NF-κB in Gastric Cancer Development and Therapy

Chaithongyot, Supattra; Jantaree, Phatcharida; Sokolova, Olga; Naumann, Michael

doi:10.3390/biomedicines9080870

Cited by 25 publications

(16 citation statements)

References 176 publications

(190 reference statements)

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“…Treatment and reversal of CAG are important strategies for controlling gastric cancer. Years of experimental studies have proved that traditional Chinese medicine is endowed Additionally, studies showed that the NF-κB inflammatory signaling pathway is often in a state of persistent abnormal activation in gastric cancer [11,12]. It has been found that Helicobacter pylori infection and the inflammatory response caused by environmental factors constitutively activate NF-κB [13][14][15].…”

Section: Discussionmentioning

confidence: 99%

Curcumol Undermines SDF-1α/CXCR4/NF-κB Signaling Pathway to Suppress the Progression of Chronic Atrophic Gastritis (CAG) and Gastric Cancer

Kong

Zhu

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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CAG is the most common precancerous disease of gastric cancer, which belongs to a kind of chronic gastritis. CAG is in close association with gastric cancer, which makes itself a critical node clinically in cancer prevention and treatment. Curcumol is a main active monomer in Fuzheng Huowei decoction, which has the properties of antioxidant, antiviral, and antitumor. In this study, the expression of SDF-1α/CXCR4/NF-κB was detected by in vivo and in vitro methods. Then, we found that the expressions of NF-κB, SDF-1α, CXCR4, and p-NF-κB were decreased in the curcumol treatment group. Curcumol inhibited gastric cancer cells’ viability, migration, and invasion and induced their apoptosis. After adding the lentivirus overexpressing SDF-1α to the curcumol treatment group, it was found that SDF-1α, CXCR4, NF-κB, and p-NF-κB protein expressions were all increased, and the effect of curcumol on gastric cancer cells was reversed. In the nude mouse experiment, the tumor volume in the curcumol + SDF-1α group was the largest, and the tumor volume in the Fuzheng Huowei decoction + NC group was the smallest. In conclusion, curcumol effectively protects gastric tissue and inhibits the viability of gastric cancer cells, and curcumol regulates SDF-1α/CXCR4/NF-κB to play a therapeutic role in chronic atrophic gastritis and gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Curcumol Undermines SDF-1α/CXCR4/NF-κB Signaling Pathway to Suppress the Progression of Chronic Atrophic Gastritis (CAG) and Gastric Cancer

Kong

Zhu

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…This modification targets IkB through ubiquitination and consequent degradation by the 26S proteasome. NF-κB is thus released and can translocate to the nucleus where it promotes gene transcription [ 36 ].…”

Section: The Effect Of Parthenolide On Gene Expression Profilementioning

confidence: 99%

Parthenolide and Its Soluble Analogues: Multitasking Compounds with Antitumor Properties

et al. 2022

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Due to its chemical properties and multiple molecular effects on different tumor cell types, the sesquiterpene lactone parthenolide (PN) can be considered an effective drug with significant potential in cancer therapy. PN has been shown to induce either classic apoptosis or alternative caspase-independent forms of cell death in many tumor models. The therapeutical potential of PN has been increased by chemical design and synthesis of more soluble analogues including dimethylaminoparthenolide (DMAPT). This review focuses on the molecular mechanisms of both PN and analogues action in tumor models, highlighting their effects on gene expression, signal transduction and execution of different types of cell death. Recent findings indicate that these compounds not only inhibit prosurvival transcriptional factors such as NF-kB and STATs but can also determine the activation of specific death pathways, increasing intracellular reactive oxygen species (ROS) production and modifications of Bcl-2 family members. An intriguing property of these compounds is its specific targeting of cancer stem cells. The unusual actions of PN and its analogues make these agents good candidates for molecular targeted cancer therapy.

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“…The discovery of NF‐κB occurred almost 30 years ago and it can exist in both homodimeric and heterodimeric forms. NF‐κB proteins were first recognized in B lymphocytes and it is capable of binding to B motif in enhancer element of κ light‐chain gene to affect expression level (Chaithongyot et al, 2021; Puar et al, 2018; Sawhney et al, 2007). Overall, NF‐κB can predominantly mediate its signaling through canonical and noncanonical pathways (Napetschnig & Wu, 2013).…”

Section: Introductionmentioning

confidence: 99%

NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition

Mirzaei

Saghari

Bassiri

et al. 2022

Journal Cellular Physiology

118

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Metastasis of tumor cells is a complex challenge and significantly diminishes the overall survival and prognosis of cancer patients. The epithelial‐to‐mesenchymal transition (EMT) is a well‐known mechanism responsible for the invasiveness of tumor cells. A number of molecular pathways can regulate the EMT mechanism in cancer cells and nuclear factor‐kappaB (NF‐κB) is one of them. The nuclear translocation of NF‐κB p65 can induce the transcription of several genes involved in EMT induction. The present review describes NF‐κB and EMT interaction in cancer cells and their association in cancer progression. Due to the oncogenic role NF‐κB signaling, its activation enhances metastasis of tumor cells via EMT induction. This has been confirmed in various cancers including brain, breast, lung and gastric cancers, among others. The ZEB1/2, transforming growth factor‐β, and Slug as inducers of EMT undergo upregulation by NF‐κB to promote metastasis of tumor cells. After EMT induction driven by NF‐κB, a significant decrease occurs in E‐cadherin levels, while N‐cadherin and vimentin levels undergo an increase. The noncoding RNAs can potentially also function as upstream mediators and modulate NF‐κB/EMT axis in cancers. Moreover, NF‐κB/EMT axis is involved in mediating drug resistance in tumor cells. Thus, suppressing NF‐κB/EMT axis can also promote the sensitivity of cancer cells to chemotherapeutic agents.

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NF-κB in Gastric Cancer Development and Therapy

Cited by 25 publications

References 176 publications

Curcumol Undermines SDF-1α/CXCR4/NF-κB Signaling Pathway to Suppress the Progression of Chronic Atrophic Gastritis (CAG) and Gastric Cancer

Curcumol Undermines SDF-1α/CXCR4/NF-κB Signaling Pathway to Suppress the Progression of Chronic Atrophic Gastritis (CAG) and Gastric Cancer

Parthenolide and Its Soluble Analogues: Multitasking Compounds with Antitumor Properties

NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition

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