Fluorescence detection and depletion of T47D breast cancer cells from human mononuclear cell-enriched blood preparations by photodynamic treatment: Basic in vitro experiments towards the removal of circulating tumor cells

The imaging of tumor cells and tumor tissue samples is very important for cancer detection and therapy. We have taken advantages of fluorescent silica nanoparticles (FSiNPs) coupled with a molecular recognition element that allows for effective in vitro and ex vivo imaging of tumor cells and tissues. In this study, we report on the targeting and imaging of MDA-MB-231 human breast cancer cells using arginine-glycine-aspartic acid (RGD) peptide-labeled FSiNPs. When linked with RGD peptide using the cyanogen bromide (CNBr) method, the FSiNPs exhibited high target binding to αvβ3 integrin receptor (ABIR)-positive MDA-MB-231 breast cancer cells in vitro. Further study regarding the ex vivo imaging of tumor tissue samples was also carried out by intravenously injecting RGD peptide-labeled FSiNPs into athymic nude mice bearing the MDA-MB-231 tumors. Tissue images demonstrated that the high integrin αvβ3 expression level of the MDA-MB-231 tumors was clearly visible due to the special targeting effects of the RGD peptide-labeled FSiNPs, and the tumor fluorescence reached maximum intensity at 1 h postinjection. Our results break new ground for using FSiNPs to optically image tumors, and may also broaden the applications of silica nanoparticles in biomedicine.

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P11.10 The IFNγ pathway mediates brain metastasis formation of breast cancer

Neuro-Oncology ◽

10.1093/neuonc/noz126.156 ◽

2019 ◽

Vol 21 (Supplement_3) ◽

pp. iii44-iii44

Author(s):

R Pedrosa ◽

J M Kros ◽

B Schrijver ◽

R Marques ◽

P Leenen ◽

...

Keyword(s):

Breast Cancer ◽

T Cells ◽

T Cell ◽

T Lymphocytes ◽

Cancer Cells ◽

Tumor Cells ◽

Breast Cancer Cells ◽

T Cell Response ◽

Activated T Cells

Abstract BACKGROUND In previous work we showed the prominence of the T-cell response in the formation of brain metastases of primary ER negative breast cancers (Mustafa et al, Acta Neuropathol 2018). We also showed that breast cancer cells co-cultured with stimulated T lymphocytes overexpress Guanylate-binding protein 1 (GBP1) accompanying increased trespassing ability through an in vitro blood-brain barrier (BBB) model. In addition, we demonstrated a predilection for metastasizing to brain of breast cancer cells that were co-cultured with activated T cells in a mouse model. We now scrutinize the importance of the IFNγ pathway for tresspassing of the tumor cells through the BBB following T cell contact. MATERIAL AND METHODS Anti-hIFN-γ-IgA antibodies were used to neutralize the IFNγ effects on the tumor cells. The effects on the tumor cells is only due to native IFNγ produced by activated T cells, not by recombinant IFNγ. Since the IFNγ expression itself enhances its expression by the T cells, we blocked IFNγ receptors prior to adding CD3+ T cell conditioned media to the breast cancer cells. The receptor blocking was achieved by antibodies to the IFNγα and IFNγβ subunits. Activation of the STAT1 pathway was monitored by GBP1 expression. For functional read-out the in vitro BBB model was used. RESULTS The presence of T-lymphocyte-secreted IFNγ in the primary breast cancer microenvironment activates the STAT1-dependent IFNγ pathway in breast cancer cells, endowing them with an increased ability to trespass the in vitro BBB. Moreover, direct inhibition of soluble IFNγ, or blocking of the IFNγ-specific receptor in breast cancer cells significantly decreases their ability to cross the BBB. CONCLUSION The results illustrate the specific action of T lymphocytes in the formation of cerebral metastasis involves the IFNγ signaling pathway as one of the crucial entangled pathways Subsequent studies should aim at the interference with the IFNγ pathway to develop preventive strategies against the formation of cerebral metastases of breast cancer.

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Molecular Mechanism by which Diosbulbin B Regulates the TP63 Gene in Triple-Negative Breast Cancer

10.21203/rs.3.rs-122887/v1 ◽

2020 ◽

Author(s):

LIU LIU ◽

Qiufeng Lao ◽

Shengle Li ◽

Weiyi Pang

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Molecular Mechanism ◽

Triple Negative Breast Cancer ◽

Breast Cancer Cells ◽

Triple Negative ◽

In Vitro Experiments ◽

Active Components ◽

Dioscorea Bulbifera

Abstract BackgroundDioscorea bulbifera L. is mainly used for antitumor therapy in clinical practice. Studies have shown that the drug-containing serum obtained from Dioscorea bulbifera L. induces the apoptosis and inhibits the proliferation of rat breast cancer cells. However, the main active compounds and the molecular mechanism in triple-negative breast cancer are still unclear.MethodsThe TCMSP, GeneCards, GEO and TCGA databases were used to identify genes that intersect the target genes of Dioscorea bulbifera L., active Dioscorea bulbifera L. components and triple-negative breast cancer targets, and Kaplan-Meier and GSEA methods were used to analyze the survival and pathway enrichment of the intersecting genes, respectively. Subsequently, in vitro experiments were performed for verification.ResultsA total of 14 active components were screened, and the targets of the active components were combined with triple-negative breast cancer-related targets and differentially expressed genes obtained from the GeneCards database. Three genes (CCNB1, PGR and TP63) are related to the anti-breast cancer effects of Dioscorea bulbifera L., and TP63 (P<0.05) is related to breast cancer survival. The GSEA showed that the TP63 gene is related to the apoptosis pathway, and TP63 gene analysis in the TCGA clinical database showed the greatest expression difference in triple-negative breast cancer. The in vitro experiments showed that diosbulbin B, the main antitumor compound in Dioscorea bulbifera L., may inhibit the proliferation and migration of MDA-MB-231 breast cancer cells and induce their apoptosis by promoting the expression of the TP63 gene.ConclusionThe present study fully elucidated the active components, potential targets and molecular mechanisms of Dioscorea bulbifera L. against triple-negative breast cancer and provided a new method for revealing the scientific basis and therapeutic mechanism of Chinese medicine in treating diseases.

