99mTc-HYNIC-(tricine/EDDA)-FROP peptide for MCF-7 breast tumor targeting and imaging

Background: Breast cancer is a malignant disease with high mortality rate among women in the world. It is necessary to diagnose breast cancer at the early stage before it metastasizes in patients. Objective: The aim of this study is the evaluation of 99mTc-(tricine)-HYNIC-Lys-FROP for breast tumor imaging. Method: Lys-FROP peptide was labeled with 99mTc using HYNIC as chelator and tricine as co-ligand. Specific binding of this radiolabeled peptide on breast cancerous cell was assessed in different cell lines as well as in tumor-bearing mice. Results: HYNIC-Lys-FROP peptide was labeled with 99mTc at radiochemical purity more than 99%. It was observed high stability in normal saline and serum about 95%. The highest cellular uptake was observed in MCF-7 breast tumor cells treated with 99mTc-(tricine)-HYNIC-Lys-FROP as compared to other cell lines (lung, ovarian, T47D breast cancer cell lines). Biodistribution results in female MCF-7 tumor-bearing mice showed the relatively high tumor uptake and tumor-muscle ratio as 3.82 ± 0.66 after 15 min post-injection of 99mTc-(tricine)- HYNIC-Lys-FROP. Tumor uptake was reduced in mice that were co-injected with excess of unlabeled peptide to be 0.91 ± 0.08. Conclusion: Findings showed this radiolabeled peptide is a promising candidate for tumor targeting and molecular imaging of breast cancer.

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Effects of interaction between estradiol-17? and progesterone on the proliferation of cloned breast tumor cells (MCF-7 and T47D)

Journal of Cellular Physiology ◽

10.1002/jcp.1041240305 ◽

1985 ◽

Vol 124 (3) ◽

pp. 386-390 ◽

Cited By ~ 19

Author(s):

Robert W. Schatz ◽

Ana M. Soto ◽

Carlos Sonnenschein

Keyword(s):

Tumor Cells ◽

Breast Tumor ◽

Breast Tumor Cells ◽

Mcf 7

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METHYL 10-EPI-PHEOPHORBIDE A FROM MCF-7 CELLS ACTIVE LAYER OF THE INDONESIAN FICUS DELTOIDEA JACK LEAVES

International Journal of Pharmacy and Pharmaceutical Sciences ◽

10.22159/ijpps.2017v9i8.18750 ◽

2017 ◽

Vol 9 (8) ◽

pp. 183 ◽

Cited By ~ 2

Author(s):

Anggia Murni ◽

Novriyandi Hanif ◽

Masaki Kita ◽

Latifah K. Darusman

Keyword(s):

Active Layer ◽

Column Chromatography ◽

Breast Tumor ◽

High Performance ◽

Chemical Structure ◽

High Resolution Mass Spectrometry ◽

Assay Method ◽

Pheophorbide A ◽

Ficus Deltoidea ◽

Mcf 7

Objective: To isolate and elucidate a cytotoxic principle against breast tumor MCF-7 cells of the Indonesian terrestrial plant Ficus deltoidea Jack leaves.Methods: F. deltoidea leaves collected at National Park of mount Gede-Pangrango, Indonesia have been subjected to chemical and biological work. F. deltoidea leaves were extracted with 96% aqueous ethanol (EtOH) and was then partitioned into three layers n-hexane, dichloromethane (CH2Cl2), and n-butanol (n-BuOH). All layers were checked for their activity against breast tumor MCF-7 cells using MTT assay method. A portion of the most active layer was purified using open column chromatography to give fraction that has toxicity against zebra fish embryos. Based on the assay-guided isolation, compound 1 was isolated. The chemical structure of 1 was elucidated using nuclear magnetic resonance (NMR) and high-resolution mass spectrometry (HRMS) data as well as comparing data with literature.Results: The CH2Cl2 layer of F. deltoidea leaves was found to inhibit breast tumor MCF-7 cells with IC50 10 µg/ml which was the most toxic among the layers. A portion of the most active layer was purified using open column chromatography to give 7 fractions. The fraction 5 showed toxicity against zebrafish embryos (LC50 35 µg/ml, 48 hpf). This fraction was purified using high performance liquid chromatography (HPLC) octadecylsilyl (ODS) column with gradient elution 70% aqueous acetonitrile (MeCN) to 100% MeCN (linear gradient) for 40 min with UV detection at 254 nm (tR = 30.99 min) to give compound 1. The chemical structure of 1 was revealed as a chlorin-type compound named methyl 10-epi-pheophorbide A.Conclusion: Methyl 10-epi-pheophorbide A was isolated for the first time from the active fraction of the Indonesian F. deltoidea leaves or tabat barito. The chemical structure including absolute stereo chemistry was elucidated using NMR and HRMS data as well as by comparison with the literature values. The 13C NMR data has been added to complete the previous report.

