scholarly journals A Combination of an Antimitotic and a Bromodomain 4 Inhibitor Synergistically Inhibits the Metastatic MDA-MB-231 Breast Cancer Cell Line

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Thandi Mqoco ◽  
André Stander ◽  
Anna-Mart Engelbrecht ◽  
Anna M Joubert
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Chemotherapeutic Agents ◽  
Breast Cancer Cell Lines ◽  
Mcf 7

Current chemotherapeutic agents have many side effects and are toxic to normal cells, providing impetus to identify agents that can effectively eliminate tumorigenic cells without damaging healthy cells. The aim of this study was to examine whether combining a novel BRD4 inhibitor, ITH-47, with the antimitotic estradiol analogue, ESE-15-ol, would have a synergistic effect on inhibiting the growth of two different breast cancer cell lines in vitro. Our docking and molecular dynamics studies showed that compared to JQ1, ITH-47 showed a similar binding mode with hydrogen bonds forming between the ligand nitrogens of the pyrazole, ASN99, and water of the BRD4 protein. Data from cell growth studies revealed that the GI50 of ITH-47 and ESE-15-ol after 48 hours of exposure was determined to be 15 μM and 70 nM, respectively, in metastatic MDA-MB-231 breast cancer cells. In tumorigenic MCF-7 breast cancer cells, the GI50 of ITH-47 and ESE-15-ol was 75 μM and 60 nM, respectively, after 48 hours of exposure. Furthermore, the combination of 7.5 μM and 14 nM of ITH-47 and ESE-15-ol, respectively, resulted in 50% growth inhibition of MDA-MB-231 cells resulting in a synergistic combination index (CI) of 0.7. Flow cytometry studies revealed that, compared to the control, combination-treated MDA-MB-231 cells had significantly more cells present in the sub-G1 phase and the combination treatment induced apoptosis in the MDA-MB-231 cells. Compared to vehicle-treated cells, the combination-treated cells showed decreased levels of the BRD4, as well as c-Myc protein after 48 hours of exposure. In combination, the selective BRD4 inhibitor, ITH-47, and ESE-15-ol synergistically inhibited the growth of MDA-MB-231 breast cancer cells, but not of the MCF-7 cell line. This study provides evidence that resistance to BRD4 inhibitors may be overcome by combining inhibitors with other compounds, which may have treatment potential for hormone-independent breast cancers.

The α2δ1 subunit of the voltage-gated calcium channel as a potential candidate for breast cancer tumor initial cells biomarker

2021 ◽  
pp. 1-11
Author(s):  
Meng Li ◽  
Wenmin Zhang ◽  
Xiaodan Yang ◽  
Guo An ◽  
Wei Zhao
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Self Renewal

BACKGROUND: The voltage-gated calcium channel subunit alpha 2 delta 1 (α2δ1) is a functional tumor initial cells (TICs) marker for some solid cancer cells. This study aimed to investigate whether α2δ1 can be used as a potential TIC marker for breast cancer cells. METHODS: α2δ1+ and α2δ1- cells were identified and sorted from the breast cancer cell lines MDA-MB-231, MDA-MB-435s and ZR-75-1 by Immunofluorescence (IF) and Fluorescent-activated cell sorting (FACS) analyses. Spheroid formation in vitro and tumorigenesis in NOD/SCID mice were assessed to determine the self-renewal and serial transplantation abilities of these cells. Using a lentivirus infection system for α2δ1 in breast cancer cell lines, we determined the mRNA levels of stemnessassociated genes by quality real-time PCR (qRT-PCR). Boyden chamber and wounding assays were further performed to detect the migration of α2δ1 overexpression cells. Bioinformatics explored the relationship of molecular classification of breast cancer and drug resistance. RESULTS: α2δ1 presents on the cytomembrane of breast cancer cells, with a positive rate of 1.5–3%. The α2δ1+ cells in breast cancer cell lines have a stronger self-renewal ability and tumor initiating properties in vitro and in vivo. Overexpressing α2δ1 successfully enhanced the sphere-forming efficiency, and upregulated the expression of stemness-associated genes, and increased cell migration. However, seldom significant was available between estrogen receptor +/- (ER+/-), progesterone receptor (PR+/-), and Her2+/-. CONCLUSIONS: Breast cancer cells positive for the α2δ1 charactered tumor initiation, and α2δ1 is a potential TIC marker for breast cancer that further promotes the migration.

