scholarly journals Metabolically activated macrophages in mammary adipose tissue link obesity to triple-negative breast cancer

2018 ◽  
Author(s):  
Payal Tiwari ◽  
Ariane Blank ◽  
Chang Cui ◽  
Kelly Q. Schoenfelt ◽  
Guolin Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Tumor Formation ◽  
List Type ◽  
Dependent Manner ◽  
Macrophage Phenotype ◽  
Adipose Tissue Macrophages

SUMMARYObesity is associated with increased incidence and severity of triple-negative breast cancer (TNBC); however, mechanisms underlying this relationship are incompletely understood. Macrophages, which accumulate in adipose tissue and are activated during obesity, are an attractive mechanistic link. Here, we show that, during obesity, murine and human mammary adipose tissue macrophages adopt a pro-inflammatory, metabolically- activated (MMe) macrophage phenotype that promotes TNBC stem-like markers and functions, including increased tumorsphere growthin vitroand tumor-initiating potentialin vivo. We demonstrate that MMe macrophages release cytokines in an NADPH oxidase 2 (NOX2)-dependent manner that signal through glycoprotein 130 (GP130) on TNBC cells to promote their stem-like properties. Accordingly, deletingNox2in myeloid cells or depleting GP130 in TNBC cells attenuates the ability of obesity to drive TNBC tumor formation. Our studies implicate MMe macrophage accumulation in mammary adipose tissue during obesity as a mechanism for promoting TNBC stemness and tumorigenesis.HIGHLIGHTS⁘Obesity promotes TNBC tumor formation and stemness.⁘Mammary adipose tissue macrophages are metabolically activated (MMe) in obese mice and humans.⁘MMe macrophages in mammary adipose tissue contribute to obesity-induced stemness.⁘MMe macrophages promote TNBC stemness through GP130 signaling.

scholarly journals Metabolically activated adipose tissue macrophages link obesity to triple-negative breast cancer

2019 ◽  
Vol 216 (6) ◽  
pp. 1345-1358 ◽  
Author(s):  
Payal Tiwari ◽  
Ariane Blank ◽  
Chang Cui ◽  
Kelly Q. Schoenfelt ◽  
Guolin Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Tumor Formation ◽  
Dependent Manner ◽  
Macrophage Phenotype ◽  
M1 Macrophages ◽  
Adipose Tissue Macrophages ◽  
Macrophage Accumulation

Obesity is associated with increased incidence and severity of triple-negative breast cancer (TNBC); however, mechanisms underlying this relationship are incompletely understood. Here, we show that obesity reprograms mammary adipose tissue macrophages to a pro-inflammatory metabolically activated phenotype (MMe) that alters the niche to support tumor formation. Unlike pro-inflammatory M1 macrophages that antagonize tumorigenesis, MMe macrophages are pro-tumorigenic and represent the dominant macrophage phenotype in mammary adipose tissue of obese humans and mice. MMe macrophages release IL-6 in an NADPH oxidase 2 (NOX2)–dependent manner, which signals through glycoprotein 130 (GP130) on TNBC cells to promote stem-like properties including tumor formation. Deleting Nox2 in myeloid cells or depleting GP130 in TNBC cells attenuates obesity-augmented TNBC stemness. Moreover, weight loss reverses the effects of obesity on MMe macrophage inflammation and TNBC tumor formation. Our studies implicate MMe macrophage accumulation in mammary adipose tissue as a mechanism for promoting TNBC stemness and tumorigenesis during obesity.

scholarly journals Adipose derived mesenchymal stem cell secretome formulation as a biotherapeutic to inhibit growth of drug resistant triple negative breast cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ragima Nadesh ◽  
Krishnakumar N. Menon ◽  
Lalitha Biswas ◽  
Ullas Mony ◽  
K. Subramania Iyer ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Standard Of Care ◽  
Breast Cancer Cell Lines ◽  
Dependent Manner

