Learning)
Open AccessReview Noncanonical NF-κB in Cancer
Biomedicines 2018, 6(2), 66; https://doi.org/10.3390/biomedicines6020066
Received: 10 May 2018 / Revised: 31 May 2018 / Accepted: 4 June 2018 / Published: 5 June 2018
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Abstract
The NF-κB pathway is a critical regulator of immune responses and is often dysregulated in cancer. Two NF-κB pathways have been described to mediate these responses, the canonical and the noncanonical. While understudied compared to the canonical NF-κB pathway, noncanonical NF-κB and its
[...] Read more.
The NF-κB pathway is a critical regulator of immune responses and is often dysregulated in cancer. Two NF-κB pathways have been described to mediate these responses, the canonical and the noncanonical. While understudied compared to the canonical NF-κB pathway, noncanonical NF-κB and its components have been shown to have effects, usually protumorigenic, in many different cancer types. Here, we review noncanonical NF-κB pathways and discuss its important roles in promoting cancer. We also discuss alternative NF-κB-independent functions of some the components of noncanonical NF-κB signaling. Finally, we discuss important crosstalk between canonical and noncanonical signaling, which blurs the two pathways, indicating that understanding the full picture of NF-κB regulation is critical to deciphering how this broad pathway promotes oncogenesis. Full article
(This article belongs to the Special Issue Roles of NF-kB in Cancer and Their Therapeutic Approaches)
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Open AccessReview Utilizing Peptide Ligand GPCRs to Image and Treat Pancreatic Cancer
Biomedicines 2018, 6(2), 65; https://doi.org/10.3390/biomedicines6020065
Received: 15 May 2018 / Accepted: 28 May 2018 / Published: 2 June 2018
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Abstract
It is estimated that early detection of pancreatic ductal adenocarcinoma (PDAC) could increase long-term patient survival by as much as 30% to 40% (Seufferlein, T. et al., Nat. Rev. Gastroenterol. Hepatol. 2016, 13, 74–75). There is an unmet need for reagents
[...] Read more.
It is estimated that early detection of pancreatic ductal adenocarcinoma (PDAC) could increase long-term patient survival by as much as 30% to 40% (Seufferlein, T. et al., Nat. Rev. Gastroenterol. Hepatol. 2016, 13, 74–75). There is an unmet need for reagents that can reliably identify early cancerous or precancerous lesions through various imaging modalities or could be employed to deliver anticancer treatments specifically to tumor cells. However, to date, many PDAC tumor-targeting strategies lack selectivity and are unable to discriminate between tumor and nontumor cells, causing off-target effects or unclear diagnoses. Although a variety of approaches have been taken to identify tumor-targeting reagents that can effectively direct therapeutics or imaging agents to cancer cells (Liu, D. et al., J. Controlled Release 2015, 219, 632–643), translating these reagents into clinical practice has been limited, and it remains an area open to new methodologies and reagents (O’Connor, J.P. et al., Nat. Rev. Clin. Oncol. 2017, 14, 169–186). G protein–coupled receptors (GPCRs), which are key target proteins for drug discovery and comprise a large proportion of currently marketed therapeutics, hold significant promise for tumor imaging and targeted treatment, particularly for pancreatic cancer. Full article
(This article belongs to the Special Issue Cancer Biomarkers and Targets in Digestive Organs)
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Open AccessConference Report Frontiers in Gastrointestinal Oncology: Advances in Multi-Disciplinary Patient Care
Biomedicines 2018, 6(2), 64; https://doi.org/10.3390/biomedicines6020064
Received: 25 April 2018 / Revised: 9 May 2018 / Accepted: 11 May 2018 / Published: 1 June 2018
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Abstract
Cancers of the digestive system remain highly lethal; therefore, the care of patients with malignant diseases of the digestive tract requires the expertise of providers from multiple health disciplines. Progress has been made to advance the understanding of epidemiology and genetics, diagnostic and
