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Naturally Occurring Histone Deacetylase (HDAC) Inhibitors in the Treatment of Cancers
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Sujatha Puttalingaiah, Murthy V. Greeshma, Mahadevaswamy G. Kuruburu, Venugopal R. Bovilla, SubbaRao V. Madhunapantula
Recent studies have shown that HDACis have the potential of modulating immune functions as they were involved in controlling the NF-κB and STAT3 pathways (Dickinson et al., 2010; Schotterl et al., 2015). NF-κB plays a critical role in the innate and adaptive immune responses, cell proliferation, inhibition of apoptosis, promotion of cell migration, invasion and stimulation of angiogenesis and metastasis, which lead to the acceleration of cancer progression (Grivennikov et al., 2010).
Nuclear Factor Kappa-B: Bridging Inflammation and Cancer
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Mohammad Aslam Khan, Girijesh Kumar Patel, Haseeb Zubair, Nikhil Tyagi, Shafquat Azim, Seema Singh, Aamir Ahmad, Ajay Pratap Singh
NF-κB transcriptionally regulates expression of genes which are involved in cell survival, apoptosis, differentiation and immune responses [42, 43]. As discussed above, NF-κB family consists of five members. Both the precursors (NF-κB1/p105 and NF-κB2/ p100) contain IκB-homologous regions at the C-terminal that function as NF-κB inhibitors. Proteolytic processing removes inhibitory domains, allowing the processed proteins (NF-κB1/ p50 and NF-κB2/p52) to enter into the nucleus. Inside the nucleus, p50 and p52 form homodimers or heterodimers with Rel family proteins [42]. All these NF-κB associated proteins have Rel homology domain (RHD) at the N-terminal region. Some of the NF-κB proteins (p65, c-Rel and RelB) contain transcriptional activation domain (TAD) at C-terminal, and these TAD containing proteins positively regulate transcriptional activity. On the other hand, two TAD lacking proteins, p52 and p100, negatively regulate gene expression when bound as homodimer, but can activate gene expression when recruited with other TAD containing proteins like p65. RelB and cRel [44]. Activation of NF-κB pathway is either by classical/canonical or the alternate/non-canonical signaling pathways.
Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
NF-κB is a major transcription factor which tightly controls DNA transcription, cell survival, and immune responses to infection, and controls many genes involved in inflammatory processes. Up-regulated expression of NF-κB is common in chronic inflammation which can promote the initiation of cancer. Some chemopreventive agents are thought to work by down-regulating NF-κB expression thus leading to cellular protection from DNA damage caused by inflammation. Another example is Nrf2, a dual-specificity phosphatase that plays a key role in inactivating several MAP kinase isoforms during inflammatory processes. Some chemopreventive agents are thought to work by inhibiting NF-κB or Nrf2.
The involvement of Nrf2/HO-1/cytoglobin and Ang-II/NF-κB signals in the cardioprotective mechanism of lansoprazole against cisplatin-induced heart injury
Published in Toxicology Mechanisms and Methods, 2023
Emad H. M. Hassanein, Fares E. M. Ali, Zuhair M. Mohammedsaleh, Ahmed M. Atwa, Mohamed Elfiky
Nuclear factor-kappa B (NF-κB) is the strategic regulator of inflammation. Because of its transcriptional role in maintaining proinflammatory states in heart diseases, NF-κB has a central role in the toxicological mechanism of heart diseases, and its prolonged activation promotes heart failure (Hall et al. 2006; Gordon et al. 2011). The NF-κB expression has been shown to be activated or induced by various signals. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway activate NF-κB (Loh et al. 2019). The renin-angiotensin system (RAS) plays a critical role in cardiovascular and renal physiology. Furthermore, the classic RAS system components renin, angiotensin-converting enzyme (ACE), and angiotensin-II (Ang-II) are proinflammatory and induce oxidative stress, resulting in organ injury (Crowley et al. 2005; Benigni et al. 2010; Garg et al. 2012).
How do nuclear factor kappa B (NF-κB)1 and NF-κB2 defects lead to the incidence of clinical and immunological manifestations of inborn errors of immunity?
Published in Expert Review of Clinical Immunology, 2023
Nazanin Fathi, Hanieh Mojtahedi, Marzieh Nasiri, Hassan Abolhassani, Mahsa Yousefpour Marzbali, Marzie Esmaeili, Fereshte Salami, Furozan Biglari, Nima Rezaei
Low switched memory B cells are a remarkable manifestation in NF-κB-deficient patients, so recurrent infections it is not surprising in defective memory B cells status. It appears that p105 and p65 deficiency prevent pre-pro-B cells from passing, and pre-BCR expression is associated with an increase in NF-κB activity and the induction of anti-apoptotic signals [47]. There is evidence of a decrease in immature bone marrow B cells in a murine model, with the lack of either NF-κB1 or NF-κB2 genes. Immature B cells might be sensitized to pro-apoptotic signals by following BCR ligation if constitutive NF-κB activity is downregulated [42]. MZB cell production is sensitive to perturbations in NF-κB activation, as these cells completely fall with p100-, p105-, or RelB knockout [48]. Since NF-κB is also responsible for activating anti-apoptotic genes’ transcription, regulating NF-κB responses is essential to affect the balance between cell viability and cell death. Some patients with NF-κB mutations showed high levels of CD21low B cells, which are commonly expanded in autoimmune diseases. CD21low B cells may be a consequence of imperfect calcium signaling and weak proliferation as a result of BCR activation that may be affected by the defect NF-κB signaling pathway [49]. Increased levels of inflammatory chemokine receptors are expressed by CD21low B cells, which are related to autoinflammatory manifestations in NF-κB mutations. It is noteworthy that the mechanism of the defect of switching memory B in NF-κB-related signaling still has a major gap.
Phytochemicals with protective effects against acute pancreatitis: a review of recent literature
Published in Pharmaceutical Biology, 2022
Yao Tang, Mingli Sun, Zhenning Liu
The transcription factor NF-κB is an important nuclear factor that plays a variety of evolutionarily conserved roles in a plethora of cellular and biological processes. NF-κB affects many cellular responses including inflammation, apoptosis and proliferation by regulating target gene expression. During the development of AP, NF-κB is activated rapidly in pancreatic acinar cells, and then multiple inflammatory cytokines (TNF, IL-6 and IL-1β) and chemokines (MCP-1 and MIP-1α) are significantly increased which can affect vascular permeability and contribute to thrombosis, haemorrhage and tissue necrosis (Steinle et al. 1999). Substantial evidence indicates NF-κB activation to be a key event in the progression of AP (Jakkampudi et al. 2016); therefore, inhibition of NF-κB activation and proinflammatory cytokines release may be a good therapeutic strategy for the attenuation of AP.