AbstractIn the present study, a protocol was developed for processing of human adipose derived mesenchymal stem cell secretome formulation of varying concentration. Its molecular composition was evaluated, and its effectiveness in vitro using breast cancer cell lines, and in vivo in a nude mice breast cancer model was studied to determine its role in suppressing triple negative breast cancer in a dose dependent manner. Because the secretome could have value as an add-on therapy along with a current drug, the effectiveness of the secretome both in monotherapy and in combination therapy along with paclitaxel was evaluated. The results showed significant cell kill when exposed to the secretome above 20 mg/ml at which concentration there was no toxicity to normal cells. 70 mg/ml of SF showed 90 ± 10% apoptosis and significant decrease in CD44+/CD24−, MDR1+ and PDL-1+ cancer cells. In vivo, the tumor showed no growth after daily intra tumor injections at 50 mg/ml and 100 mg/ml doses whereas substantial tumor growth occurred after saline intra tumor injection. The study concludes that SF is a potential biotherapeutic for breast cancer and could be used initially as an add-on therapy to other standard of care to provide improved efficacy without other adverse effects.

scholarly journals A novel sequential treatment of palbociclib enhances the effect of cisplatin in RB-proficient triple-negative breast cancer

2020 ◽  
Author(s):  
Yajing Huang ◽  
Hao Wu ◽  
Xingrui Li
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cyclin D1 ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Sequential Treatment ◽  
Phase Cell ◽  
Dependent Manner ◽  
Effect Of Pd

Abstract Background: Triple-negative breast cancer (TNBC) is a highly aggressive malignancy lack of sensitivity to chemo-, endocrine and targeted therapy. CDK4/6 inhibitors, combined with endocrine therapy, have been proven to be effective in postmenopausal women with HR-positive, HER2-negative advanced or metastatic breast cancer. So we investigated that whether CDK4/6 inhibitor palbociclib (PD) could enhance effects of cisplatin (CDDP) on TNBC.Methods: The effects of different drug regimens of PD and CDDP on MDA-MB-231 and RB-knockdown MDA-MB-231 (sh-MDA-MB-231) cells were assessed in vitro and vivo. MDA-MB-468 and RB-overexpression MDA-MB-468 cells were used to assess the effect of PD-CDDP regimen in vitro. Immunoblotting illustrated cyclin D1/RB/E2F axis signaling pathway.Results: PD induced G1 phase cell cycle arrest in MDA-MB-231 cell line. However, synchronous treatment with PD and CDDP for 24h, PD used for 24h and then followed by CDDP or CDDP used for 24h and then followed by PD all had no influence on cell apoptosis of MDA-MB-231 cells. We further investigated the effect of PD or CDDP withdrawal on sequential treatment and found that PD used for 48h and then withdrawn for 48h followed by CDDP (PD-CDDP) could significantly increase apoptosis, inhibit cell viability and colony formation of MDA-MB-231 cells, while in other regimens PD and CDDP represented additive or antagonistic response. Preferential use of PD could increase DNA damage by CDDP as measured through γH2AX. These findings above were negative in sh-MDA-MB-231 cells and cell function experiments of MDA-MB-468 and RB-overexpression MDA-MB-468 cells could draw similar conclusions, which indicated that PD enhanced the sensitivity of TNBC cells to CDDP in a RB dependent manner. In vivo, this combination treatment inhibited tumor growth and Ki-67 expression compared with single drug treatments in MDA-MB-231 xenograft models. Western blotting analysis presented that PD enhanced sensitivity to CDDP through CDK4/6-cyclin D-RB-E2F pathway. Conclusions: Pre-treatment with PD synchronized tumor cell cycle through CDK4/6-cyclin D1-RB-E2F pathway, which could increase anti-tumor effect of CDDP. PD-CDDP might be an effective treatment for RB-proficient TNBC patients.

scholarly journals Resibufogenin Suppresses Triple-Negative Breast Cancer Angiogenesis by Blocking VEGFR2-Mediated Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Ting Yang ◽  
Yi-Xin Jiang ◽  
Ye Wu ◽  
Dong Lu ◽  
Rui Huang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Antitumor Effect ◽  
Triple Negative ◽  
Network Formation ◽  
Umbilical Vein ◽  
Dependent Manner ◽  
Antiangiogenic Activity

