Potential of bacterial culture media in biofabrication of metal nanoparticles and the therapeutic potential of the as-synthesized nanoparticles in conjunction with artemisinin against MDA-MB-231 breast cancer cells

2018 ◽  
Vol 234 (5) ◽  
pp. 6951-6964 ◽  
Author(s):  
Badrealam Farheen Khan ◽  
Hamidullah ◽  
Sonam Dwivedi ◽  
Rituraj Konwar ◽  
Swaleha Zubair ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metal Nanoparticles ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Bacterial Culture ◽  
Therapeutic Potential ◽  
Culture Media

scholarly journals Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway

2019 ◽  
Vol 21 (1) ◽  
pp. 131 ◽  
Author(s):  
Jinxia Qiu ◽  
Tao Zhang ◽  
Xinying Zhu ◽  
Chao Yang ◽  
Yaxing Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mouse Model ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Caspase 3 ◽  
Therapeutic Potential ◽  
B Cell Lymphoma ◽  
Flavonoid Glycosides

Hyperoside (quercetin 3-o-β-d-galactopyranoside) is one of the flavonoid glycosides with anti-inflammatory, antidepressant, and anti-cancer effects. But it remains unknown whether it had effects on breast cancer. Here, different concentrations of hyperoside were used to explore its therapeutic potential in both breast cancer cells and subcutaneous homotransplant mouse model. CCK-8 and wound healing assays showed that the viability and migration capability of Michigan Cancer Foundation-7 (MCF-7) and 4T1 cells were inhibited by hyperoside, while the apoptosis of cells were increased. Real-time quantitative PCR (qRT-PCR) and western blot analysis were used to detect mRNA and the protein level, respectively, which showed decreased levels of B cell lymphoma-2 (Bcl-2) and X-linked inhibitor of apoptosis (XIAP), and increased levels of Bax and cleaved caspase-3. After exploration of the potential mechanism, we found that reactive oxygen species (ROS) production was reduced by the administration of hyperoside, which subsequently inhibited the activation of NF-κB signaling pathway. Tumor volume was significantly decreased in subcutaneous homotransplant mouse model in hyperoside-treated group, which was consistent with our study in vitro. These results indicated that hyperoside acted as an anticancer drug through ROS-related apoptosis and its mechanism included activation of the Bax–caspase-3 axis and the inhibition of the NF-κB signaling pathway.

Effects of the Gold Nanoparticles (AuNPs) on the Proliferation and Morphological Characteristics of Human Breast Cancer Cells (MCF-7) in Culture

2017 ◽  
Vol 268 ◽  
pp. 254-258 ◽  
Author(s):  
Nur Shafawati Rosli ◽  
Azhar Abdul Rahman ◽  
Azlan Abdul Aziz ◽  
Shaharum Shamsuddin ◽  
Nurul Sabihah Zakaria
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Culture Media ◽  
Morphological Changes ◽  
Morphological Characteristics ◽  
Morphological Observation ◽  
Duration Of Treatment ◽  
Significant Difference ◽  
Mcf 7

Ultrastructural characteristic and morphological changes of untreated and treated breast cancer MCF-7 cells were observed by energy-filtered transmission electron microscope (EFTEM). Morphological observation of MCF-7 after being treated with 13 nm, 50 nm, and 70 nm AuNPs, were looking unhealthy and dying out of the populace, the observed cells were more reduced and dying as treatment with 50 nm and 70 nm AuNPs. Cells detachment, clumping, shrunken, and dispersed cells in the culture medium and floating cells were also observed. The observed morphological changes increase in 50 nm and 70 nm AuNPs than in 13 nm AuNPs, which is less toxic to MCF-7 cells. The presented morphological analysis has established that 13 nm AuNPs showed less toxic to MCF-7 breast cancer cells. Whereas, control cells of MCF-7 were treated with only complete culture media, despite the duration of treatment, whereby the cells maintained most of their morphological features and observed to have a typical morphology of healthy cells that are well attached to the surface. These results indicate that AuNPs were clustered in the cells and there was no significant difference between images of different sizes of AuNPs observed in the cells, because the AuNPs always clustered together inside the cells.

C/EBPδ Modulates Cell Growth, Differentiation and Apoptosis of Myeloid Leukemia, Prostate and Breast Cancer Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4300-4300
Author(s):  
Sigal Gery ◽  
Sakae Stanosaki ◽  
Takayuki Ikezoe ◽  
Wolf K. Hofmann ◽  
Adrian F. Gombart ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Myeloid Leukemia ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Critical Role ◽  
Leukemic Cells ◽  
Granulocytic Differentiation ◽  
Mcf 7

