Arthrospira Platensis Mediated Green Biosynthesis of Silver Nanoparticlesas Breast Cancer Controlling Agent: In-vitro and In-vivo Safety Approach.

2021 ◽  
Author(s):  
Nehal El Deeb ◽  
Mai A. Abo-Eleneen ◽  
Omyma A. Awad ◽  
Atef M. Abo-Shady
Keyword(s):  
Breast Cancer ◽  
Survival Rates ◽  
Arthrospira Platensis ◽  
Active Metabolites ◽  
Protein Marker ◽  
Anticancer Efficacy ◽  
Protein Levels ◽  
Albino Mice

Abstract Biogenic Silver Nanoparticle (bio-AgNPs) is one of the most fascinating nanomaterials used in the biomedical purposes. In the current study, we biosynthesized AgNPs (bio-AgNPs) using Arthrospira platensis(A-bio-AgNPs), Microcystis aeruginosa(M-bio-AgNPs)and Chlorella vulgaris(C-bio-AgNPs) active metabolites and evaluated their anticancer efficacy against breast cancer. The recovered bio-AgNPs were characterized using Scanning and Transmission Electron Microscopy (SEM and TEM) and their safety profiles were monitoring in-vitro on PBMCs cells and in-vivo on Albino mice. The obtained results indicated the safety usage of bio-AgNPs at concentration of 0.1 mg/ml on PBMCs cells and 1.5mg/ml on the Albino mice. The bio-AgNPs displayed dose-dependent cytotoxic effects against HepG-2, CaCO-2 and MCF-7 cell lines by inducing ROS and arresting the treated cells in G0/G1 and sub G0 phases. In addition, A-bio-AgNPs induced breast cancer cellular apoptosis by down regulating the expression of survivin, MMP7, TGF and Bcl2 genes. Upon A-bio-AgNPs treatment, a significant reduction in tumor growth and prolonged survival rates were recorded in breast cancer BALB/c model. Furthermore, A-bio-AgNPs treatment significant decreased theKi 67 protein marker from 60% (in the untreated group) to 20% and increased Caspase 3 protein levels to 65% (in treated groups) comparing with 45% (in Doxorubicin treated groups).

scholarly journals Arthrospira platensis Mediated Biosynthesis of Silver Nanoparticles as Breast Cancer Proliferation and Differentiation Controlling agent: In-vitro and In-vivo Safety Approach

2021 ◽  
Author(s):  
Nehal El Deeb ◽  
Mai Abo-Eleneen ◽  
Omyma Awad ◽  
Atef Aboshady
Keyword(s):  
Breast Cancer ◽  
Silver Nanoparticles ◽  
Arthrospira Platensis ◽  
Mice Model ◽  
Cancer Proliferation ◽  
Protein Marker ◽  
Ki 67 ◽  
Protein Levels

Abstract Biogenic Silver nanoparticles (AgNPs) are one of the most fascinating nanomaterials used in biomedical purposes. In the current study, we biosynthesized AgNPs using Arthrospira platensis, Microcystis aeruginosa and Chlorella vulgarisactive metabolites and evaluate their efficacy against breast cancer. The recovered AgNPs was characterized using scanning and transmission electron microscopy (SEM and TEM). The safety usage of bio-AgNPs was tested in-vitro on PBMCs cells and in-vivo. The obtained results indicated the safety usage of bio-AgNPs at concentration 0.1 mg/ml on PBMCs cells and 1.5mg/ml on the tested Albino mice. The bio-AgNPs displayed dose-dependent cytotoxicity (0.1 mg/ml) against HepG-2, CaCO-2 and MCF-7 cell lines via ROS induction and arresting treated cells in G0/G1 and sub G0 phases. In addition, Arthrospira bio-AgNPs treatment induced cellular apoptosis in breast cancer cells via the down regulation of survivin, MMP7, TGF and Bcl2 genes expressions. Upon Arthrospira bio-AgNPs treatment, a great delay in tumor growth and prolonged survival were recorded in breast cancer mice model. Furthermore, after Arthrospira bio-AgNPs treatment, a great reduction in Ki 67 protein marker from 60% to be 20% and was recorded and an elevation in Caspase 3 protein levels was recorded in treated groups with percentage 65% comparing with 45% in Doxorubicin treated groups.

