Activation of Nm23-H1 to suppress breast cancer metastasis via redox regulation

Lee, Kong Joo

doi:10.1038/s12276-021-00575-1

Cited by 17 publications

(15 citation statements)

References 98 publications

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“…This metastatic ability may be regulated by carotenoids on many levels, including the expression of important pro- and antimetastatic factors such as Nm23-H1; uPA; matrix metalloproteinases, e.g., MMP-1, -2, -3, -7, -8, -9, -12, and -13; MT1-MMP and MT3-MMP; endogenous tissue inhibitors of metalloproteinases (TIMPs), e.g., TIMP-1, -2, -3, and -4; transforming growth factor-β1 (TGF-β1); Rho subfamily, including RhoA, Rac1, and Cdc42; transmembrane E-cadherin; and surface glycoprotein, including CD44 and CXCR4, and HIF-1α. Carotenoids can also regulate pro-angiogenic factors, such as VEGF and cytokines or toll-like receptors (TLRs) [ 41 , 117 , 123 , 124 , 125 ]; these factors can contribute to the destruction and remodelling of the ECM compounds, which is a basic step in the further progression of the tumour.…”

Section: Resultsmentioning

confidence: 99%

Dietary Carotenoids in Head and Neck Cancer—Molecular and Clinical Implications

Starska

2022

Nutrients

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Head and neck cancer (HNC) is one of the most common cancers in the world according to GLOBCAN. In 2018, it was reported that HNC accounts for approximately 3% of all human cancers (51,540 new cases) and is the cause of nearly 1.5% of all cancer deaths (10,030 deaths). Despite great advances in treatment, HNC is indicated as a leading cause of death worldwide. In addition to having a positive impact on general health, a diet rich in carotenoids can regulate stages in the course of carcinogenesis; indeed, strong epidemiological associations exist between dietary carotenoids and HNS, and it is presumed that diets with carotenoids can even reduce cancer risk. They have also been proposed as potential chemotherapeutic agents and substances used in chemoprevention of HNC. The present review discusses the links between dietary carotenoids and HNC. It examines the prospective anticancer effect of dietary carotenoids against intracellular cell signalling and mechanisms, oxidative stress regulation, as well as their impact on apoptosis, cell cycle progression, cell proliferation, angiogenesis, metastasis, and chemoprevention; it also provides an overview of the limited preclinical and clinical research published in this arena. Recent epidemiological, key opinion-forming systematic reviews, cross-sectional, longitudinal, prospective, and interventional studies based on in vitro and animal models of HNC also indicate that high carotenoid content obtained from daily supplementation has positive effects on the initiation, promotion, and progression of HNC. This article presents these results according to their increasing clinical credibility.

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Section: Resultsmentioning

confidence: 99%

Dietary Carotenoids in Head and Neck Cancer—Molecular and Clinical Implications

Starska

2022

Nutrients

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“…RORA interacts with nucleoside diphosphate kinases, including NM23-1 and NM23-2. NM23-1 is a tumor metastasis suppressor candidate gene 24 , 25 , and NM23-2 plays a role in organogenesis and differentiation 26 , 27 . RORA is also a potential target in breast cancer that negatively modulates angiogenesis 11 .…”

Section: Discussionmentioning

confidence: 99%

The suppressive functions of Rora in B lineage cell proliferation and BCR/ABL1-induced B-ALL pathogenesis

Li¹,

Wang²,

He³

et al. 2022

Int. J. Biol. Sci.

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RORA plays an important role in regulating circadian rhythms, inflammation, metabolism and cellular development. Herein, we explore the roles of Rora in B cell proliferation and differentiation, as well as in Ph + B-ALL. By using Rora loxp/loxp Mx-1-Cre mice, Rora was deleted in hematopoietic cells post Pipc induction. Rora deficiency mice were associated with an obvious accumulation of B cells in the peripheral blood, bone marrow, and spleen. On the other hand, activation of Rora with Cholesterol sulfate (CS) was associated with decreased B cell numbers. RNA-seq analysis revealed that the transcription level of Lmo1 was decreased in Rora deficient B cells. Moreover, the expression of RORA was shown to be decreased in Ph + B-ALL cells compared to peripheral blood derived B cells from healthy donors. The overexpression of Rora in BaF3 cells with BCR/ABL1 was also associated with impeded the cell growth and an increased apoptotic rate compared to cells transduced with BCR/ABL1 alone. The co-expression of BCR/ABL1 and Rora induced B-ALL mouse model was associated with the significant inhibition of BCR/ABL1-transformed cell growth and prolonged the survival of the diseased mice. These results suggest a novel role for Rora in B cell development and Ph + leukemogenesis.

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“…Notably, in KEGG analysis, most of enriched proteins involved the nervous-system pathways, including Alzheimer disease and Parkinson disease (Succinate Dehydrogenase Complex Flavoprotein Subunit A, SDHA and 26S Proteasome Ubiquitin Receptor, ADRM1) associated with metal accumulation in the brain 64 (Figure 4d and Table S7). Significantly high enriched proteasome here possibly comes from that emerging data identified mammalian proteins of interest exhibiting histidine phosphorylation, including Pselectin, annexin I and the 20S proteasome 65,66 . Moreover, as active histidine residues are commonly found in enzyme active sites and metal-binding sites 67,68 , Gene Ontology (GO) 69 terms analysis for 78 highly enriched proteins described their classes of biological process (BP), cellular component (CC) and molecule function (MF).…”

Section: Proteome-wide Profiling In Human Cellsmentioning

confidence: 91%