Determination of Vulpinic Acid Effect on Apoptosis and mRNA Expression Levels in Breast Cancer Cell Lines

2019 ◽  
Vol 18 (14) ◽  
pp. 2032-2041 ◽  
Author(s):  
Nil Kılıç ◽  
Sümer Aras ◽  
Demet Cansaran-Duman
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Human Breast

Objective: Breast cancer is one of the most common diseases among women worldwide and it is characterized by a high ratio of malignancy and metastasis and low rate of survival of patients. Due to limited treatment options, the discovery of alternative therapeutic agents and clarifying the molecular mechanism of breast cancer development may offer new hope for its treatment. Lichen secondary metabolites may be one of these therapeutic agents. Methods: In this study, the effects of Vulpinic Acid (VA) lichen secondary metabolite on the cell viability and apoptosis of breast cancer cells and non-cancerous cell line were investigated. Quantitative polymerase chain reaction was also performed to determine changes in the expression of apoptosis-related genes at a molecular level. Results: The results demonstrated that VA significantly inhibited the cell viability and induced apoptosis of human breast cancer cells. The highest rates of decreased growth were determined using the IC50 value of VA for 48h on MCF-7 breast cancer cell. Interestingly, VA treatment significantly reduced cell viability in all examined breast cancer cell lines compared to their non-cancerous human breast epithelial cell line. This is the first study on the investigation of the effects of VA on the molecular mechanisms associated with the expression of apoptosis-related genes in breast cancer cell lines. Results demonstrated that the gene expression of P53 genes was altered up to fourteen-fold levels in SK-BR-3 cell lines whereas it reached 2.5-fold in the MCF-12A cell line after treatment with VA. These observations support that VA induces apoptosis on the breast cancer cells compared with the non-cancerous human breast epithelial cell line. Conclusion: It is implicated that VA may be a promising novel molecule for the induction of apoptosis on breast cancer cells.

scholarly journals Increased 12-Lipoxygenase Expression in Breast Cancer Tissues and Cells. Regulation by Epidermal Growth Factor1

1997 ◽  
Vol 82 (6) ◽  
pp. 1790-1798 ◽  
Author(s):  
Rama Natarajan ◽  
Robert Esworthy ◽  
Wei Bai ◽  
Jia-Li Gu ◽  
Sharon Wilczynski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Breast Epithelial Cell ◽  
Mrna Levels ◽  
Epidermal Growth ◽  
Mcf 7

Abstract The interaction of growth factors, such as epidermal growth factor (EGF) with their receptors, on breast cancer cells can lead to the hydrolysis of phospholipids and release of fatty acids, such as arachidonic acid, which can be further metabolized by the lipoxygenase (LO) pathway. Several LO products have been shown to stimulate oncogenes and have mitogenic and chemotactic effects. In this study, we have evaluated the regulation of 12-LO activity and expression in breast cancer cells and tissues. Leukocyte-type 12-LO messenger RNA (mRNA) expression was studied by a specific RT-PCR method in matched, normal, uninvolved and cancer-involved breast tissue RNA samples from six patients. In each of these six patients, the cancer-involved section showed a much higher level of 12-LO mRNA than the corresponding normal section. 12-LO mRNA levels also were greater in two breast cancer cell lines, MCF-7 and COH-BR1, compared with the nontumorigenic breast epithelial cell line, MCF-10F. The growth of the MCF-7 cells was significantly inhibited by two specific LO blockers but not by a cyclooxygenase blocker. Treatment of serum-starved MCF-7 cells with EGF for 4 h led to a dose-dependent increase in the formation of the 12-LO product, 12-hydroxyeicosatetraenoic acid. EGF treatment also increased the levels of the leukocyte-type 12-LO protein expression at 24 h. These results suggest that activation of the 12-LO pathway may play a key role in basal and EGF-induced breast cancer cell growth.

scholarly journals WD-3 inhibits the proliferation of breast cancer cells by regulating the glycolytic pathway

2020 ◽  
Author(s):  
Xiaodan Zhu ◽  
Lu Zhao ◽  
Jianliang You ◽  
Yiqun Ni ◽  
Zhipeng Wei ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Hexokinase 2 ◽  
Mcf 7