scholarly journals Repurposing of Fluvastatin as an Anticancer Agent against Breast Cancer Stem Cells via Encapsulation in a Hyaluronan-Conjugated Liposome

Pharmaceutics ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 1133
Author(s):  
Ji Yu ◽  
Dae Shin ◽  
Jin-Seok Kim
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Body Weight Loss ◽  
Breast Cancer Stem Cells ◽  
Anticancer Efficacy

Fluvastatin (FLUVA), which is a common anti-hypercholesterolemia drug, exhibits potential anticancer activity as it suppresses the proliferation, angiogenesis, and metastasis of breast cancer cells via inhibiting 3-hydroxy-methyl glutaryl-coenzyme A (HMG-CoA) reductase. In this study, hyaluronan-conjugated FLUVA-encapsulating liposomes (HA-L-FLUVA) were evaluated for their anticancer efficacy in vitro and in vivo. The particle size, zeta potential, and encapsulation efficiency of HA-L-FLUVA were 158.36 ± 1.78 nm, −24.85 ± 6.26 mV, and 35%, respectively. Growth inhibition of breast cancer stem cells (BCSCs) by HA-L-FLUVA was more effective than that by free FLUVA. The half maximal inhibitory concentration (IC50) values of FLUVA, L-FLVUA, and HA-L-FLUVA were 0.16, 0.17, and 0.09 μM, respectively. The in vivo anticancer effect of HA-L-FLUVA in combination with doxorubicin (DOX) was more effective than that of free FLUVA, free DOX, and HA-L-FLUVA. The longest survival of mice was achieved by treatment with FLUVA (15 mg/kg) and HA-L-FLUVA (15 mg/kg) + DOX (3 mg/kg), followed by HA-L-FLUVA (15 mg/kg), Dulbecco’s phosphate buffered saline, and DOX (3 mg/kg). No more than 10% body weight loss was observed in the mice injected with FLUVA, indicating that the drug was not toxic. Taken together, these results indicate that HA-L-FLUVA could serve as an effective anticancer drug by inhibiting the growth of both breast cancer cells and cancer stem cells.

scholarly journals The anticancer efficacy of paclitaxel liposomes modified with low-toxicity hydrophobic cell-penetrating peptides in breast cancer: an in vitro and in vivo evaluation

RSC Advances ◽  
2018 ◽  
Vol 8 (43) ◽  
pp. 24084-24093 ◽  
Author(s):  
Qi Zhang ◽  
Jing Wang ◽  
Hao Zhang ◽  
Dan Liu ◽  
Linlin Ming ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Delivery ◽  
Cell Penetrating Peptides ◽  
Cell Penetrating Peptide ◽  
In Vivo Evaluation ◽  
Anticancer Efficacy ◽  
Cell Penetrating ◽  
Low Toxicity

Hydrophobic cell penetrating peptide PFVYLI-modified liposomes have been developed for the targeted delivery of PTX into tumors.

scholarly journals DCTPP1, an Oncogene Regulated by miR-378a-3p, Promotes Proliferation of Breast Cancer via DNA Repair Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Ming Niu ◽  
Ming Shan ◽  
Yang Liu ◽  
Yanni Song ◽  
Ji-guang Han ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Survival Rates ◽  
The Other ◽  
Poor Survival ◽  
Induced Apoptosis ◽  
Cell Growth And Proliferation

Breast cancer (BRCA) is one of the most deadly cancers worldwide, with poor survival rates that could be due to its high proliferation. Human all-alpha dCTP pyrophosphatase 1 (DCTPP1) is implicated in numerous diseases, including cancers. However, its role in BRCA is unclear. In this study, we used bioinformatic analyses of the ONCOMINE, UALCAN, and GEPIA databases to determine the expression pattern of DCTPP1 in BRCA. We found that elevated DCTPP1 levels correlate with poor BRCA prognosis. DCTPP1 silencing inhibited BRCA cell proliferation and induced apoptosis in vitro, as well as in vivo. Our data show that this tumorigenic effect depends on DNA repair signaling. Moreover, we found that DCTPP1 is directly modulated by miR-378a-3p, whose downregulation is linked to BRCA progression. Our results showed down-regulation of miR-378a-3p in BRCA. Upregulation of miR-378a-3p, on the other hand, can inhibit BRCA cell growth and proliferation. This study shows that reduced miR-378a-3p level enhances DCTPP1 expression in BRCA, which promotes proliferation by activating DNA repair signaling in BRCA.

