Multifunctional Carbon dot anchored halloysite nanotube: nanovehicle for cisplatin drug release, cytotoxicity on breast cancer cells and DNA binding studies

2022 ◽  
pp. 100827
Author(s):  
M.K. Prashanth ◽  
K. Chaitra ◽  
Prakash Krishnaiah ◽  
K.N. Prashanth ◽  
K. Yogesh kumar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Binding ◽  
Drug Release ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Binding Studies ◽  
Halloysite Nanotube ◽  
Carbon Dot ◽  
Dna Binding Studies

scholarly journals A Novel Organometallic Rhenium Salt: DNA-Binding and Cytotoxicity Studies on Pancreatic, Breast and Lymphoma Cancers

2021 ◽  
Author(s):  
Christopher C. Krauss ◽  
Birsen Y. Varisli ◽  
Angela J. Winstead ◽  
Paul T. Wilder ◽  
David J. Weber ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Binding ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Carbonyl Complexes ◽  
Binding Studies ◽  
Pancreatic Cancer Cells ◽  
Cytotoxicity Studies ◽  
Estrogen Receptor Positive ◽  
Dna Binding Studies

Abstract DNA-binding studies of a variety of rhenium(I) tricarbonyl complexes are known. Primarily the rhenium complexes bind to DNA through intercalation or minor groove or both. We synthesized a novel organometallic salt of the type, [Re(µ-H)Re]+[Re(µ-OR)3Re]-. The UV-vis and emission spectroscopic titrations and viscosity studies indicate that the salt binds to DNA through partial intercalation. A variety of mono-, di-, and trinuclear rhenium(I) carbonyl complexes are known to exhibit cytotoxicity against numerous cancer cell lines. Examples of the cytotoxicity of tetranuclear rhenium (I) tricarbonyl complexes are rare. We have found that the tetranuclear, novel organometallic salt is highly potent on numerous cancer cells. The IC50 values (concentrations required to induce 50% cell deaths) are 0.220 µM on BxPC-3 pancreatic cancer cells, 0.298 µM on estrogen receptor positive MCF-7 breast cancer cells, 0.948 µM on triple negative MDA-MB-231 breast cancer cells, and 0.300 µM on U-937 lymphoma cells.

scholarly journals Screening antiproliferative drug for breast cancer from bisbenzylisoquinoline alkaloid tetrandrine and fangchinoline derivatives by targeting BLM helicase

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Wangming Zhang ◽  
Shuang Yang ◽  
Jinhe Liu ◽  
Linchun Bao ◽  
He Lu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Binding ◽  
Small Molecules ◽  
Cancer Cells ◽  
Small Molecule ◽  
Breast Cancer Cells ◽  
Dna Unwinding ◽  
Protein Levels ◽  
Blm Helicase ◽  
Bisbenzylisoquinoline Alkaloids

Abstract Background The high expression of BLM (Bloom syndrome) helicase in tumors involves its strong association with cell expansion. Bisbenzylisoquinoline alkaloids own an antitumor property and have developed as candidates for anticancer drugs. This paper aimed to screen potential antiproliferative small molecules from 12 small molecules (the derivatives of bisbenzylisoquinoline alkaloids tetrandrine and fangchinoline) by targeting BLM642–1290 helicase. Then we explore the inhibitory mechanism of those small molecules on proliferation of MDA-MB-435 breast cancer cells. Methods Fluorescence polarization technique was used to screen small molecules which inhibited the DNA binding and unwinding of BLM642–1290 helicase. The effects of positive small molecules on the ATPase and conformation of BLM642–1290 helicase were studied by the malachite green-phosphate ammonium molybdate colorimetry and ultraviolet spectral scanning, respectively. The effects of positive small molecules on growth of MDA-MB-435 cells were studied by MTT method, colony formation and cell counting method. The mRNA and protein levels of BLM helicase in the MDA-MB-435 cells after positive small molecule treatments were examined by RT-PCR and ELISA, respectively. Results The compound HJNO (a tetrandrine derivative) was screened out which inhibited the DNA binding, unwinding and ATPase of BLM642–1290 helicase. That HJNO could bind BLM642–1290helicase to change its conformationcontribute to inhibiting the DNA binding, ATPase and DNA unwinding of BLM642–1290 helicase. In addition, HJNO showed its inhibiting the growth of MDA-MB-435 cells. The values of IC50 after drug treatments for 24 h, 48 h and 72 h were 19.9 μmol/L, 4.1 μmol/L and 10.9 μmol/L, respectively. The mRNA and protein levels of BLM helicase in MDA-MB-435 cells increased after HJNO treatment. Those showed a significant difference (P < 0.05) compared with negative control when the concentrations of HJNO were 5 μmol/L and 10 μmol/L, which might contribute to HJNO inhibiting the DNA binding, ATPase and DNA unwinding of BLM helicase. Conclusion The small molecule HJNO was screened out by targeting BLM642–1290 helicase. And it showed an inhibition on MDA-MB-435 breast cancer cells expansion.

