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Isotoosendanin exerts inhibition on triple-negative breast cancer through abrogating TGF-β-induced EMT via directly targeting TGFβR1

ABSTRACT: In this study, analysis of mRNA sequencing was used to identify potential biological signalling pathways involved in the inhibition of triple negative breast cancer metastasis by ITSN.

ORGANISM(S): Mus musculus

PROVIDER: GSE217003 | GEO | 2023/08/08

REPOSITORIES: GEO

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Isotoosendanin exerts inhibition on triple-negative breast cancer through abrogating TGF-β-induced EMT via directly targeting TGFβR1

Project description:Isotoosendanin exerts inhibition on triple-negative breast cancer through abrogating TGF-β-induced EMT via directly targeting TGFβR1

| PRJNA896562 | ENA

Isotoosendanin exerts inhibition on triple-negative breast cancer through abrogating TGF-β-induced epithelial-mesenchymal transition via directly targeting TGFβR1.

Project description:As the most aggressive breast cancer, triple-negative breast cancer (TNBC) is still incurable and very prone to metastasis. The transform growth factor β (TGF-β)-induced epithelial-mesenchymal transition (EMT) is crucially involved in the growth and metastasis of TNBC. This study reported that a natural compound isotoosendanin (ITSN) reduced TNBC metastasis by inhibiting TGF-β-induced EMT and the formation of invadopodia. ITSN can directly interact with TGF-β receptor type-1 (TGFβR1) and abrogated the kinase activity of TGFβR1, thereby blocking the TGF-β-initiated downstream signaling pathway. Moreover, the ITSN-provided inhibition on metastasis obviously disappeared in TGFβR1-overexpressed TNBC cells in vitro as well as in mice bearing TNBC cells overexpressed TGFβR1. Furthermore, Lys232 and Asp351 residues in the kinase domain of TGFβR1 were found to be crucial for the interaction of ITSN with TGFβR1. Additionally, ITSN also improved the inhibitory efficacy of programmed cell death 1 ligand 1 (PD-L1) antibody for TNBC in vivo via inhibiting the TGF-β-mediated EMT in the tumor microenvironment. Our findings not only highlight the key role of TGFβR1 in TNBC metastasis, but also provide a leading compound targeting TGFβR1 for the treatment of TNBC metastasis. Moreover, this study also points out a potential strategy for TNBC treatment by using the combined application of anti-PD-L1 with a TGFβR1 inhibitor.

| S-EPMC10372922 | biostudies-literature

Expression data for triple-negative breast cancer (TNBC) cells following chemotherapy

Project description:The mechanisms behind drug resistance and sensitivity in breast cancers relies on complex signalling pathways that involve the up or downregulation of certain genes. Many of these genes are involved in adhesion, growth, epithelial/mesenchymal transitions, and apoptosis. We used microarrays to assess differences in gene expression in triple-negative breast cancer cells in response to treatment. We examined the triple-negative human cell line HCC1806 treated with docetaxel or control DMSO. The purpose is to find out the early drug induced changes in this cell line.

2015-07-10 | E-GEOD-70690 | biostudies-arrayexpress

ICAM1 promotes bone metastasis via integrin-mediated TGF-β/EMT signaling in triple-negative breast cancer.

Project description:Bone-related events caused by breast cancer bone metastasis substantially compromise the survival and quality of life of patients. Because triple-negative breast cancer (TNBC) lacks hormone receptors and Her2-targeted therapeutic options, progress in the treatment of TNBC bone metastasis has been very slow. Intercellular adhesion molecule 1 (ICAM1) is highly expressed in various cancers and plays an important role in tumorigenesis and metastasis. However, the effect and mechanism of ICAM1 in TNBC bone metastasis are still unknown. We found that ICAM1 was highly expressed in TNBC and correlated with prognosis in TNBC patients. Cell lines with high expression of ICAM1 exhibited enhanced bone metastasis in tumor-bearing mice, and silencing ICAM1 expression significantly inhibited bone metastasis in mice. ICAM1 interacted with integrins to activate the epithelial-to-mesenchymal transition program through TGF-β/SMAD signaling, ultimately enhancing cell invasiveness. Therefore, the findings of the present study provide a strong rationale for the application of ICAM1-targeted therapy in TNBC patients with bone metastasis.

| S-EPMC9633300 | biostudies-literature

Expression data for triple-negative breast cancer (TNBC) cells following chemotherapy

2015-07-10 | GSE70690 | GEO

Dezocine, An Opioid Analgesic, Exerts Antitumor Effects in Triple-Negative Breast Cancer by Targeting Nicotinamide Phosphoribosyltransferase.