scholarly journals Nanoparticles Loaded with the BET Inhibitor JQ1 Block the Growth of Triple Negative Breast Cancer Cells In Vitro and In Vivo

Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 91 ◽  
Author(s):  
Valentina Maggisano ◽  
Marilena Celano ◽  
Rocco Malivindi ◽  
Ines Barone ◽  
Donato Cosco ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Anticancer Efficacy ◽  
Bet Inhibitor ◽  
Physico Chemical ◽  
And Migration

Inhibition of bromo-and extra-terminal domain (BET) proteins, epigenetic regulators of genes involved in cell viability, has been efficiently tested in preclinical models of triple negative breast cancer (TNBC). However, the use of the selective BET-inhibitor JQ1 on humans is limited by its very short half-life. Herein, we developed, characterized and tested a novel formulation of nanoparticles containing JQ1 (N-JQ1) against TNBC in vitro and in vivo. N-JQ1, prepared using the nanoprecipitation method of preformedpoly-lactid-co-glycolic acid in an aqueous solution containing JQ1 and poloxamer-188 as a stabilizer, presented a high physico-chemical stability. Treatment of MDA-MB 157 and MDA-MB 231 TNBC cells with N-JQ1 determined a significant decrease in cell viability, adhesion and migration. Intra-peritoneal administration (5 days/week for two weeks) of N-JQ1 in nude mice hosting a xenograft TNBC after flank injection of MDA-MB-231 cells determined a great reduction in the growth and vascularity of the neoplasm. Moreover, the treatment resulted in a minimal infiltration of nearby tissues. Finally, the encapsulation of JQ1 in nanoparticles improved the anticancer efficacy of this epigenetic compound against TNBC in vitro and in vivo, opening the way to test it in the treatment of TNBC.

scholarly journals EXTH-29. GALECTIN-3 AS A POTENTIAL THERAPEUTIC TARGET IN RECURRENT ATYPICAL AND MALIGNANT MENINGIOMA

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi88-vi88
Author(s):  
Arabinda Das ◽  
Jaime Martinez Santos ◽  
Indira Kanginakudru ◽  
Daniel G McDonald ◽  
Libby Kosnik Infinger ◽  
...  
Keyword(s):  
Therapeutic Target ◽  
Survival Rates ◽  
Laboratory Data ◽  
Standard Of Care ◽  
Potential Therapeutic Target ◽  
Protein Levels ◽  
Signaling Transduction Pathway ◽  
Galectin 3

Abstract Atypical and malignant meningiomas are rare tumors that unlike WHO I meningiomas are characteristically more aggressive in nature and are associated with higher recurrence risks of recurrence. In fact despite aggressive treatment of malignant meningiomas, the average 5-year survival rates are in the range of 30% to 60%. Still the standard of care for atypical and malignant meningiomas (AM and MM) has yet to be established. Our laboratory data demonstrated that galectin-3 (Gal-3), a multifunctional β-galactoside-binding protein, is highly expressed in AM and MM as compared to normal tissue. However, the biological functions of Gal-3 in meningioma cells are not fully understood. To address this, we used either small interfering RNA (siRNA) to knock down Gal-3 expression or Gal-3 inhibitor, TD139 to suppress Gal-3 expression in in vitro cell culture model. Silencing or inhibiting of Gal-3 expression significantly decreased the protein levels of urokinase-type plasminogen activator receptor (uPAR) as well as uPAR’s downstream signaling transduction pathway, including phosphorylation of AKT. In both cases, we found that silencing of Gal-3 or inhibiting Gal-3 expression decreased the proliferative activity, and migratory potential of AM and MM cells. Furthermore, we demonstrated that TD139 inhibits MM growth in an in vivo xenograft MM model. Taken together, our results suggest that Gal-3 modulates uPAR expression and that Gal-3 may be a potential therapeutic target for the treatment of atypical and malignant meningiomas.

