Alternations of NF-κB Signaling by Natural Compounds in Muscle-Derived Cancers

Radzka, Justyna; Łapińska, Zofia; Szwedowicz, Urszula; Gajewska-Naryniecka, Agnieszka; Gizak, Agnieszka; Kulbacka, Julita

doi:10.3390/ijms241511900

Cited by 6 publications

(4 citation statements)

References 97 publications

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“…This process further accelerates the transcription of various proinflammatory cytokines, proteinases, and prostaglandins, contributing to the activation of inflammatory cells (macrophages and neutrophils) ( 45 ). On the other hand, the alternative signaling pathway of NF-κB is primarily involved in lymphoid organogenesis and the activation of the adaptive immune response ( 46 ). In contrast to the canonical NF-κB signaling pathway, the alternative signaling pathway is activated by a subset of Tumor Necrosis Factor Receptor (TNFR) superfamily members, including CD40, the lymphotoxin-β receptor (LTβR), receptor activator of NF-κB ligand (RANK), and B lymphocyte stimulating factor receptor (BAFFR) ( 47 ).…”

Section: Nf-κb “Identity Card”mentioning

confidence: 99%

The roles and mechanisms of the NF-κB signaling pathway in tendon disorders

Li,

Luo

et al. 2024

Front. Vet. Sci.

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Both acute and chronic tendon injuries are the most frequently occurring musculoskeletal diseases in human and veterinary medicine, with a limited repertoire of successful and evidenced-based therapeutic strategies. Inflammation has been suggested as a key driver for the formation of scar and adhesion tissue following tendon acute injury, as well as pathological alternations of degenerative tendinopathy. However, prior efforts to completely block this inflammatory process have yet to be largely successful. Recent investigations have indicated that a more precise targeted approach for modulating inflammation is critical to improve outcomes. The nuclear factor-kappaB (NF-κB) is a typical proinflammatory signal transduction pathway identified as a key factor leading to tendon disorders. Therefore, a comprehensive understanding of the mechanism or regulation of NF-κB in tendon disorders will aid in developing targeted therapeutic strategies for human and veterinary tendon disorders. In this review, we discuss what is currently known about molecular components and structures of basal NF-κB proteins and two activation pathways: the canonical activation pathway and the non-canonical activation pathway. Furthermore, we summarize the underlying mechanisms of the NF-κB signaling pathway in fibrosis and adhesion after acute tendon injury, as well as pathological changes of degenerative tendinopathy in all species and highlight the effect of targeting this signaling pathway in tendon disorders. However, to gain a comprehensive understanding of its mechanisms underlying tendon disorders, further investigations are required. In the future, extensive scientific examinations are warranted to full characterize the NF-κB, the exact mechanisms of action, and translate findings into clinical human and veterinary practice.

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Section: Nf-κb “Identity Card”mentioning

confidence: 99%

The roles and mechanisms of the NF-κB signaling pathway in tendon disorders

Li,

Luo

et al. 2024

Front. Vet. Sci.

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“…As different studies have shown, NF-κB modulates a plethora of cellular processes, including cell proliferation, angiogenesis, and apoptosis suppression, making it an important link in promoting inflammation, cancer proliferation, and drug resistance [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 ]. NF-κB is activated in an inflammatory milieu and regulates various pro-inflammatory cytokines (TNFα, IL-6, IL-1β) as well as STAT3, a transcription factor that activates proliferative and survival genes in cancer cells [ 10 , 17 , 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, while apoptosis activation is always desired in cancer treatment, autophagy has a much more complex role and can induce tumor suppression or tumor proliferation, depending on the tumor stage [ 25 , 26 , 27 , 28 ]. Due to increasing multidrug resistance in cancer, numerous studies are now using natural products to target NF-κB and induce apoptosis or autophagy, leading to cancer suppression [ 3 , 16 , 29 , 30 , 31 , 32 , 33 ]. Furthermore, many of these phytochemicals, such as curcumin, resveratrol, and lycopene, exert their anti-cancer activity not only by targeting NF-κB but also by controlling epigenetic modifications, which are key regulators of apoptosis and autophagy [ 30 , 32 , 33 , 34 , 35 , 36 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, while apoptosis activation is always desired in cancer treatment, autophagy has a much more complex role and can induce tumor suppression or tumor proliferation, depending on the tumor stage [25][26][27][28]. Due to increasing multidrug resistance in cancer, numerous studies are now using natural products to target NF-κB and induce apoptosis or autophagy, leading to cancer suppression [3,16,[29][30][31][32][33]. Furthermore, many of these phytochemicals, such as In several cases, dimeric NIQs have proven enhanced activities as compared to their monomeric analogs in several anti-infective test systems (e.g., against HIV, Plasmodium) [1,2,4,6].…”