Resibufogenin (RBF), an active compound from Bufo bufonis, has been used for the treatment of multiple malignant cancers, including pancreatic cancer, colorectal cancer, and breast cancer. However, whether RBF could exert its antitumor effect by inhibiting angiogenesis remains unknown. Here, we aimed to explore the antiangiogenic activity of RBF and its underlying mechanism on human umbilical vein endothelial cell (HUVEC), and the therapeutic efficacy with regard to antiangiogenesis in vivo using two triple-negative breast cancer (TNBC) models. Our results demonstrated that RBF can inhibit the proliferation, migration, and tube formation of HUVECs in a dose-dependent manner. Spheroid sprouts were thinner and shorter after RBF treatment in vitro 3D spheroid sprouting assay. RBF also significantly suppressed VEGF-mediated vascular network formation in vivo Matrigel plug assay. In addition, Western blot analysis was used to reveal that RBF inhibited the phosphorylation of VEGFR2 and its downstream protein kinases FAK and Src in endothelial cells (ECs). Molecular docking simulations showed that RBF affected the phosphorylation of VEGFR2 by competitively binding to the ATP-bound VEGFR2 kinase domain, thus preventing ATP from providing phosphate groups. Finally, we found that RBF exhibited promising antitumor effect through antiangiogenesis in vivo without obvious toxicity. The present study first revealed the high antiangiogenic activity and the underlying molecular basis of RBF, suggesting that RBF could be a potential antiangiogenic agent for angiogenesis-related diseases.

scholarly journals Identifying the Effect of Ursolic Acid Against Triple-Negative Breast Cancer: Coupling Network Pharmacology With Experiments Verification

2021 ◽  
Vol 12 ◽  
Author(s):  
Yubao Zhang ◽  
Xiaoran Ma ◽  
Huayao Li ◽  
Jing Zhuang ◽  
Fubin Feng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Ursolic Acid ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Gene Set Enrichment Analysis ◽  
Dependent Manner ◽  
P53 Signaling ◽  
P53 Signaling Pathway

Triple negative breast cancer (TNBC) is a subtype of breast cancer with complex heterogeneity, high invasiveness, and long-term poor prognosis. With the development of molecular pathology and molecular genetics, the gene map of TNBC with distinctive biological characteristics has been outlined more clearly. Natural plant extracts such as paclitaxel, vinblastine, colchicine etc., have occupied an important position in the treatment of hormone-independent breast cancer. Ursolic acid (UA), a triterpenoid acid compound derived from apple, pear, loquat leaves, etc., has been reported to be effective in a variety of cancer treatments, but there are few reports on the treatment of TNBC. This study performed comprehensive bioinformatics analysis and in vitro experiments to identify the effect of UA on TNBC treatment and its potential molecular mechanism. Our results showed that UA could not only reduce the proliferation, migration, and invasion in MDA-MB-231 and MDA-MB-468 cell lines with a dose-dependent manner but also induce cell cycle arrest and apoptosis. Meanwhile, we collected the gene expression data GSE45827 and GSE65194 from GEO for comparison between TNBC and normal cell type and obtained 724 DEGs. Subsequently, PLK1 and CCNB1 related to TNBC were screened as the key targets via topological analysis and molecular docking, and gene set enrichment analysis identified the key pathway as the p53 signaling pathway. In addition, quantitative real-time PCR and western blot verified the key genes were PLK1 and CCNB1. In vivo and in vitro experiments showed that UA could inhibit the growth of TNBC cells, and down-regulate the protein expression levels of PLK1 and CCNB1 by mediating p53 signaling pathway. These findings provide strong evidence for UA intervention in TNBC via multi-target therapy.

scholarly journals P01.07 Depletion of CD206high tumour-associated macrophages using a nanoconjugate limits tumour burden & dissemination in metastatic triple negative breast cancer in mice

