Thioredoxin-1 inhibitor, 1-methylpropyl 2-imidazolyl disulfide, inhibits the growth, migration and invasion of colorectal cancer cell lines

Wang, Fule; Lin, Feiyan; Zhang, Peili; Ni, Wuhua; Bi, Lei; Wu, Jianbo; Jiang, Lei

doi:10.3892/or.2014.3652

Cited by 28 publications

(22 citation statements)

References 36 publications

(31 reference statements)

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“…Accordingly, DATS may directly inhibit HIF‐1α transcriptional activity through suppressing its protein expression. The direct upstream signal of HIF‐1α is the Trx‐1 redox system . Trx‐1 promotes HIF‐1α transcriptional activity by influencing HIF‐1α protein expression and the binding of HIF‐1α dimer to its co‐activator, as we found in this study.…”

Section: Discussionsupporting

confidence: 74%

“…The direct upstream signal of HIF‐1α is the Trx‐1 redox system . Trx‐1 promotes HIF‐1α transcriptional activity by influencing HIF‐1α protein expression and the binding of HIF‐1α dimer to its co‐activator, as we found in this study. DATS inhibited Trx‐1 protein expression in a dose‐dependent manner under normoxic or hypoxic condition.…”

Section: Discussionsupporting

confidence: 74%

“…The direct upstream signal of HIF-1α is the Trx-1 redox system. 41 Trx-1 promotes HIF-1α transcriptional activity by influencing HIF-1α protein expression and the binding of HIF-1α dimer to its co-activator, [41][42][43][44] as we found in this study.…”

Section: Diminution Of Hif-1α Was Independent Of Transcription Mtomentioning

confidence: 66%

“…D), suggesting that increased HIF‐1α protein contributed to the inhibition of HIF‐1α transcriptional activity in MDA‐MB‐231 cells by DATS. Trx‐1 can affect HIF‐1α transactivation and directly regulate its protein levels, so, we assumed that Trx1 was a key node of HIF‐1α inhibition by DATS. Trx‐1 expressions upon normoxia and hypoxia were inhibited by DATS treatment.…”

Section: Resultsmentioning

confidence: 99%

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Diallyl trisulfides, a natural histone deacetylase inhibitor, attenuate HIF‐1α synthesis, and decreases breast cancer metastasis

Wei

Shan

et al. 2017

Molecular Carcinogenesis

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Intratumoral hypoxia promotes the distant metastasis of cancer subclones. The clinical expression level of hypoxia-inducible factor-1α (HIF-1α) reflects the prognosis of a variety of cancers, especially breast cancer. Histone deacetylase (HDAC) inhibitors can target HIF-1α protein due to von Hippel-Lindau (VHL) protein-dependent degradation. Dietary organosulfur compounds, such as those in garlic, have been reported as HDAC inhibitors. The effects of diallyl sulfide (DAS), diallyl disulfide (DADS), and diallyl trisulfide (DATS) on the ratio of firefly/Renilla luciferase activity in hypoxic MDA-MB-231 cells were determined. The mRNA expressions of HIF-1α target genes ANGPTL4, LOXL4, and LOX in hypoxic MDA-MB-231 cells were significantly down-regulated by DATS. DATS attenuated the metastatic potential of MDA-MB-231 cells in hypoxia-induced embryonic zebrafish, xenograft, and orthotopic tumors. Endothelial cell-cancer cell adhesion, wound healing, transwell, and tube formation assays showed that DATS dose-dependently inhibited the migration and angiogenesis of MDA-MB-231 cells in vitro. The expressions of L1CAM, VEGF-A, and EMT-related proteins (Slug, Snail, MMP-2) were inhibited by DATS. DATS dose-dependently inhibited HIF-1α transcriptional activity and hypoxia-induced hematogenous metastasis of MDA-MB-231 cells. It reduced the protein expression of HIF-1α, which did not involve inhibition of HIF-1α mRNA expression or ubiquitin proteasome degradation. Efficient inhibition of HIF-1α expression was required for DATS to resist breast cancer.