Number 3 Prescription (WD-3) is an herbal remedy used in traditional Chinese medicine that has been shown to improve the outcomes of patients with advanced colon and gastric cancers. This study aimed to investigate the effect of WD-3 on proliferation, glycolysis, and hexokinase 2 expression in breast cancer cells. Four breast cancer cell lines (MDA-MB-231, BT-549, MCF-7, and MCF-7/ADR-RES) were treated with different concentrations of WD-3 compared with blank control (phosphate-buffered saline). Each of the breast cancer cell lines was also divided into WD-3, paclitaxel, and blank control group. Cell proliferation and morphology were assessed by MTT assay, nuclear Hoechst 33258 staining, or immunofluorescence. Apoptosis was analyzed by flow cytometry. High performance liquid chromatography was used for measurement of ATP, ADP, and AMP. Hexokinase 2 expression was analyzed by Western blot and quantitative reverse transcription PCR. WD-3 inhibited proliferation and increased apoptosis in all four breast cancer cell lines, in a dose-dependent manner. ATP and EC (energy charge) were significantly decreased in WD-3-treated BT-549 and MDA-MB-231 cells. WD-3 significantly downregulated the protein and mRNA expression of hexokinase II in BT-549 cells, however, not in the other three breast cancer cell lines. Our findings indicate that WD-3 targets the glycolytic pathway in breast cancer cells to exert its antitumor activity.

scholarly journals Eupafolin Induces Apoptosis and Autophagy of Breast Cancer Cells Through PI3K/AKT, MAPKs and NF-κB Signaling Pathways

2021 ◽  
Author(s):  
Jiahui Wei ◽  
Yu Ding ◽  
Xinmiao Liu ◽  
Qing Liu ◽  
Yiran Lu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Breast Cancer Cell Lines ◽  
Cancer Cell Proliferation

Abstract Eupafolin is a flavonoid that can be extracted from common sage. Previous studies have reported that Eupafolin has antioxidant, anti-inflammatory and anti-tumor properties. However, no studies have investigated the role of Eupafolin in breast cancer. Herein, we investigated the effect of Eupafolin on two human breast cancer cell lines, as well as its potential mechanism of action. Next, the data showed that proliferation, migration and invasion ability of breast cancer cells that were treated with Eupafolin was significantly reduced, while the apoptosis rate was significantly increased. In addition, Eupafolin treatment caused breast cancer cell proliferation to be blocked in the S phase. Moreover, Eupafolin significantly induced autophagy in breast cancer cells, with an increase in the expression of LC3B-II/I. PI3K/AKT, MAPKs and NF-κB pathways were significantly inhibited by Eupafolin treatment. Additionally, 3-MA (a blocker of autophagosome formation) significantly reduced Eupafolin-induced activation of LC3B-II/I in breast cancer cells. Furthermore, Eupafolin displayed good in vitro anti-angiogenic activity. Additionally, anti-breast cancer activity of Eupafolin was found to be partially mediated by Cav-1. Moreover, Eupafolin treatment significantly weakened carcinogenesis of MCF-7 cells in nude mice. Therefore, this data provides novel directions on the use of Eupafolin for treatment of breast cancer.

Decrease in Cell Viability of Breast Cancer Cells by a Di-Hydroxylated Derivative of N-(2-hydroxyphenyl)-2-Propylpentanamide

2021 ◽  
Vol 21 ◽  
Author(s):  
Norma Lizeth Galindo-Alvarez ◽  
Humberto L. Mendoza-Figueroa ◽  
Martha Cecilia Rosales-Hernández ◽  
Norbert Bakalara ◽  
José Correa-Basurto
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Proliferative Activity ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Hydroxyl Groups ◽  
Mcf 7

Background: A preliminary study of the biotransformation by cytochrome P450 enzymes (CYP) of N-(2-hydroxyphenyl)-2-propylpentanamide (HO-AAVPA), an HDAC inhibitor, led to the synthesis of two hydroxylated derivatives: N-(2,4-dihydroxyphenyl)-2-propylpentanamide (5a) and N-(2,5-dihydroxyphenyl)-2-propylpentanamide (5b). Objective: The study aims to evaluate the anti-proliferative activity of these di-hydroxylated derivatives in breast cancer cell lines. Methods: MTT assays were conducted in MCF-7 and MDA-MB-231 cell lines. Additionally, in silico studies were carried out to evaluate the affinity of these derivatives with the HDAC1 enzyme. Results: Results showed that only 5b possess an enhanced anti-proliferative effect in breast cancer cell lines MCF-7 and MDA-MB-231. Docking studies revealed that the presence of hydroxyl groups, as well as the position of the additional hydroxyl groups, could have an impact on HDAC1 affinity and could explain the lack of activity of compound 5a. Conclusion: A priori, these results hypothesize that anti-proliferative activity of 5b could be related to HDAC1 inhibition and thus anti-proliferative activity in breast cancer cells.