2021 ◽  
Vol 9 (Suppl 1) ◽  
pp. A6-A7
Author(s):  
A Lepland ◽  
A Malfanti ◽  
U Haljasorg ◽  
S Dordevic ◽  
L Salumäe ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Lung Metastases ◽  
Bodyweight Loss ◽  
List Type ◽  
M2 Macrophages ◽  
Polymer Backbone

BackgroundAnti-inflammatory (M2) tumour-associated macrophages (TAMs) exert protumoural roles through angiogenesis, immunosuppression and resistance to therapies.1 M2 TAMs express the mannose receptor, CD206,2 excellent marker for targeted therapies. We have previously identified a peptide called mUNO2 that specifically binds to CD206 on M2 TAMs. Aiming to dissect the role of CD206high M2 TAMs in the tumour progression and immunosuppression, we depleted them using an mUNO and doxorubicin (Adriamycin®)-containing polymer-drug nanoconjugate (St-PGA-DOX-mUNO, ‘OximUNO’) where the polymer backbone is branched polyglutamic acid (St-PGA).3Materials and MethodsWe compared OximUNO with free DOX and the untargeted nanoconjugate St-PGA-DOX. To study the in vitro cytotoxicity of the nanoconjugates, we used M2 and M1 skewed macrophages derived from human blood buffy coat. To study the in vivo homing of nanoconjugates we used an orthotopic triple negative breast cancer (TNBC, 4T1 cells) model and a TNBC experimental metastases model in immunocompetent mice. For in vivo therapeutic efficacy studies, we used orthotopic and experimental metastases models of TNBC, and administered the compounds intraperitoneally (i.p.).ResultsIn vitro, OximUNO showed 39% higher toxicity to the primary human M2 macrophages than St-PGA-DOX, and 31% lower toxicity to the M1 macrophages than St-PGA-DOX. In vivo, OximUNO showed no change in creatinine or alanine aminotransferase values, indicating no toxic effects to the kidneys or liver. Compared to control St-PGA, i.p.-administered St-PGA-mUNO, showed improved homing to M2 TAMs in both orthotopic and experimental metastases models with low accumulation in the liver. In the orthotopic treatment study, only OximUNO significantly reduced the tumour volume and showed 56% and 38% less lung metastases than DOX and St-PGA-DOX, respectively. Additionally, DOX and St-PGA-DOX produced a significant bodyweight loss whereas OximUNO did not. Importantly, OximUNO treatment resulted in 2-5-fold increase in the ratio of CD8+/FOXP3+ expression, suggesting a shift in the immune landscape towards an immunostimulatory profile. In the experimental metastases model, OximUNO monotherapy resulted in the highest reduction of lung metastases, and this effect correlated with a significant reduction in CD206high M2 TAMs; whereas no significant effect on M2 TAMs population was observed with DOX or untargeted nanoconjugate.ConclusionsOur data suggests that the elimination of CD206high M2 TAMs with OximUNO suppresses spontaneous and experimental metastases in safe manner, shifts immune landscape towards immunostimulatory and could therefore be a potential treatment option for TNBC patients.ReferencesHughes R, Qian B-Z, Rowan C, Muthana M, Keklikoglou I, Olson OC, et al. Perivascular M2 macrophages stimulate tumor relapse after chemotherapy. Cancer Res 2015;75(17):3479–91.Scodeller P, Simón-Gracia L, Kopanchuk S, Tobi A, Kilk K, Säälik P, et al. Precision targeting of tumor macrophages with a CD206 binding peptide. Sci Rep 2017;7(1):14655.Duro-Castano A, Nebot VJ, Niño-Pariente A, Armiñán A, Arroyo-Crespo JJ, Paul A, et al. Capturing ‘extraordinary’ soft-assembled charge-like polypeptides as a strategy for nanocarrier design. Adv Mater 2017;29(39):1702888.Disclosure InformationA. Lepland: None. A. Malfanti: None. U. Haljasorg: None. S. Dordevic: None. L. Salumäe: None. P. Peterson: None. T. Teesalu: None. M.J. Vicent: None. P. Scodeller: None.