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Section: Discussionsupporting

confidence: 74%

Section: Discussionsupporting

confidence: 74%

Section: Diminution Of Hif-1α Was Independent Of Transcription Mtomentioning

confidence: 66%

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

Diallyl trisulfides, a natural histone deacetylase inhibitor, attenuate HIF‐1α synthesis, and decreases breast cancer metastasis

Wei

Shan

et al. 2017

Molecular Carcinogenesis

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“…Cell cycle analysis was performed with propidium iodide (Sigma‐Aldrich) staining as described previously . Briefly, 2 × 10 5 cells per well in 6‐well plates were transfected with 100 nM has‐miR‐124 mimics for 48 hrs.…”

Section: Methodsmentioning

confidence: 99%

miR‐124 interacts with the Notch1 signalling pathway and has therapeutic potential against gastric cancer

Jiang

Lin

et al. 2015

J Cellular Molecular Medi

Self Cite

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Aberrant Notch signalling plays an important role in cancer progression. However, little is known about the interaction between miRNA and the Notch signalling pathway and its role in gastric cancer (GC). In this study, we found that miR‐124 was down‐regulated in GC compared with adjacent normal tissue. Forced expression of miR‐124 inhibited GC cell growth, migration and invasion, and induced cell cycle arrest. miR‐124 negatively regulated Notch1 signalling by targeting JAG1. miR‐124 levels were also shown to be inversely correlated with JAG1 expression in GC. Furthermore, we found that the overexpression of the intracellular domain of Notch1 repressed miR‐124 expression, promoted GC cell growth, migration and invasion. Conversely, blocking Notch1 using a γ‐secretase inhibitor up‐regulated miR‐124 expression, inhibited GC cell growth, migration and invasion. In conclusion, our data demonstrates a regulatory feedback loop between miR‐124 and Notch1 signalling in GC cells, suggesting that the miR‐124/Notch axis may be a potential therapeutic target against GC.

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The thioredoxin system: Balancing redox responses in immune cells and tumors

Muri

Köpf

2022

Eur J Immunol

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The thioredoxin (TRX) system is an important contributor to cellular redox balance and regulates cell growth, apoptosis, gene expression, and antioxidant defense in nearly all living cells. Oxidative stress, the imbalance between reactive oxygen species (ROS) and antioxidants, can lead to cell death and tissue damage, thereby contributing to aging and to the development of several diseases, including cardiovascular and allergic diseases, diabetes, and neurological disorders. Targeting its activity is also considered as a promising strategy in the treatment of cancer. Over the past years, immunologists have established an essential function of TRX for activation, proliferation, and responses in T cells, B cells, and macrophages. Upon activation, immune cells rearrange their redox system and activate the TRX pathway to promote proliferation through sustainment of nucleotide biosynthesis, and to support inflammatory responses in myeloid cells by allowing NF-κB and NLRP3 inflammasome responses. Consequently, targeting the TRX system may therapeutically be exploited to inhibit immune responses in inflammatory conditions. In this review, we summarize recent insights revealing key roles of the TRX pathway in immune cells in health and disease, and lessons learnt for cancer therapy.

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Thioredoxin-1 inhibitor, 1-methylpropyl 2-imidazolyl disulfide, inhibits the growth, migration and invasion of colorectal cancer cell lines

Cited by 28 publications

References 36 publications

Diallyl trisulfides, a natural histone deacetylase inhibitor, attenuate HIF‐1α synthesis, and decreases breast cancer metastasis

Diallyl trisulfides, a natural histone deacetylase inhibitor, attenuate HIF‐1α synthesis, and decreases breast cancer metastasis

miR‐124 interacts with the Notch1 signalling pathway and has therapeutic potential against gastric cancer

The thioredoxin system: Balancing redox responses in immune cells and tumors

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