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Subtle changes in network composition impact the biodistribution and tumor accumulation of nanogels

Chemical Communications ◽

10.1039/c8cc05627g ◽

2018 ◽

Vol 54 (83) ◽

pp. 11777-11780 ◽

Cited By ~ 7

Author(s):

Ilona Zilkowski ◽

Ioanna Theodorou ◽

Krystyna Albrecht ◽

Frederic Ducongé ◽

Jürgen Groll

Keyword(s):

Breast Tumor ◽

Tumor Targeting ◽

Near Infrared ◽

Side Chain ◽

Human Breast ◽

Human Breast Tumor ◽

Tumor Xenografts ◽

Network Composition ◽

Tumor Accumulation

We studied the effect of subtle changes in side-chain chemistry and labelling with near infrared fluorophores of nanogels (NGs) prepared from thiolated poly(glycidol) on in vivo biodistribution in mice bearing human breast tumor xenografts. Side chain chemistry as well as labelling clearly influenced tumor targeting and overall biodistribution.

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Breast Tumor Targeting in a Mouse Model with a New Anti-MUC1 Monoclonal Antibody, PR81, Radiolabeled with 99mTc via the HYNIC

World Congress on Medical Physics and Biomedical Engineering 2006 - IFMBE Proceedings ◽

10.1007/978-3-540-36841-0_413 ◽

2007 ◽

pp. 1677-1680

Author(s):

M. Salouti ◽

H. Rajabi ◽

M. H. Babaei ◽

M. J. Rasaee ◽

R. Najafi ◽

...

Keyword(s):

Monoclonal Antibody ◽

Mouse Model ◽

Breast Tumor ◽

Tumor Targeting

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Potentiation of cell killing by fractionated radiation and suppression of proliferative recovery in MCF-7 breast tumor cells by the Vitamin D3 analog EB 1089

The Journal of Steroid Biochemistry and Molecular Biology ◽

10.1016/j.jsbmb.2004.07.011 ◽

2004 ◽

Vol 92 (5) ◽

pp. 365-374 ◽

Cited By ~ 16

Author(s):

Gerald A. DeMasters ◽

Mona S. Gupta ◽

Kara R. Jones ◽

Myles Cabot ◽

Hongtao Wang ◽

...

Keyword(s):

Tumor Cells ◽

Vitamin D3 ◽

Breast Tumor ◽

Cell Killing ◽

Breast Tumor Cells ◽

Eb 1089 ◽

Fractionated Radiation ◽

Mcf 7

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Aloe-Emodin Induces Breast Tumor Cell Apoptosis through Upregulation of miR-15a/miR-16-1 That Suppresses BCL2

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2020/5108298 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Xuefeng Jiang ◽

Yusheng Liu ◽

Guijuan Zhang ◽

Shujun Lin ◽

Jieyan Wu ◽

...

Keyword(s):

Protein Expression ◽

Cell Apoptosis ◽

Breast Tumor ◽

Protein Translation ◽

Significant Inhibition ◽

Mrna Levels ◽

Anticancer Activities ◽

Bax Protein ◽

Aloe Emodin ◽

Mcf 7

Purpose. Aloe-emodin (AE) is a natural compound derived from aloe vera and palmatum rhubarb and shows anticancer activities in various cancers. Bcl-2 family is the main regulator of cell death or cell survival. This study describes the effects of AE on proliferation of breast tumor (BT) cells. Methods. MCF-10A, MCF-10AT, MCF-7, and MDA-MB-231 cell lines were exposed to AE. Cell proliferation and apoptosis were assessed by CCK-8 and flow cytometry. Protein levels were measured by Western blotting. The levels of mRNA and miRNA were examined by RT-PCR. Bioinformatics was applied to screen miRNAs that bind to 3′-UTR of mRNA. Results. The results showed that AE selective activity inhibited the proliferation and induced apoptosis of MCF-10AT and MCF-7 cells but exhibited no significant inhibition in MCF10A and MDA-MB-231 cells. Mechanistically, AE dose-dependently decreased the protein expression of Bcl-2 and Bcl-xl, while it increased Bax protein expression in MCF-10AT and MCF-7 cells. The levels of Bcl-xl and Bax mRNA were altered by AE treatment, which was consistent with the protein expression results. However, Bcl-2 mRNA levels were not affected in either cell line, suggesting that AE may modulate the protein translation of Bcl-2 through miRNAs. In all candidate miRNAs that bind to 3′-UTR of Bcl-2, miR-15a and miR-16-1 were dose-dependently downregulated by AE. Moreover, inhibition of miR-15a/16-1 could eliminate the inhibition of MCF-10AT and MCF-7 cells growth by AE and could reverse the downregulation of AE-induced Bcl-2 protein level. Conclusion. Our research provides an important basis that AE induces BT cell apoptosis through upregulation of miR-15a/miR-16-1 that suppresses BCL2.

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