scholarly journals B4GALNT2 Gene Promotes Proliferation, and Invasiveness and Migration Abilities of Model Triple Negative Breast Cancer (TNBC) Cells by Interacting With HLA-B Protein

2021 ◽  
Vol 11 ◽  
Author(s):  
Pu Yu ◽  
Lili Zhu ◽  
Kang Cui ◽  
Yabing Du ◽  
Chaojie Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Tumor Formation ◽  
The Cancer Genome Atlas ◽  
G1 Phase ◽  
And Migration

B4GALNT2 gene encodes the enzyme β1,4-N-acetylgalactosaminyltransferase 2 that biosynthesizes the histo-blood group antigen Sda, which is expressed on the surface of erythrocytes and in body secretions. Analysis of The Cancer Genome Atlas (TCGA) database revealed that this gene was highly expressed in breast cancer tissues in comparison with adjacent healthy ones. In-vitro lentivirus-assisted B4GALNT2 gene knockdown experiments in model triple negative breast cancer (TNBC) cell lines (HCC1937 and MDA-MB-231) showed inhibition in cell proliferation, decrease in cell viability, promotion of cell apoptosis and inhibitions in cell migration and invasiveness abilities in comparison with empty lentivirus transfectant controls. Also, in cell cycle tests, the number of cells in the G1 phase increased, in the S phase decreased and did not change in the G2/M phase (indicative of the presence of a block in the G1 phase). In-vivo tumor formation experiments in mice revealed that knockdown of the B4GALNT2 gene in MDA-MB-231 cells inhibited their proliferation. Using co-immunoprecipitation (Co-IP) mass spectroscopy-assisted analysis, it was found that HLA-B protein [a product of the human leukocyte antigen (HLA) class I gene] interacts with B4GALNT2 protein. In-vitro overexpression of HLA-B in B4GALNT2-knocked down MDA-MB-231 cell lines significantly recovered the cell proliferation, viability and migration ability of B4GALNT2 gene. These indicate that HLA-B is one of the interaction proteins in the downstream pathway of the B4GALNT2 gene.

scholarly journals CX-5461 Enhances the Efficacy of APR-246 via Induction of DNA Damage and Replication Stress in Triple-Negative Breast Cancer

2021 ◽  
Vol 22 (11) ◽  
pp. 5782
Author(s):  
Ashwini Makhale ◽  
Devathri Nanayakkara ◽  
Prahlad Raninga ◽  
Kum Kum Khanna ◽  
Murugan Kalimutho
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Triple Negative Breast Cancer ◽  
Combination Treatment ◽  
Triple Negative ◽  
Annexin V ◽  
Replication Stress ◽  
Breast Cancer Cell Lines ◽  
Combination Strategy

Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer lacking targeted therapy. Here, we evaluated the anti-cancer activity of APR-246, a P53 activator, and CX-5461, a RNA polymerase I inhibitor, in the treatment of TNBC cells. We tested the efficacy of individual and combination therapy of CX-5461 and APR-246 in vitro, using a panel of breast cancer cell lines. Using publicly available breast cancer datasets, we found that components of RNA Pol I are predominately upregulated in basal-like breast cancer, compared to other subtypes, and this upregulation is associated with poor overall and relapse-free survival. Notably, we found that the treatment of breast cancer cells lines with CX-5461 significantly hampered cell proliferation and synergistically enhanced the efficacy of APR-246. The combination treatment significantly induced apoptosis that is associated with cleaved PARP and Caspase 3 along with Annexin V positivity. Likewise, we also found that combination treatment significantly induced DNA damage and replication stress in these cells. Our data provide a novel combination strategy by utilizing APR-246 in combination CX-5461 in killing TNBC cells that can be further developed into more effective therapy in TNBC therapeutic armamentarium.

scholarly journals GCH1 induces immunosuppression through metabolic reprogramming and IDO1 upregulation in triple-negative breast cancer

