Enterolactone modulates the ERK/NF-κB/Snail signaling pathway in triple-negative breast cancer cell line MDA-MB-231 to revert the TGF-β-induced epithelial–mesenchymal transition

Mali, Aniket V; Joshi, Asavari; Hegde, Mahabaleshwar V.; Kadam, Shivajirao

doi:10.20892/j.issn.2095-3941.2018.0012

Cited by 52 publications

(28 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TGF-β, a major inducer of EMT, is overexpressed in breast cancer, and is associated with malignant progression and poor prognosis (16). Adding TGF-β to epithelial cells in culture induces EMT in vitro (17,18). TGF-β induces EMT through a Smad-dependent pathway.…”

Section: Discussionmentioning

confidence: 99%

DCST1-AS1 Promotes TGF-β-Induced Epithelial–Mesenchymal Transition and Enhances Chemoresistance in Triple-Negative Breast Cancer Cells via ANXA1

Tang

Chen²,

Chen

et al. 2020

Front. Oncol.

View full text Add to dashboard Cite

Triple-negative breast cancer (TNBC) is a highly metastatic breast cancer subtype, and the primary systemic treatment strategy involves conventional chemotherapy. DC-STAMP domain containing 1-antisense 1 (DCST1-AS1) is a long non-coding RNA that promotes TNBC migration and invasion. Studying the role of DCST1-AS1 in promoting epithelial-mesenchymal transition (EMT) and chemoresistance will provide a new strategy for TNBC therapy. In the present study, we found that DCST1-AS1 regulates the expression or secretion of EMT-related proteins E-cadherin, snail family zinc finger 1 (SNAI1), vimentin, matrix metallopeptidase 2 (MMP2), and matrix metallopeptidase 9 (MMP9). Interference with DCST1-AS1 impaired TGF-β-induced TNBC cell invasion and migration. DCST1-AS1 directly binds to ANXA1 in BT-549 cells and affects the expression of ANXA1. DCST1-AS1 enhances TGF-β/Smad signaling in BT-549 cells through ANXA1 to promote EMT. The combination of DCST1-AS1 and ANXA1 also contributes to enhancement of the resistance of BT-549 cells to doxorubicin and paclitaxel. In conclusion, DCST1-AS1 promotes TGF-β-induced EMT and enhances chemoresistance in TNBC cells through ANXA1, and therefore represents a potentially promising target for metastatic breast cancer therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

DCST1-AS1 Promotes TGF-β-Induced Epithelial–Mesenchymal Transition and Enhances Chemoresistance in Triple-Negative Breast Cancer Cells via ANXA1

Tang

Chen²,

Chen

et al. 2020

Front. Oncol.

View full text Add to dashboard Cite

show abstract

“…ASX inhibits migration in the TNBC and ER + breast cancer cells examined in these experiments. The MDA-MB-231 TNBC line is highly metastatic [ 32 ] but its migratory capacity is attenuated by ASX treatment.…”

Section: Discussionmentioning

confidence: 99%

Effects of Astaxanthin on the Proliferation and Migration of Breast Cancer Cells In Vitro

et al. 2018

View full text Add to dashboard Cite

Astaxanthin (ASX) is a marine-based ketocarotenoid; an accessory pigment in plants in that it has many different potential functions. ASX is an antioxidant that is notably more potent than many other antioxidants. Antioxidants have anti-inflammatory and oxidative stress-reducing properties to potentially reduce the incidence of cancer or inhibit the expansion of tumor cells. In this study, we tested the hypothesis that ASX would inhibit proliferation and migration of breast cancer cells in vitro. We found that application of ASX significantly reduced proliferation rates and inhibited breast cancer cell migration compared to control normal breast epithelial cells. Based on these results, further investigation of the effects of ASX on not only breast cancer cells, but other forms of tumor cells, should be carried out.

show abstract

“…The NF-κB signaling pathway is closely related to tumorigenesis, invasion, and metastasis. [24][25][26] Yang et al found that p65-regulated EMT induced by the low-dose irradiation of cervical cancer cell lines promotes invasiveness and metastasis. 27 Interestingly, studies have reported that CXCL1 promotes breast cancer metastasis via NF-κB.…”

Section: Discussionmentioning

confidence: 99%

<p>Low-Dose Radiation Promotes Invasion and Migration of A549 Cells by Activating the CXCL1/NF-κB Signaling Pathway</p>

Li¹,

Wu²,

Han³

et al. 2020

OTT

View full text Add to dashboard Cite

Radiation has well-known and well-characterized direct toxic effects on cells and tissues. However, low-dose ionizing irradiation (LDIR) can also enhance the invasion and migration of tumor cells, and the mechanisms underlying these effects remain unclear. The present study aimed to investigate changes induced in the migration and invasion of A549 cells after LDIR and to explore the potential molecular mechanism. Materials and Methods: A549 cells were irradiated with X-rays at different doses (0, 2, 4, and 6 Gy) and cultured for 24 or 48 h. Apoptosis and proliferation were evaluated by lactate dehydrogenase release, CCK8, colony formation, and flow cytometry assays. Wound-healing and transwell assays were performed to detect migration and invasion ability. CXCL1 or p65 were knocked down using lentivirus-mediated siRNA in A549 cell lines. Knockdown efficiency of CXCL1 and p65 was assessed by RT-qPCR. Western blotting and immunofluorescence were used to determine the changes in protein levels. Results: In cells irradiated with a dose of 6 Gy, after 48 h, apoptosis was clearly induced while proliferation was inhibited. Irradiation with 4 Gy resulted in the upregulation of CXCL1 expression and activation of the NF-κB signaling pathway. Moreover, upon 4 Gy irradiation, migration, invasion, and epithelial-mesenchymal transition (EMT) were significantly enhanced in A549 cells. Importantly, CXCL1 or p65 knockdown inhibited radiationinduced migration, invasion, and EMT. Conclusion: Low-dose radiation upregulates CXCL1 expression and activates the NF-κB signaling to regulate EMT in A549 cells, thereby promoting invasion and migration. These results provide new insights into the prevention of tumor invasion and metastasis induced by radiotherapy.

show abstract

Enterolactone modulates the ERK/NF-κB/Snail signaling pathway in triple-negative breast cancer cell line MDA-MB-231 to revert the TGF-β-induced epithelial–mesenchymal transition

Cited by 52 publications

References 53 publications

DCST1-AS1 Promotes TGF-β-Induced Epithelial–Mesenchymal Transition and Enhances Chemoresistance in Triple-Negative Breast Cancer Cells via ANXA1

DCST1-AS1 Promotes TGF-β-Induced Epithelial–Mesenchymal Transition and Enhances Chemoresistance in Triple-Negative Breast Cancer Cells via ANXA1

Effects of Astaxanthin on the Proliferation and Migration of Breast Cancer Cells In Vitro

<p>Low-Dose Radiation Promotes Invasion and Migration of A549 Cells by Activating the CXCL1/NF-κB Signaling Pathway</p>

Contact Info

Product

Resources

About