Project description:Opioids are a potential adjuvant treatment for certain cancers; while they are primarily used to relieve chronic pain, these drugs may also affect cancer progression and recurrence. Dezocine is one opioid commonly used in China, but its effects on cancer cells are unknown. Here, we demonstrated the inhibitory effect of dezocine on triple-negative breast cancer (TNBC) cells, and determined the underlying molecular mechanism. We found that dezocine suppressed cell proliferation, migration and invasion, and induced apoptosis in TNBC cells. Xenograft models demonstrated the inhibitory effects of dezocine treatment on TNBC tumor growth in vivo. The anticancer effects of dezocine were independent of opioid receptors, which are not highly expressed by normal breast or breast cancer tissues. A pull-down assay and LC-MS/MS analysis indicated that dezocine directly targets NAMPT: computer modeling verified that the free energy of dezocine kinetically bound into the pocket of NAMPT was -17.4 kcal/mol. Consequently, dezocine treatment inhibited NAMPT enzyme activity, resulting in cellular NAD abolishment. We confirmed the dezocine-induced inhibition of cell proliferation by both NAMPT knockdown and upon treatment with the inhibitor FK866. Our results suggest that both dezocine and NAMPT might represent novel therapeutic targets for TNBC.

| S-EPMC8072669 | biostudies-literature

Triple therapy reduced metastasis in triple-negative breast cancer.

Project description:Triple therapy reduced metastasis in triple-negative breast cancer.

| PRJNA832953 | ENA

Inhibition of ERR? suppresses epithelial mesenchymal transition of triple negative breast cancer cells by directly targeting fibronectin.

Project description:Triple-negative breast cancer (TNBC) patients have poor prognosis due to the aggressive metastatic behaviors. Our study reveals that expression of estrogen related receptor ? (ERR?) is significantly (p < 0.01) positively associated with high grade tumors and lymph node metastasis, while negatively correlated with overall survival (OS), in 138 TNBC patients. Targeted inhibition of ERR? by its inverse agonist XCT-790 or si-RNA obviously inhibits in vitro motility of TNBC cells. While over expression of ERR? triggers the invasion and migration of TNBC cells. Further, si-ERR? and XCT-790 inhibit the epithelial mesenchymal transition (EMT) of TNBC cells with increasing the expression of E-cadherin and decreasing fibronectin (FN) and vimentin. While XCT-790 has no effect on the expression of EMT related transcription factors such as Snail or Slug. Further, inhibitors of MAPK, PI3K/Akt, NF-?B signal molecules, which are activated by XCT-790, can not attenuate the suppression effects of XCT-790 on EMT. Alternatively, luciferase reporter gene assays and ChIP analysis indicate that ERR? can directly bind with FN promoter at ERR response element-3 (ERRE-1), ERRE-3, and ERRE-4, while XCT-790 reduces this bond. In vivo data show that ERR? expression is significantly (p < 0.05) correlated with FN in clinical TNBC patients. In MDA-MB-231 tumor xenograft models, XCT-790 decreases the expression of FN, inhibits the growth and lung metastasis, and suppresses the EMT. Our results demonstrate that ERR? functions as a metastasis stimulator and its targeted inhibition may be a new therapeutic strategy for TNBC treatment.

| S-EPMC4694852 | biostudies-other

Triple Negative Breast Cancer RNA Sequencing

Project description:We propose to definitively characterise the somatic genetics of triple negative breast cancer through generation of comprehensive catalogues of somatic mutations in breast cancer cases by high coverage genome sequencing coupled with integrated transcriptomic and methylation analyses.

2015-04-16 | E-ERAD-113 | biostudies-arrayexpress

Triple Negative Breast tumors: SPARC Positive Tumors vs SPARC Negative Tumors

Project description:The aim of this study was evaluate the transcriptome changes in the comparison between triple negative tumors with increased SPARC expression and triple negative tumors with decreased SPARC expression according to Nagai et al., 2011 (Breast Cancer Res Treat (2011) 126:1–14) The results generated could be of particular interest to better define the prognostic impact of SPARC expression in triple negative breast tumors

2018-07-01 | GSE98931 | GEO

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