Radioiodinated Ginger Compounds (6-gingerol and 6-shogaol) and Incorporation Assays on Breast Cancer Cells

2020 ◽  
Vol 20 (9) ◽  
pp. 1129-1139 ◽  
Author(s):  
Kadriye B. Karatay ◽  
Ayfer Yurt Kılçar ◽  
Emine Derviş ◽  
Fazilet Z. Biber Müftüler
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Breast Carcinoma Cell Line ◽  
Active Components ◽  
High Yields ◽  
Mcf 7

Background: 6-Gingerol (6G) and 6-Shogaol (6S) are the main active components of ginger. 6-Gingerol is known for its anti-metastatic and anti-invasive pharmacological activities on cancer cells, besides, 6-Shogaol also inhibits breast cancer cell invasion. Objective: In this study, radioiodination (131I) of 6G and 6S was aimed. Additionally, it is aimed to monitor their incorporation behavior on breast cancer cell lines. Methods: 6-Gingerol was isolated from the fresh ginger-roots extract, additionally, dehydrated to obtain 6-Shogaol. 6G and 6S were radioiodinated using iodogen method. Quality control studies of radioiodinated ginger compounds (6G and 6S) were performed by thin layer radio-chromatography. In vitro studies of radioiodinated ginger compounds on MCF-7 and MDA-MB-231 cells were performed with incorporation assays. Results: 6-Gingerol and 6-Shogaol were radioiodinated (131I-6G and 131I-6S) in high yields over 95%. 131I-6S demonstrated higher incorporation values than 131I-6G on MDA-MB-231 cells. Incorporation behavior of 131I-6G and 131I-6S was similar to MCF-7 cells. Conclusion: It has been observed that ginger compounds were radioiodinated successfully and 131I-6S have a noteworthy incorporation on MDA-MB-231 cells which is a known breast carcinoma cell line with highly invasive characteristics.

Soluble Inflammatory Mediators Proteinase-3 and Neutrophil Elastase Are Targeted by PR1-Specific Immunotherapy After Cellular Uptake and Cross Presentation of PR1 Peptide by Breast Cancer Cells

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2089-2089
Author(s):  
Gheath Alatrash ◽  
Elizabeth Mittendorf ◽  
Anna Sergeeva ◽  
Pariya Sukhumalchandra ◽  
Na Qiao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cross Presentation ◽  
Mcf 7

Abstract Abstract 2089 The human leukocyte antigen (HLA)-A2 restricted nonapeptide PR1 (VLQELNVTV) was shown to be immunogenic in leukemia. A phase I/II clinical trial has been initiated with PR1 peptide vaccine and to date has demonstrated clinical efficacy, including complete remission and immunologic responses in patients with acute (AML) and chronic (CML) myeloid leukemia, as well as myelodysplastic syndrome. PR1 is derived from the serine proteases proteinase-3 (P3) and neutrophil elastase (NE), which are normally found within neutrophil azurophil granules and are released into the inflammatory milieu. We have shown that P3 and NE are taken up and cross presented by antigen presenting cells and that their cross presentation elicits PR1 immunity. Because P3 and NE are present in breast cancer biopsies, we hypothesized that P3/NE may be taken up by breast cancer cells and cross presented to PR1-CTL. We recently demonstrated that the breast cancer cell lines MDA-MB-231, MDA-MB-453, MCF-7 and HER18 do not endogenously express NE and that NE is taken up by these cell lines. In this report, using PCR, western blot and flow cytometry, we show that P3 also is NOT endogenously expressed by the breast cancer cell lines MDA-MB-231, MDA-MB-453, MCF-7 or HER18. Using confocal microscopy, we demonstrate that P3 is taken up by these breast cancer cell lines within 10 minutes of pulsing and localizes to LAMP-2 containing lysosomal vesicles by 4 hours, suggesting its processing for presentation by (HLA)-I (i.e. HLA-A2). Using 8F4, the novel PR1-HLA-A2 monoclonal antibody, we show that PR1 is cross presented from P3 by 3 of 4 HLA-A2+ breast cancer cell lines (MDA-MB-231, MDA-MB-453-A2+, MCF-7), and from NE by 1 of 4 breast cancer cell lines (MDA-MB-231). Next, we studied whether PR1 presentation made cells susceptible to PR1-specific killing by PR1-CTL and the 8F4 monoclonal antibody. We show that following 12-hour pulsing of the MDA-MB-231 cell line with NE or P3, PR1 CTLs killed up to 31% and 38% of the NE- or P3-pulsed breast cancer cells respectively, vs. <1% of ovalbumin (ova)-pulsed MDA-MB-231cells. Additionally, in a complement mediated cytotoxicity assay using 8F4 antibody, pulsing of MDA-MB-231 cells with P3 led to 60% cytotoxicity (vs. 40% in ova-pulsed cells). In conclusion, this study shows that 1) PR1 is cross presented by breast cancer cells following uptake of soluble P3 and NE and 2) PR1 expression makes breast cancer a target of PR1-specific immunotherapy. If uptake of P3 or NE, present in the inflammatory milieu of other solid tumors, also leads to PR1 cross presentation, then PR1-based immunotherapy may be useful to treat other non-hematopoietic tumors. These results support a new paradigm linking inflammation and innate immunity to adaptive immune responses to cancer. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Role of WISP-2/CCN5 in the Maintenance of a Differentiated and Noninvasive Phenotype in Human Breast Cancer Cells