Abstract C/EBPδ belongs to the family of highly conserved CCAAT/enhancer binding protein (C/EBP) transcription factors. Members of this family play a critical role in the regulation of mitotic growth arrest and differentiation in numerous cell types. To examine the consequences of C/EPBδ expression, we transfected C/EPBδ into CML myeloid leukemia (KCL22, K562), prostate (LNCaP, PC3, DU145), and breast (MCF-7, T47D, MDA-MB-231) cancer cell lines. C/EBPδ expression resulted in a proliferative arrest and an increase in apoptosis of the myeloid leukemia cells, as well as the prostate cells LNCaP and PC3, and the breast cells MCF-7 and T47D. In contrast, DU145 prostate and MDA-MB-231 breast cancer cells were not inhibited by C/EBPδ, indicating that the biologically properties of C/EBPδ depend upon its cellular context. We further studied the molecular mechanisms underlying the affect of C/EPBδ expression in CML leukemic cells. Myeloid differentiation of KCL22 and K562 blast cells as shown by morphologic changes and induction of secondary specific granule genes, occurred within 4 days of inducing expression of C/EBPδ. Furthermore, expression of C/EBPδ was associated with downregulation of c-Myc and cyclin E, and upregulation of the forkhead transcription factor FoxO1a (FKHR) and the cyclin-dependent kinase inhibitor p27Kip1. In addition, microarray analysis showed that C/EBPδ mRNA is upregulated during granulocytic differentiation of normal CD34+ bone marrow cells, suggesting that C/EBPδ is involved in lineage-specific differentiation. Taken together, these results show that expression of C/EBPδ in BCR-ABL-positive CML cells in blast crisis, is sufficient for neutrophil differentiation and suggest that ectopic induction of C/EBPδ in the blastic phase of CML, as well as in certain cases of prostate and breast cancers, may hold promising therapeutic potential.

scholarly journals Typhonium flagelliforme decreases telomerase expression in HeLa cervical cancer cells

2016 ◽  
Vol 35 (1) ◽  
pp. 3
Author(s):  
Endang Purwaningsih ◽  
Yulia Suciati ◽  
Etty Widayanti
Keyword(s):  
Breast Cancer ◽  
Cervical Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Culture Media ◽  
Vero Cells ◽  
Telomerase Activity ◽  
Multiple Comparison Test ◽  
Cervical Cancer Cells ◽  
Experimental Laboratory

<p><strong>Background</strong><br /> Cancer cells have a relatively high telomerase activity compared to normal cells, so that cancer cells have the ability for continued proliferation and uncontrolled mitosis. Telomerase is an enzyme responsible for the length of telomeres, DNA segments located at the ends of eukaryotic chromosomes. Natural materials such as rodent tuber (<em>Typhonium flagelliforme</em>) have anticancer potential. The purpose of the present study was to determine the effects of <em>Typhonium flagelliforme </em>extract on telomerase expression in HeLa cervical cancer and T47D breast cancer cells.</p><p><br /> <strong>Methods </strong></p><p>This experimental laboratory study was conducted on cultured HeLa and T47D cancer cell lines, with normal Vero cells as controls, and using RPMI and M199 culture media. The study comprised three groups, i.e. controls, and groups receiving <em>Typhonium flagelliforme </em>extract at doses of ½ IC50 and IC50. Telomerase expression was measured by immunohistochemistry (IHC). Analysis of variance and LSD multiple comparison test were used to analyze the data.</p><p><strong> </strong></p><p><strong>Results </strong><br /> Telomerase expression in cancer cells showed significantly higher values compared to normal Vero cells. <em>Typhonium flagelliforme</em> extract was capable of significantly decreasing telomerase expression in cancer cells receiving the extract.</p><p><strong> </strong></p><strong>Conclusion </strong><br /> <em>Typhonium flagelliforme</em> extract at different doses is capable of decreasing telomerase expression more effectively in cervical cancer cells than in breast cancer cells. This study shows that <em>Typhonium flagelliforme</em> may have anti-cancer activity, necessitating further investigations.

scholarly journals Therapeutic potential of xanthones from Swertia chirata in breast cancer cells

2020 ◽  
Vol 152 (3) ◽  
pp. 285
Author(s):  
Prosenjit Saha ◽  
Atish Barua ◽  
Pritha Choudhury ◽  
Suvra Mandal ◽  
ChinmayKumar Panda
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Therapeutic Potential ◽  
Swertia Chirata

scholarly journals Unacylated ghrelin and AZP531 suppress the 3D growth of breast cancers

2020 ◽  
Author(s):  
CheukMan C. Au ◽  
John B. Furness ◽  
Kara Britt ◽  
Sofya Oshchepkova ◽  
Heta Ladumor ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Mechanism Of Action ◽  
Breast Cancer Cells ◽  
Therapeutic Potential ◽  
3D Culture ◽  
Mapk Signaling ◽  
Unacylated Ghrelin ◽  
Ghrelin Receptor

ABSTRACTBreast cancer is the most common type of cancer in women and notwithstanding important therapeutic advances, it remains the second leading cause of cancer-related death in the US. Despite extensive research relating to the hormone ghrelin, responsible for the stimulation of growth hormone release and appetite, little is known of the effects of its unacylated form, especially in cancer. One major area of research relates to its reported effects to increase insulin sensitivity in diabetics, this being the basis for the development of unacylated ghrelin analog, AZP531 or livoletide, now in clinical trials for the treatment of Prader-Willi Syndrome. The mechanism of action of unacylated ghrelin is largely uncharacterized, in any system, because it does not bind to or activate the cognate ghrelin receptor, GHSR1a. The present study aimed to characterize effects of unacylated ghrelin on breast cancer cells, define its mechanism of action, and explore the therapeutic potential of unacylated ghrelin or analog AZP531. We report potent effects of unacylated ghrelin, at picomolar doses, on the growth of breast cancer cells, dependent on 3D culture and activation of Gαi. Suppression of MAPK signaling by unacylated ghrelin leads to cell cycle arrest and apoptosis. AZP531 also suppresses the growth of breast cancer cells in vitro and in xenografts, and may be a novel approach for the safe and effective treatment of breast cancer.