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Cancers of the digestive system remain highly lethal; therefore, the care of patients with malignant diseases of the digestive tract requires the expertise of providers from multiple health disciplines. Progress has been made to advance the understanding of epidemiology and genetics, diagnostic and screening evaluation, treatment modalities, and supportive care for patients with gastrointestinal cancers. At the Multi-Disciplinary Patient Care in Gastrointestinal Oncology conference at the Hershey Country Club in Hershey, Pennsylvania on 29 September 2017, the faculty members of the Penn State Health Milton S. Hershey Medical Center presented a variety of topics that focused on this oncological specialty. In this continuing medical education-certified conference, updates on the population sciences including health disparities and resistance training were presented. Progress made in various diagnostic evaluation and screening procedures was outlined. New developments in therapeutic modalities in surgical, radiation, and medical oncology were discussed. Cancer genetic testing and counseling and the supportive roles of music and arts in health and cancer were demonstrated. In summary, this disease-focused medical conference highlighted the new frontiers in gastrointestinal oncology, and showcase the multi-disciplinary care provided at the Penn State Cancer Institute. Full article
(This article belongs to the Special Issue Cancer Biomarkers and Targets in Digestive Organs)
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Open AccessArticle Assisted Tip Sonication Approach for Graphene Synthesis in Aqueous Dispersion
Biomedicines 2018, 6(2), 63; https://doi.org/10.3390/biomedicines6020063
Received: 15 April 2018 / Revised: 19 May 2018 / Accepted: 20 May 2018 / Published: 28 May 2018
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Abstract
Graphene (G) is a newcomer material that holds promising properties for many applications. The production of high quality G with a good yield is a long-standing goal for many researchers. This work emphasizes synthesis of dispersed graphene nanoplatelets (DGP) through aqueous dispersion technique
[...] Read more.
Graphene (G) is a newcomer material that holds promising properties for many applications. The production of high quality G with a good yield is a long-standing goal for many researchers. This work emphasizes synthesis of dispersed graphene nanoplatelets (DGP) through aqueous dispersion technique in surfactant/water solution with the aid of tip sonication. A chemical method was also used to prepare graphene oxide (GO) and reduced graphene oxide (RGO) for comparison. Elemental analysis revealed the C:O ratio to be 12:1 for DGP but much lower for other graphene structures. Optical characterization of DGP, GO and RGO with UV and Raman spectroscopy confirmed the ideal structure of DGP. Moreover, X-ray diffraction (XRD) revealed the amorphous structure of DGP. Transmission electron microscope (TEM) imaging showed that DGP was composed of a few flat layers, unlike the wrinkled and partially bent multilayered G. Topological study of the DGP surface with scanning electron microscope (SEM) depicted its rough surface with (ra) value of 35 nm, as revealed using an atomic force microscope (AFM). Electrochemical measurements confirmed the higher conductivity of DGP over graphene prepared by chemical method due to lack of structural defects. Its perfect structure facilitates the mobility of charge carriers that makes it preferable in optoelectronic applications. Full article
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Open AccessArticle Deubiquitinylase USP47 Promotes RelA Phosphorylation and Survival in Gastric Cancer Cells
Biomedicines 2018, 6(2), 62; https://doi.org/10.3390/biomedicines6020062
Received: 13 February 2018 / Revised: 11 May 2018 / Accepted: 12 May 2018 / Published: 22 May 2018
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Abstract
Every year, gastric cancer causes around 819,000 deaths worldwide. The incidence of gastric cancer in the western world is slowly declining, but the prognosis is unpromising. In Germany, the 5-year-survival rate is around 32%, and the average life span after diagnosis is 6
[...] Read more.