2021 ◽  
Vol 9 (7) ◽  
pp. e002383
Author(s):  
Jin-Li Wei ◽  
Si-Yu Wu ◽  
Yun-Song Yang ◽  
Yi Xiao ◽  
Xi Jin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Molecular Taxonomy ◽  
Underlying Mechanism ◽  
Metabolic Reprogramming ◽  
Sequencing Data ◽  
Aryl Hydrocarbon

PurposeRegulatory T cells (Tregs) heavily infiltrate triple-negative breast cancer (TNBC), and their accumulation is affected by the metabolic reprogramming in cancer cells. In the present study, we sought to identify cancer cell-intrinsic metabolic modulators correlating with Tregs infiltration in TNBC.Experimental designUsing the RNA-sequencing data from our institute (n=360) and the Molecular Taxonomy of Breast Cancer International Consortium TNBC cohort (n=320), we calculated the abundance of Tregs in each sample and evaluated the correlation between gene expression levels and Tregs infiltration. Then, in vivo and in vitro experiments were performed to verify the correlation and explore the underlying mechanism.ResultsWe revealed that GTP cyclohydrolase 1 (GCH1) expression was positively correlated with Tregs infiltration and high GCH1 expression was associated with reduced overall survival in TNBC. In vivo and in vitro experiments showed that GCH1 increased Tregs infiltration, decreased apoptosis, and elevated the programmed cell death-1 (PD-1)-positive fraction. Metabolomics analysis indicated that GCH1 overexpression reprogrammed tryptophan metabolism, resulting in L-5-hydroxytryptophan (5-HTP) accumulation in the cytoplasm accompanied by kynurenine accumulation and tryptophan reduction in the supernatant. Subsequently, aryl hydrocarbon receptor, activated by 5-HTP, bound to the promoter of indoleamine 2,3-dioxygenase 1 (IDO1) and thus enhanced the transcription of IDO1. Furthermore, the inhibition of GCH1 by 2,4-diamino-6-hydroxypyrimidine (DAHP) decreased IDO1 expression, attenuated tumor growth, and enhanced the tumor response to PD-1 blockade immunotherapy.ConclusionsTumor-cell-intrinsic GCH1 induced immunosuppression through metabolic reprogramming and IDO1 upregulation in TNBC. Inhibition of GCH1 by DAHP serves as a potential immunometabolic strategy in TNBC.

scholarly journals Selection of aptamers against triple negative breast cancer cells using high throughput sequencing

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Débora Ferreira ◽  
Joaquim Barbosa ◽  
Diana A. Sousa ◽  
Cátia Silva ◽  
Luís D. R. Melo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
High Throughput ◽  
Triple Negative Breast Cancer ◽  
High Throughput Sequencing ◽  
Triple Negative ◽  
Metastatic Breast ◽  
Target Cells ◽  
Cancer Tissue ◽  
Surface Receptors

AbstractTriple-negative breast cancer is the most aggressive subtype of invasive breast cancer with a poor prognosis and no approved targeted therapy. Hence, the identification of new and specific ligands is essential to develop novel targeted therapies. In this study, we aimed to identify new aptamers that bind to highly metastatic breast cancer MDA-MB-231 cells using the cell-SELEX technology aided by high throughput sequencing. After 8 cycles of selection, the aptamer pool was sequenced and the 25 most frequent sequences were aligned for homology within their variable core region, plotted according to their free energy and the key nucleotides possibly involved in the target binding site were analyzed. Two aptamer candidates, Apt1 and Apt2, binding specifically to the target cells with $$K_{d}$$ K d values of 44.3 ± 13.3 nM and 17.7 ± 2.7 nM, respectively, were further validated. The binding analysis clearly showed their specificity to MDA-MB-231 cells and suggested the targeting of cell surface receptors. Additionally, Apt2 revealed no toxicity in vitro and showed potential translational application due to its affinity to breast cancer tissue sections. Overall, the results suggest that Apt2 is a promising candidate to be used in triple-negative breast cancer treatment and/or diagnosis.

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