Matriptase activation and shedding with HAI-1 is induced by steroid sex hormones in human prostate cancer cells, but not in breast cancer cells

2006 ◽  
Vol 291 (1) ◽  
pp. C40-C49 ◽  
Author(s):  
Ken-ichi Kiyomiya ◽  
Ming-Shyue Lee ◽  
I-Chu Tseng ◽  
Hong Zuo ◽  
Robert J. Barndt ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Synthesis ◽  
Cancer Cells ◽  
Sex Hormones ◽  
Breast Cancer Cells ◽  
Culture Media ◽  
Protein Synthesis Inhibitor ◽  
Lncap Cells ◽  
Synthesis Inhibitor ◽  
Steroid Sex Hormones

Matriptase and its cognate inhibitor, hepatocyte growth factor activator inhibitor-1 (HAI-1), have been implicated in carcinoma onset and malignant progression. However, the pathological mechanisms of matriptase activation are not defined. Steroid sex hormones play crucial roles in prostate and breast cancer. Therefore, we investigated the questions of whether and how steroid sex hormones regulate matriptase activation in these cancer cells. Treatment of cells with 17β-estradiol had no effect on activation of matriptase in hormone-starved breast cancer cells, in part due to their high constitutive level of activated matriptase. In striking contrast, very low levels of activated matriptase were detected in hormone-starved lymph node prostatic adenocarcinoma (LNCaP) cells. Robust activation of matriptase was observed as early as 6 h after exposure of these cells to 5α-dihydrotestosterone (DHT). Activation of matriptase was closely followed by shedding of the activated matriptase with >90% of total activated matriptase present in the culture media 24 h after DHT treatment. Activated matriptase was shed in a complex with HAI-1 and may result from simultaneously proteolytic cleavages of both membrane-bound proteins. Latent matriptase and free HAI-1 were also shed into culture media. As a result of shedding, the cellular levels of matriptase and HAI-1 were significantly reduced 24 h after exposure to DHT. DHT-induced matriptase activation and shedding were significantly inhibited by the androgen antagonist bicalutamide, by the RNA transcription inhibitor actinomycin D, and by the protein synthesis inhibitor cycloheximide. These results suggest that in LNCaP cells, androgen induces matriptase activation via the androgen receptor, and requires transcription and protein synthesis.

scholarly journals hTERT Downregulation Attenuates Resistance to DOX, Impairs FAK-Mediated Adhesion, and Leads to Autophagy Induction in Breast Cancer Cells

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 867
Author(s):  
Aleksandra Romaniuk-Drapała ◽  
Ewa Totoń ◽  
Natalia Konieczna ◽  
Marta Machnik ◽  
Wojciech Barczak ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Therapeutic Potential ◽  
Telomerase Activity ◽  
Telomere Maintenance ◽  
Population Doubling ◽  
Cell Cycle Distribution ◽  
Human Telomerase Reverse Transcriptase ◽  
Human Telomerase

Telomerase is known to contribute to telomere maintenance and to provide cancer cell immortality. However, numerous reports are showing that the function of the enzyme goes far beyond chromosome ends. The study aimed to explore how telomerase downregulation in MCF7 and MDA-MB-231 breast cancer cells affects their ability to survive. Consequently, sensitivity to drug resistance, proliferation, and adhesion were assessed. The lentiviral-mediated human telomerase reverse transcriptase (hTERT) downregulation efficiency was performed at gene expression and protein level using qPCR and Western blot, respectively. Telomerase activity was evaluated using the Telomeric Repeat Amplification Protocol (TRAP) assay. The study revealed that hTERT downregulation led to an increased sensitivity of breast cancer cells to doxorubicin which was demonstrated in MTT and clonogenic assays. During a long-term doubling time assessment, a decreased population doubling level was observed. Interestingly, it did not dramatically affect cell cycle distribution. hTERT downregulation was accompanied by an alteration in β1-integrin- and by focal adhesion kinase (FAK)-driven pathways together with the reduction of target proteins phosphorylation, i.e., paxillin and c-Src. Additionally, autophagy activation was observed in MDA-MB-231 cells manifested by alternations in Atg5, Beclin 1, LC3II/I ratio, and p62. These results provide new evidence supporting the possible therapeutic potential of telomerase downregulation leading to induction of autophagy and cancer cells elimination.

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