Every year, gastric cancer causes around 819,000 deaths worldwide. The incidence of gastric cancer in the western world is slowly declining, but the prognosis is unpromising. In Germany, the 5-year-survival rate is around 32%, and the average life span after diagnosis is 6 to 9 months. Therapy of gastric cancer patients comprises a gastrectomy and perioperative or adjuvant chemotherapy. However, resistance of gastric cancer cells to these agents is widespread; thus, improved chemotherapeutic approaches are required. Nuclear factor kappa B (NF-κB) transcription factors are associated with anti-apoptosis, carcinogenesis, and chemoresistance, and thus, constitute attractive targets for therapeutic intervention. In immunoblots, we show that ubiquitin specific protease 47 (USP47) promotes β-transducin repeat-containing protein (βTrCP) stability and phosphorylation of RelA. Furthermore, after knockdown of USP47 by RNA interference, we analyzed in gastric cancer cell lines metabolic activity/viability in an MTT assay, and apoptotic cell death by Annexin V staining and poly(ADP-Ribose) polymerase (PARP)-1, caspase 3, and caspase 8 cleavage, respectively. We found that USP47 contributes to cell viability and chemoresistance in NCI-N87 gastric carcinoma cells treated with etoposide and camptothecin. Inhibition of USP47 might be a suitable strategy to downregulate NF-κB activity, and to overcome chemoresistance in gastric cancer. Full article
(This article belongs to the Special Issue Roles of NF-kB in Cancer and Their Therapeutic Approaches)
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Open AccessArticle Osteocytes Specific GSK3 Inhibition Affects In Vitro Osteogenic Differentiation
Biomedicines 2018, 6(2), 61; https://doi.org/10.3390/biomedicines6020061
Received: 27 March 2018 / Revised: 24 April 2018 / Accepted: 13 May 2018 / Published: 21 May 2018
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Abstract
Osteocytes, the most important regulators of bone processes, are producers of molecules (usually proteins) that act as signals in order to communicate with nearby cells. These factors control cell division (proliferation), differentiation, and survival. Substantial evidence showed different signaling pathways activated by osteocytes
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Osteocytes, the most important regulators of bone processes, are producers of molecules (usually proteins) that act as signals in order to communicate with nearby cells. These factors control cell division (proliferation), differentiation, and survival. Substantial evidence showed different signaling pathways activated by osteocytes and involved in osteoblast differentiation, in particular in the last decade, when the Wingless-related integration site (WNT) pathway assumed a critical large importance. WNT activation by inhibiting glycogen synthase kinase 3 (GSK-3) causes bone anabolism, making GSK3 a potential therapeutic target for bone diseases. In our study, we hypothesized an important role of the osteocyte MLO-Y4 conditioned medium in controlling the differentiation process of osteoblast cell line 2T3. We found an effect of diminished differentiation capability of 2T3 upon conditioning with medium from murine long bone osteocyte-Y4 cells (MLO-Y4) pre-treated with GSK3 inhibitor CHIR2201. The novel observations of this study provide knowledge about the inhibition of GSK3 in MLO-Y4 cells. This strategy could be used as a plausible target in osteocytes in order to regulate bone resorption mediated by a loss of osteoblasts activity through a paracrine loop. Full article
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Open AccessReview Metabolic Regulation of Hypoxia-Inducible Transcription Factors: The Role of Small Molecule Metabolites and Iron
Biomedicines 2018, 6(2), 60; https://doi.org/10.3390/biomedicines6020060
Received: 24 April 2018 / Revised: 11 May 2018 / Accepted: 15 May 2018 / Published: 17 May 2018
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Abstract
Hypoxia-inducible transcription factors (HIFs) facilitate cellular adaptations to low-oxygen environments. However, it is increasingly recognised that HIFs may be activated in response to metabolic stimuli, even when oxygen is present. Understanding the mechanisms for the crosstalk that exists between HIF signalling and metabolic
[...] Read more.
Hypoxia-inducible transcription factors (HIFs) facilitate cellular adaptations to low-oxygen environments. However, it is increasingly recognised that HIFs may be activated in response to metabolic stimuli, even when oxygen is present. Understanding the mechanisms for the crosstalk that exists between HIF signalling and metabolic pathways is therefore important. This review focuses on the metabolic regulation of HIFs by small molecule metabolites and iron, highlighting the latest studies that explore how tricarboxylic acid (TCA) cycle intermediates, 2-hydroxyglutarate (2-HG) and intracellular iron levels influence the HIF response through modulating the activity of prolyl hydroxylases (PHDs). We also discuss the relevance of these metabolic pathways in physiological and disease contexts. Lastly, as PHDs are members of a large family of 2-oxoglutarate (2-OG) dependent dioxygenases that can all respond to metabolic stimuli, we explore the broader role of TCA cycle metabolites and 2-HG in the regulation of 2-OG dependent dioxygenases, focusing on the enzymes involved in chromatin remodelling. Full article
(This article belongs to the Special Issue Hypoxia)
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Open AccessReview The NF-κB Activating Pathways in Multiple Myeloma
Biomedicines 2018, 6(2), 59; https://doi.org/10.3390/biomedicines6020059
Received: 12 March 2018 / Revised: 14 May 2018 / Accepted: 14 May 2018 / Published: 16 May 2018
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Abstract
Multiple myeloma(MM), an incurable plasma cell cancer, represents the second most prevalent hematological malignancy. Deregulated activity of the nuclear factor kappaB (NF-κB) family of transcription factors has been implicated in the pathogenesis of multiple myeloma. Tumor microenvironment-derived cytokines and cancer-associated genetic mutations signal
[...] Read more.