scholarly journals Lipid-Based Nanocarriers Provide Prolonged Anticancer Activity for Palbociclib: In Vitro and in Vivo Evaluations

2021 ◽  
Author(s):  
Parichehr Hassanzadeh ◽  
Elham Arbabi ◽  
Fatemeh Rostami
Keyword(s):  
Breast Cancer ◽  
Cancer Therapy ◽  
Cell Cycle Progression ◽  
Critical Role ◽  
Survival Rates ◽  
Physicochemical Characteristics ◽  
In Vivo Models ◽  
Estrogen Receptor Positive

Breast cancer therapy has remained one of the major healthcare challenges. Based on the critical role of cyclin-dependent kinase 4/6 (CDK 4/6) in cell cycle progression, targeting this signaling appears promising for cancer therapy. Palbociclib, a selective CDKs 4/6 inhibitor, is the first-line treatment for estrogen receptor-positive breast cancer. However, poor absorption or side effects may negatively affect its efficiency. This prompted us to incorporate palbociclib into the nanostructured lipid carriers (NLCs) and evaluate the anticancer effect of the nanoformulation (Pa-NLCs) in in vitro and in vivo models of breast cancer. Pa-NLCs were developed by high-pressure homogenization followed by assessment of the physicochemical characteristics and bioactivities in MCF-7 breast cancer cells and female Wistar rats exposed to the carcinogen 7,12-dimethylbenz(a)anthracene (DMBA). The prepared Pa-NLCs demonstrated suitable physicochemical characteristics, including the controlled release pattern, efficient cellular uptake, and cytotoxicity, while free palbociclib failed to show significant effects. Rats treated with Pa-NLCs exhibited significantly reduced tumor volumes, increased survival rates, and histopathological improvement. Free palbociclib was significantly less efficient than Pa-NLCs. Pa-NLCs, by improving the pharmacological profile of palbociclib and providing longer-lasting effects, can be considered as a promising nanoformulation against breast cancer.

scholarly journals Luteolin Prevents Cardiac Dysfunction and Improves the Chemotherapeutic Efficacy of Doxorubicin in Breast Cancer

2021 ◽  
Vol 8 ◽  
Author(s):  
Youyang Shi ◽  
Feifei Li ◽  
Man Shen ◽  
Chenpin Sun ◽  
Wei Hao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mitochondrial Fission ◽  
Mitochondrial Morphology ◽  
Protective Effects ◽  
Myocardial Cells ◽  
Related Protein ◽  
Zebrafish Model ◽  
Protein Levels

Background: Doxorubicin (Dox) is one of the most effective chemotherapy agents used in the treatment of solid tumors and hematological malignancies. However, it causes dose-related cardiotoxicity that may lead to heart failure in patients. Luteolin (Lut) is a common flavonoid that exists in many types of plants. It has been studied for treating various diseases such as hypertension, inflammatory disorders, and cancer. In this study, we evaluated the cardioprotective and anticancer effects of Lut on Dox-induced cardiomyopathy in vitro and in vivo to explore related mechanisms in alleviating dynamin-related protein (Drp1)-mediated mitochondrial apoptosis.Methods: MTT and LDH assay were used to determine the viability and toxicity of cardiomyocytes treated with Dox and Lut. Flow cytometry was used to examine ROS levels, and electron and confocal microscopy was employed to assess the mitochondrial morphology. The level of apoptosis was examined by Hoechst 33258 staining. The protein levels of myocardial fission protein and apoptosis-related protein were examined using Western blot. Transcriptome analysis of the protective effect of Lut against Dox-induced cardiac toxicity in myocardial cells was performed using RNA sequencing technology. The protective effects of Lut against cardiotoxicity mediated by Dox in zebrafish were quantified. The effect of Lut increase the antitumor activity of Dox in breast cancer both in vitro and in vivo were further employed.Results: Lut ameliorated Dox-induced toxicity in H9c2 and AC16 cells. The level of oxidative stress was downregulated by Lut after Dox treatment of myocardial cells. Lut effectively reduced the increased mitochondrial fission post Dox stimulation in cardiomyocytes. Apoptosis, fission protein Drp1, and Ser616 phosphorylation were also increased post Dox and reduced by Lut. In the zebrafish model, Lut significantly preserved the ventricular function of zebrafish after Dox treatment. Moreover, in the mouse model, Lut prevented Dox-induced cardiotoxicity and enhanced the cytotoxicity in triple-negative breast cancer by inhibiting proliferation and metastasis and inducing apoptosis.