The biological activity of G-quadruplex DNA binding papaverine-derived ligand in breast cancer cells

2008 ◽  
Vol 27 (4) ◽  
pp. 289-296 ◽  
Author(s):  
Blazej Rubis ◽  
Mariusz Kaczmarek ◽  
Natalia Szymanowska ◽  
Elzbieta Galezowska ◽  
Andrzej Czyrski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Biological Activity ◽  
Dna Binding ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Quadruplex Dna ◽  
G Quadruplex

scholarly journals Estrogen Withdrawal-Induced NF-κB Activity and Bcl-3 Expression in Breast Cancer Cells: Roles in Growth and Hormone Independence

2003 ◽  
Vol 23 (19) ◽  
pp. 6887-6900 ◽  
Author(s):  
M. A. Christine Pratt ◽  
Tanya E. Bishop ◽  
Dawn White ◽  
Gordon Yasvinski ◽  
Michel Ménard ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Binding ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Stable Form ◽  
Estrogen Withdrawal ◽  
Hormone Independence ◽  
Mcf 7

ABSTRACT About one-third of breast cancers express a functional estrogen (β-estradiol [E2]) receptor (ER) and are initially dependent on E2 for growth and survival but eventually progress to hormone independence. We show here that ER+, E2-independent MCF-7/LCC1 cells derived from E2-dependent MCF-7 cells contain elevated basal NF-κB activity and elevated expression of the transcriptional coactivator Bcl-3 compared with the parental MCF-7 line. LCC1 NF-κB activity consists primarily of p50 dimers, although low levels of a p65/p50 complex are also present. The ER− breast cancer cell lines harbor abundant levels of both NF-κB complexes. In contrast, nuclear extracts from MCF-7 cells contain a significantly lower level of p50 and p65 than do LCC1 cells. Estrogen withdrawal increases both NF-κB DNA binding activity and expression of Bcl-3 in MCF-7 and LCC1 cells in vitro and in vivo. Tumors derived from MCF-7 cells ectopically expressing Bcl-3 remain E2 dependent but display a markedly higher tumor establishment and growth rate compared to controls. Expression of a stable form of IκBα in LCC1 cells severely reduced nuclear expression of p65 and the p65/p50 DNA binding heterodimer. Whereas LCC1 tumors in nude mice were stable or grew, LCC1(IκBα) tumors regressed after E2 withdrawal. Thus, both p50/Bcl-3- and p65/p50-associated NF-κB activities are activated early in progression and serve differential roles in growth and hormone independence, respectively. We propose that E2 withdrawal may initiate selection for hormone independence in breast cancer cells by activation of NF-κB and Bcl-3, which could then supplant E2 by providing both survival and growth signals.

scholarly journals Development and Characterization of Nanoliposomal Hydroxyurea Against BT-474 Breast Cancer Cells

2019 ◽  
Vol 10 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Azam Akbari ◽  
Azim Akbarzadeh ◽  
Morteza Rafiee Tehrani ◽  
Reza Ahangari Cohan ◽  
Mohsen Chiani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Release ◽  
Zeta Potential ◽  
Cancer Cells ◽  
Cellular Uptake ◽  
Breast Cancer Cells ◽  
Drug Carriers ◽  
Diffusion Method ◽  
Diphenyl Tetrazolium Bromide

Purpose: Hydroxyurea (HU) is a well-known chemotherapy drug with several side effects which limit its clinical application. This study was conducted to improve its therapeutic efficiency against breast cancer using liposomes as FDA-approved drug carriers. Methods: PEGylated nanoliposomes-containing HU (NL-HU) were made via a thin-film hydration method, and assessed in terms of zeta potential, size, morphology, release, stability, cellular uptake, and cytotoxicity. The particle size and zeta potential of NL-HU were specified by zeta-sizer. The drug release from liposomes was assessed by dialysis diffusion method. Cellular uptake was evaluated by flow cytometry. The cytotoxicity was designated by methyl thiazolyl diphenyl-tetrazolium bromide (MTT) test. Results: The size and zeta value of NL-HU were gotten as 85 nm and -27 mV, respectively. NL-HU were spherical.NL-HU vesicles were detected to be stable for two months. The slow drug release and Weibull kinetic model were obtained. Liposomes considerably enhanced the uptake of HU into BT-474 human breast cancer cells. The cytotoxicity of NL-HU on BT-474 cells was found to be significantly more than that of free HU. Conclusion: The results confirmed these PEGylated nanoliposomes containing drug are potentially suitable against in vitro model of breast cancer.