Multiple myeloma(MM), an incurable plasma cell cancer, represents the second most prevalent hematological malignancy. Deregulated activity of the nuclear factor kappaB (NF-κB) family of transcription factors has been implicated in the pathogenesis of multiple myeloma. Tumor microenvironment-derived cytokines and cancer-associated genetic mutations signal through the canonical as well as the non-canonical arms to activate the NF-κB system in myeloma cells. In fact, frequent engagement of both the NF-κB pathways constitutes a distinguishing characteristic of myeloma. In turn, NF-κB signaling promotes proliferation, survival and drug-resistance of myeloma cells. In this review article, we catalog NF-κB activating genetic mutations and microenvironmental cues associated with multiple myeloma. We then describe how the individual canonical and non-canonical pathways transduce signals and contribute towards NF-κB -driven gene-expressions in healthy and malignant cells. Furthermore, we discuss signaling crosstalk between concomitantly triggered NF-κB pathways, and its plausible implication for anomalous NF-κB activation and NF-κB driven pro-survival gene-expressions in multiple myeloma. Finally, we propose that mechanistic understanding of NF-κB deregulations may provide for improved therapeutic and prognostic tools in multiple myeloma. Full article
(This article belongs to the Special Issue Roles of NF-kB in Cancer and Their Therapeutic Approaches)
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Open AccessReview The Crosstalk of Endoplasmic Reticulum (ER) Stress Pathways with NF-κB: Complex Mechanisms Relevant for Cancer, Inflammation and Infection
Biomedicines 2018, 6(2), 58; https://doi.org/10.3390/biomedicines6020058
Received: 21 April 2018 / Revised: 8 May 2018 / Accepted: 11 May 2018 / Published: 16 May 2018
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Abstract
Stressful conditions occuring during cancer, inflammation or infection activate adaptive responses that are controlled by the unfolded protein response (UPR) and the nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-κB) signaling pathway. These systems can be triggered by chemical compounds
[...] Read more.
Stressful conditions occuring during cancer, inflammation or infection activate adaptive responses that are controlled by the unfolded protein response (UPR) and the nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-κB) signaling pathway. These systems can be triggered by chemical compounds but also by cytokines, toll-like receptor ligands, nucleic acids, lipids, bacteria and viruses. Despite representing unique signaling cascades, new data indicate that the UPR and NF-κB pathways converge within the nucleus through ten major transcription factors (TFs), namely activating transcription factor (ATF)4, ATF3, CCAAT/enhancer-binding protein (CEBP) homologous protein (CHOP), X-box-binding protein (XBP)1, ATF6α and the five NF-κB subunits. The combinatorial occupancy of numerous genomic regions (enhancers and promoters) coordinates the transcriptional activation or repression of hundreds of genes that collectively determine the balance between metabolic and inflammatory phenotypes and the extent of apoptosis and autophagy or repair of cell damage and survival. Here, we also discuss results from genetic experiments and chemical activators of endoplasmic reticulum (ER) stress that suggest a link to the cytosolic inhibitor of NF-κB (IκB)α degradation pathway. These data show that the UPR affects this major control point of NF-κB activation through several mechanisms. Taken together, available evidence indicates that the UPR and NF-κB interact at multiple levels. This crosstalk provides ample opportunities to fine-tune cellular stress responses and could also be exploited therapeutically in the future. Full article
(This article belongs to the Special Issue Roles of NF-kB in Cancer and Their Therapeutic Approaches)
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Open AccessCorrection Correction: Riedlinger, T. et al. The Direct and Indirect Roles of NF-κB in Cancer: Lessons from Oncogenic Fusion Proteins and Knock-In Mice. Biomedicines, 2018, 6, 36
Biomedicines 2018, 6(2), 57; https://doi.org/10.3390/biomedicines6020057
Received: 11 May 2018 / Revised: 14 May 2018 / Accepted: 14 May 2018 / Published: 16 May 2018
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Abstract
We would like to report an error in a previously published paper[...] Full article
(This article belongs to the Special Issue Roles of NF-kB in Cancer and Their Therapeutic Approaches)
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