2007 ◽  
Vol 28 (3) ◽  
pp. 1114-1123 ◽  
Author(s):  
Asmaà Fritah ◽  
Cécile Saucier ◽  
Olivier De Wever ◽  
Marc Bracke ◽  
Ivan Bièche ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cancer Cell Lines ◽  
Tissue Growth ◽  
Breast Cancer Cell Lines ◽  
Mcf 7

ABSTRACT WISP-2/CCN5 is an estrogen-regulated member of the “connective tissue growth factor/cysteine-rich 61/nephroblastoma overexpressed” (CCN) family of the cell growth and differentiation regulators. The WISP-2/CCN5 mRNA transcript is undetectable in normal human mammary cells, as well as in highly aggressive breast cancer cell lines, in contrast with its higher level in the breast cancer cell lines characterized by a more differentiated phenotype. We report here that knockdown of WISP-2/CCN5 by RNA interference in estrogen receptor alpha (ERα)-positive MCF-7 breast cancer cells induced an estradiol-independent growth linked to a loss of ERα expression and promoted epithelial-to-mesenchymal transdifferentiation. In contrast, forced expression of WISP-2/CCN5 directed MCF-7 cells toward a more differentiated phenotype. When introduced into the poorly differentiated, estrogen-independent, and invasive MDA-MB-231 breast cancer cells, WISP-2/CCN5 was able to reduce their proliferative and invasive phenotypes. In a series of ERα-positive tumor biopsies, we found a positive correlation between the expression of WISP-2/CCN5 and ID2, a transcriptional regulator of differentiation in normal and transformed breast cells. We propose that WISP-2/CCN5 is an important regulator involved in the maintenance of a differentiated phenotype in breast tumor epithelial cells and may play a role in tumor cell invasion and metastasis.

scholarly journals Enhanced Cytotoxic Activity of Docetaxel-Loaded Silk Fibroin Nanoparticles against Breast Cancer Cells

Polymers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1416
Author(s):  
Ahmed Al Saqr ◽  
Shahid Ud Din Wani ◽  
H. V. Gangadharappa ◽  
Mohammed F. Aldawsari ◽  
El-Sayed Khafagy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Silk Fibroin ◽  
Breast Cancer Cells ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines

Despite decades of research, breast cancer therapy remains a great challenge. Docetaxel is an antimicrotubule agent that is effectively used for the treatment of breast cancer. However, its clinical use is significantly hampered by its low water solubility and systemic toxicity. The current study was designed to prepare docetaxel (DXL)-loaded silk-fibroin-based nanoparticles (SF-NPs) and to screen their potential antitumor activity against breast cancer cell lines. DXL-loaded SF-NPs were prepared using a nanoprecipitation technique and were evaluated for particle size, zeta potential, entrapment efficiency, and in vitro release profile. In addition, DXL-loaded SF-NPs were screened for in vitro cytotoxicity, cellular uptake, and apoptotic potential against MCF-7 and MDA-MB-231 breast cancer cell lines. The prepared DXL-loaded SF-NPs were 178 to 198 nm in diameter with a net negative surface charge and entrapment efficiency ranging from 56% to 72%. In vitro release studies exhibited a biphasic release profile of DXL from SF-NPs with sustained drug release for 72 h. In vitro cell studies revealed that entrapment of DXL within SF-NPs significantly improved cytotoxic potential against breast cancer cell lines, compared to the free drug, and enhanced cellular uptake of DXL by breast cancer cells. Furthermore, the accumulation in the G2/M phase was significantly higher in cells treated with DXL-loaded SF-NPs than in cells treated with free DXL. Collectively, the superior antitumor activities of DXL-loaded SF-NPs against breast cancer cells, compared to free DXL, could be ascribed to improved apoptosis and cell cycle arrest. Our results highlighted the feasibility of using silk fibroin nanoparticles as a nontoxic biocompatible delivery vehicle for enhanced therapeutic outcomes in breast cancer.

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