Preparation and In-vitro Evaluation of Levan Micelles: A Polyfructan Based Nano-carrier for Breast Cancer Targeted Delivery

2019 ◽  
Vol 9 (2) ◽  
pp. 97-107 ◽  
Author(s):  
Parth Patel ◽  
Yadvendrakumar Agrawal
Keyword(s):  
Breast Cancer ◽  
Kinetic Model ◽  
Drug Release ◽  
Critical Micelle Concentration ◽  
Cancer Cells ◽  
Cell Line ◽  
Targeted Delivery ◽  
Breast Cancer Cells ◽  
Ic50 Value

Background: Levans are biopolymers of fructose, produced by different microorganisms. Fructose present in the levan micelles binds with the Glucose Transporter 5 (GLUT 5) which is overexpressed in the breast cancer cells. Objective: Increased solubility of paclitaxel by loading in the GLUT 5 transporter targeted levan-based micelles may enhance its bioavailability and facilitate a targeted delivery to the breast cancer cells. Methods and Results: Critical micelle concentration of levan with an average molecular weight of 800,000 Dalton was found to be 0.125µM corresponding to 0.1mg/mL using pyrene I3/I1 method. At critical micelle concentration (CMC), levan formed very mono-disperse (PDI-0.082) micellar particles with a particle size of 153.1 ± 2.31nm and -14.6 ± 2mV zeta potential. In-vitro drug release study was performed to identify the fit kinetic model along with Fourier transform infrared analysis and Differential scanning calorimetry studies. In-vitro kinetic model fitting revealed first-order drug release from the prepared micellar composition. The drug-loaded micellar composition was studied for its anticancer activity in breast cancer cell line. The IC50 value obtained was 1.525 ± 0.11nM on MCF7 cell line. Conclusion: Paclitaxel micelles showed a nineteen-fold improvement in the IC50 value compared to free paclitaxel. Hemocompatibility study was performed with a view to parenteral administration. This solution containing drug was found to be hemocompatible when added to bovine blood in 1:4 ration. Micelles are proven fairly compatible on the basis of hemolysis test results.

Unliganded and Liganded Estrogen Receptors Protect against Cancer Invasion via Different Mechanisms

2000 ◽  
Vol 14 (7) ◽  
pp. 999-1009 ◽  
Author(s):  
Nadine Platet ◽  
Séverine Cunat ◽  
Dany Chalbos ◽  
Henri Rochefort ◽  
Marcel Garcia
Keyword(s):  
Breast Cancer ◽  
Amino Acids ◽  
Dna Binding ◽  
Cancer Cells ◽  
Zinc Finger ◽  
Transcriptional Activation ◽  
Breast Cancer Cells ◽  
Cancer Invasion ◽  
Specific Gene ◽  
Matrigel Invasion

Abstract While estrogens are mitogenic in breast cancer cells, the presence of estrogen receptor α (ERα) clinically indicates a favorable prognosis in breast carcinoma. To improve our understanding of ERα action in breast cancer, we used an original in vitro method, which combines transient transfection and Matrigel invasion assays to examine its effects on cell invasiveness. ERα expression in MDA-MB-231 breast cancer cells reduced their invasiveness by 3-fold in the absence of hormone and by 7-fold in its presence. Integrity of hormone and DNA-binding domains and activating function 2 were required for estradiol-induced inhibition, suggesting that transcriptional activation of estrogen target genes was involved. In contrast, these domains were dispensable for hormone-independent inhibition. Analysis of deletion mutants of ERα indicated that amino acids 179–215, containing the N-terminal zinc finger of the DNA-binding domain, were required for ligand-independent receptor action. Among different members of the nuclear receptor family, only unliganded ERα and ERβ reduced invasion. Calreticulin, a Ca2+-binding protein that could interact with amino acids 206–211 of ERα, reversed hormone-independent ERα inhibition of invasion. However, since calreticulin alone also inhibited invasion, we propose that this protein probably prevents ERα interaction with another unidentified invasion-regulating factor. The inhibitor role of the unliganded ER was also suggested in three ERα-positive cell lines, where ERα content was inversely correlated with cell migration. We conclude that ERα protects against cancer invasion in its unliganded form, probably by protein-protein interactions with the N-terminal zinc finger region, and after hormone binding by activation of specific gene transcription.

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