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

Antioxidants ◽

10.3390/antiox7100135 ◽

2018 ◽

Vol 7 (10) ◽

pp. 135 ◽

Cited By ~ 16

Author(s):

Buckley McCall ◽

Connor McPartland ◽

Reece Moore ◽

Anastasia Frank-Kamenetskii ◽

Brian Booth

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Tumor Cells ◽

Breast Cancer Cells ◽

Normal Breast ◽

Accessory Pigment ◽

And Migration ◽

Reducing Properties ◽

Proliferation And Migration

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.

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KCa3.1 Channels Confer Radioresistance to Breast Cancer Cells

Cancers ◽

10.3390/cancers11091285 ◽

2019 ◽

Vol 11 (9) ◽

pp. 1285 ◽

Cited By ~ 6

Author(s):

Mohr ◽

Gross ◽

Sezgin ◽

Steudel ◽

Ruth ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Tumor Cells ◽

Breast Tumor ◽

Breast Cancer Cells ◽

Therapy Response ◽

Orthotopic Mouse Model ◽

Breast Tumor Cells ◽

Fractionated Radiotherapy

KCa3.1 K+ channels reportedly contribute to the proliferation of breast tumor cells and may serve pro-tumor functions in the microenvironment. The putative interaction of KCa3.1 with major anti-cancer treatment strategies, which are based on cytotoxic drugs or radiotherapy, remains largely unexplored. We employed KCa3.1-proficient and -deficient breast cancer cells derived from breast cancer-prone MMTV-PyMT mice, pharmacological KCa3.1 inhibition, and a syngeneic orthotopic mouse model to study the relevance of functional KCa3.1 for therapy response. The KCa3.1 status of MMTV-PyMT cells did not determine tumor cell proliferation after treatment with different concentrations of docetaxel, doxorubicin, 5-fluorouracil, or cyclophosphamide. KCa3.1 activation by ionizing radiation (IR) in breast tumor cells in vitro, however, enhanced radioresistance, probably via an involvement of the channel in IR-stimulated Ca2+ signals and DNA repair pathways. Consistently, KCa3.1 knockout increased survival time of wildtype mice upon syngeneic orthotopic transplantation of MMTV-PyMT tumors followed by fractionated radiotherapy. Combined, our results imply that KCa3.1 confers resistance to radio- but not to chemotherapy in the MMTV-PyMT breast cancer model. Since KCa3.1 is druggable, KCa3.1 targeting concomitant to radiotherapy seems to be a promising strategy to radiosensitize breast tumors.

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Dinuclear CuIcomplexes of pyridyl-diazadiphosphetidines and aminobis(phosphonite) ligands: synthesis, structural studies and antiproliferative activity towards human cervical, colon carcinoma and breast cancer cells

Dalton Transactions ◽

10.1039/c4dt00832d ◽

2014 ◽

Vol 43 (29) ◽

pp. 11339-11351 ◽

Cited By ~ 18

Author(s):

Aijaz Rashid ◽

Guddekoppa S. Ananthnag ◽

Susmita Naik ◽

Joel T. Mague ◽

Dulal Panda ◽

...

Keyword(s):

Breast Cancer ◽

Antitumor Activity ◽

Cancer Cells ◽

Tumor Cells ◽

Antiproliferative Activity ◽

Breast Cancer Cells ◽

Human Tumor ◽

Structural Studies ◽

Human Tumor Cells

The CuIcomplexes showedin vitroantitumor activity against several human tumor cells 5–7 fold higher than cisplatin.

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N-hexane Extract and Fraction of Green Tea as Antiproliferation of MCM-B2 Breast Cancer Cells In Vitro

Current Biochemistry ◽

10.29244/cb.6.2.3 ◽

2020 ◽

Vol 6 (2) ◽

Author(s):

Lisni Noraida Waruwu ◽

Maria Bintang ◽

Bambang Pontjo Priosoeryanto

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Green Tea ◽

Cancer Cell ◽

Breast Cancer Cells ◽

Green Tea Extract ◽

Hexane Fraction ◽

Phytochemical Screening ◽

Tea Extract

Green tea (Camellia sinensis) is one of traditional plants that have the potential as an anticancer. The sample used in this research commercial green tea extract. The purpose of this study was to test the antiproliferation activity of green tea extract on breast cancer cell MCM-B2 in vitro. Green tea extract fractionated using three solvents, ie water, ethanol 70%, and n-hexane. Extract and fraction of green tea water have value Lethality Concentration 50 (LC50) more than 1000 ppm. The fraction of ethanol 70% and n-hexane had an LC50 value of 883.48 ppm and 600.56 ppm, respectively. The results of the phytochemical screening of green tea extract are flavonoids, tannins, and saponins, while the phytochemical screening results of n-hexane fraction are flavonoids and tannins. Antiproliferation activity was tested on breast cancer cells MCM-B2 and normal cells Vero by trypan blue staining method. The highest MCM-B2 cell inhibitory activity was achieved at a concentration of 13000 ppm green tea extract and 1000 ppm of n-hexane fraction, 59% and 59%, respectively. The extract and n-hexane fraction of green tea are not toxic to normal Vero cells characterized by not inhibiting normal cell proliferation. Keywords: antiproliferative, cancer cell MCM-B2, commercial green tea, cytotoxicity

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