Section: Introductionmentioning

confidence: 99%

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Jozimine A2, a Dimeric Naphthylisoquinoline (NIQ) Alkaloid, Shows In Vitro Cytotoxic Effects against Leukemia Cells through NF-κB Inhibition

Damiescu,

Yücer,

Klauck

et al. 2024

IJMS

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Naphthylisoquinoline (NIQ) alkaloids are rising as a promising class of secondary metabolites with pharmaceutical potential. NF-κB has already been recognized as a significant modulator of cancer proliferation and drug resistance. We have previously reported the mechanisms behind the cytotoxic effect of dioncophylline A, an NIQ monomer, in leukemia cells. In the current study, we have investigated the cytotoxic effect of jozimine A2, an NIQ dimer, on leukemia cells in comparison to a second, structurally unsymmetric dimer, michellamine B. To this end, molecular docking was applied to predict the binding affinity of the dimers towards NF-κB, which was then validated through microscale thermophoresis. Next, cytotoxicity assays were performed on CCRF-CEM cells and multidrug-resistant CEM/ADR5000 cells following treatment. Transcriptome analysis uncovered the molecular networks affected by jozimine A2 and identified the cell cycle as one of the major affected processes. Cell death modes were evaluated through flow cytometry, while angiogenesis was measured with the endothelial cell tube formation assay on human umbilical vein endothelial cells (HUVECs). The results indicated that jozimine A2 bound to NF-κB, inhibited its activity and prevented its translocation to the nucleus. In addition, jozimine A2 induced cell death through apoptosis and prevented angiogenesis. Our study describes the cytotoxic effect of jozimine A2 on leukemia cells and explains the interactions with the NF-κB signaling pathway and the anticancer activity.

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Harnessing curcumin and nanotechnology for enhanced treatment of breast cancer bone metastasis

Shakori Poshteh,

Alipour,

Varamini

2024

Discover Nano

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Breast cancer (BC) bone metastasis poses a significant clinical challenge due to its impact on patient prognosis and quality of life. Curcumin (CUR), a natural polyphenol compound found in turmeric, has shown potential in cancer therapy due to its anti-inflammatory, antioxidant, and anticancer properties. However, its metabolic instability and hydrophobicity have hindered its clinical applications, leading to a short plasma half-life, poor absorption, and low bioavailability. To enhance the drug-like properties of CUR, nanotechnology-based delivery strategies have been employed, utilizing polymeric, lipidic, and inorganic nanoparticles (NPs). These approaches have effectively overcome CUR’s inherent limitations by enhancing its stability and cellular bioavailability both in vitro and in vivo. Moreover, targeting molecules with high selectivity towards bone metastasized breast cancer cells can be used for site specific delivery of curcumin. Alendronate (ALN), a bone-seeking bisphosphonate, is one such moiety with high selectivity towards bone and thus can be effectively used for targeted delivery of curcumin loaded nanocarriers. This review will detail the process of bone metastasis in BC, elucidate the mechanism of action of CUR, and assess the efficacy of nanotechnology-based strategies for CUR delivery. Specifically, it will focus on how these strategies enhance CUR’s stability and improve targeted delivery approaches in the treatment of BC bone metastasis. Graphical abstract

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Alternations of NF-κB Signaling by Natural Compounds in Muscle-Derived Cancers

Cited by 6 publications

References 97 publications

The roles and mechanisms of the NF-κB signaling pathway in tendon disorders

The roles and mechanisms of the NF-κB signaling pathway in tendon disorders

Jozimine A2, a Dimeric Naphthylisoquinoline (NIQ) Alkaloid, Shows In Vitro Cytotoxic Effects against Leukemia Cells through NF-κB Inhibition

Harnessing curcumin and nanotechnology for enhanced treatment of breast cancer bone metastasis

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