scholarly journals A novel cystathionine γ-lyase inhibitor, I194496, inhibits the growth and metastasis of human TNBC via downregulating multiple signaling pathways

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ya Liu ◽  
Lupeng Wang ◽  
Xiuli Zhang ◽  
Yuying Deng ◽  
Limin Pan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Anticancer Activity ◽  
Signaling Pathways ◽  
Nude Mice ◽  
High Capacity ◽  
Normal Breast ◽  
Inhibitory Effects ◽  
Protein Levels

AbstractTriple-negative breast cancer (TNBC) is a high-risk subtype of breast cancer with high capacity for metastasis and lacking of therapeutic targets. Our previous studies indicated that cystathionine γ-lyase (CSE) may be a new target related to the recurrence or metastasis of TNBC. Downregulation of CSE could inhibit the growth and metastasis of TNBC. The purpose of this study was to investigate the activity of the novel CSE inhibitor I194496 against TNBC in vivo and in vitro. The anticancer activity of I194496 in vitro were detected by MTS, EdU, and transwell assays. Methylene blue assay was used to determine the H2S level. Western blot was performed to analyze the expression of related pathway proteins. Xenograft tumors in nude mice were used to analyze the anticancer activity of I194496 in vivo. I194496 exerted potent inhibitory effects than l-propargylglycine (PAG, an existing CSE inhibitor) on human TNBC cells and possessed lower toxicity in normal breast epithelial Hs578Bst cells. I194496 reduced the activity and expression of CSE protein and the release of H2S in human TNBC cells. Meanwhile, the protein levels of PI3K, Akt, phospho (p)-Akt, Ras, Raf, p-ERK, p-Anxa2, STAT3, p-STAT3, VEGF, FAK, and Paxillin were decreased in human TNBC cells administrated with I194496. Furthermore, I194496 showed more stronger inhibitory effects on human TNBC xenograft tumors in nude mice. I194496 could inhibit the growth of human TNBC cells via the dual targeting PI3K/Akt and Ras/Raf/ERK pathway and suppress the metastasis of human TNBC cells via down-regulating Anxa2/STAT3 and VEGF/FAK/Paxillin signaling pathways. CSE inhibitor I194496 might become a novel and potential agent in the treatment of TNBC.

scholarly journals MicroRNAs as a clue to overcome breast cancer treatment resistance

2021 ◽  
Author(s):  
Iris Garrido-Cano ◽  
Birlipta Pattanayak ◽  
Anna Adam-Artigues ◽  
Ana Lameirinhas ◽  
Sandra Torres-Ruiz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Epithelial To Mesenchymal Transition ◽  
Survival Rates ◽  
Treatment Resistance ◽  
Cancer Therapies ◽  
Mesenchymal Transition ◽  
Cellular Processes

AbstractBreast cancer is the most frequent cancer in women worldwide. Despite the improvement in diagnosis and treatments, the rates of cancer relapse and resistance to therapies remain higher than desirable. Alterations in microRNAs have been linked to changes in critical processes related to cancer development and progression. Their involvement in resistance or sensitivity to breast cancer treatments has been documented by different in vivo and in vitro experiments. The most significant microRNAs implicated in modulating resistance to breast cancer therapies are summarized in this review. Resistance to therapy has been linked to cellular processes such as cell cycle, apoptosis, epithelial-to-mesenchymal transition, stemness phenotype, or receptor signaling pathways, and the role of microRNAs in their regulation has already been described. The modulation of specific microRNAs may modify treatment response and improve survival rates and cancer patients’ quality of life. As a result, a greater understanding of microRNAs, their targets, and the signaling pathways through which they act is needed. This information could be useful to design new therapeutic strategies, to reduce resistance to the available treatments, and to open the door to possible new clinical approaches.

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