Browsing by Author "Eskiler, Gamze Güney"

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The anticancer activity of complex [Cu-2(mu-(C6H5)(2)CHCOO)(3)(bipy)(2))](ClO4) -solid lipid nanoparticles on MCF-7 cells
(Bentham Science, 2016-12-01) Kani, İbrahim; Dikmen, Gökhan; Eskiler, Gamze Güney; Çeçener, Gülşah; Tunca, Berrin; Egeli, Ünal; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0001-7904-883X; 0000-0002-2088-9914; 0000-0002-1619-6680; 0000-0002-3820-424X; AAH-1420-2021; AAB-6011-2022; ABI-6078-2020; AAP-9988-2020; 57190947987; 6508156530; 6602965754; 55665145000
Recent studies have focused on the potential use of metal-based complexes for the treatment of cancer. However, there are some limitations of metal-based ligands for the treatment of cancer due to their toxic effects. In the present study, a novel bimetallic Cu(II) complex, [Cu-2(mu-(C6H5)(2)CHCOO)(3) (bipy)(2))](ClO4), has firstly been synthesized and characterized by FT-IR, and X-ray crystallography. Furthermore, Cu(II) complex-loaded solid lipid nanoparticles (SLNs) were initially prepared by hot homogenization method to overcome their toxic effects. After characterization, comparative cytotoxic and apoptotic activities of the complex and Cu(II) complex-SLNs on human breast cancer cells (MCF-7) and human umbilical vein endothelial cells (HUVEC) were determined. Cu(II) complex demonstrated considerable in vitro cytotoxic effects on MCF-7 (p<0.05) and induced apoptotic cell death (88.02 +/- 3.95%) of MCF-7 cells. But, the complex has also toxic effects (69.5%) on HUVEC control cells. For this purpose, Cu(II) complex-loaded solid lipid nanoparticles (SLN) were firstly produced, with a distrubution range of 190 +/- 1.45 nm to 350 +/- 1.72 nm and zeta potentials of -27.4 +/- 1.98 mV and -18.2 +/- 1.07 mV, respectively. The scanning electron microscopy (SEM) images of SLNs were also obtained. In vitro studies have shown that Cu(II) complex-SLNs help in reducing the side effect of Cu(II) complex (29.9%) on HUVEC control cells. Therefore, metal based complex might potentially be used for cancer treatment through nanoparticle based drug delivery systems.
Association BRCA mutation status between BMN 673 (talazoparib), an oral PARP inhibitor, in triple-negative breast cancer
(Elsevier, 2018-09) Eskiler, Gamze Güney; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-1619-6680; 0000-0001-7904-883X; 0000-0002-3820-424X; ABI-6078-2020; AAH-1420-2021
Association of PALB2 sequence variants with the risk of early-onset breast cancer in patients from Turkey
(Springer, 2016-08-16) Çeçener, Gülşah; Eskiler, Gamze Güney; Egeli, Ünal; Tunca, Berrin; Alemdar, Adem; Gökgöz, Şehsuvar; Taşdelen, İsmet; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Genel Cerrahi Anabilim Dalı.; 0000-0002-3820-424X; 0000-0002-2088-9914; 0000-0002-1619-6680; 0000-0001-7904-883X; AAP-9988-2020; AAB-6011-2022; ABI-6078-2020; HIZ-7332-2022; AAH-1420-2021; 6508156530; 57190947987; 55665145000; 6602965754; 57190943001; 6603238737; 9637821500
The PALB2 gene, has been accepted as a moderate-penetrance gene associated with breast cancer susceptibility and this gene product is involved in the DNA damage repair pathway via co-localization with BRCA2. Germline PALB2 mutations are associated with an increased breast cancer risk. However, the prevalence of the diverse types of PALB2 variants depend on the population. Thus, the aim of the present study was to determine, for the first time, the prevalence of PALB2 variants in a Turkish population of BRCA1/BRCA2-negative early-onset patients with breast cancer. In total, 223 Turkish patients with BRCA1/BRCA2 negative early-onset breast cancer and 60 unaffected women were included in the study. All the coding exons and intron/exon boundaries of PALB2 were subjected to mutational analysis by heteroduplex analysis (HDA) and DNA sequencing. Eighteen PALB2 variants were found in breast cancer patients within the Turkish population. Three variants (c.271G>A, c.404C>A and c.2981T>A) have not been previously reported. In addition, nine intronic variants were described, and this study is the first to describe the c.1685-44T>A intronic variant. The prevalence of possible pathogenic PALB2 variants was found to be 4.03 % in BRCA1/2-negative Turkish patients with early-onset breast cancer. Different variants of PALB2 have been reported in the literature, and the prevalence of these variants could different for each population. This is the first study to investigate the prevalence of PALB2 variants in Turkish patients with early-onset breast cancer.
BMN 673 (talazoparib): A potent PARP inhibitor for triple negative breast cancer with different genetic profile
(Wiley, 2019-05-01) Eskiler, Gamze Güney; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; ÇEÇENER, GÜLŞAH; EGELİ, ÜNAL; TUNCA, BERRİN; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-3820-424X; 0000-0001-7904-883X; 0000-0002-1619-6680; AAP-9988-2020; ABI-6078-2020; AAH-1420-2021
The objective of the present study was to elucidate the effect of BMN 673 (talozoparib) on BRCA1 mutant (HCC1937) and wild-type (MDA-MB-231) triple negative breast cancer (TNBC). The in vitro cytotoxicity results indicated that BMN 673 had considerable inhibitory effects on HCC1937 and MDA-MB-231 cell lines by inducing apoptosis, multicaspase activity, G2/M arrest, and altering the expression levels of apoptosis-related genes (P < 0.01). Additionally, BMN 673 indicated no toxicity on MCF-10A control cells until a certain concentration and incubation time. However, BMN 673, a novel and selective poly ADP ribose polymerase inhibitor, was more potent in TNBC cells bearing BRCA1 mutant than those with wild-type BRCA1. In conclusion, our study, for the first time, demonstrated a molecular mechanism of the induction of apoptosis by BMN 673 in TNBC with different genetic profile. However, further investigations regarding the exact molecular mechanisms underlying BMN 673-inducing apoptotic death and gene-cell line associations are required.
The characterization of ascorbic acid loaded solid lipid nanoparticles
(Elsevier, 2014-07) Dikmen, Gökhan; Eskiler, Gamze Güney; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-2088-9914; AAB-6011-2022
Clinicopathologic features and genetic characteristics of the BRCA1/2 mutation in Turkish breast cancer patients
(Elsevier Science, 2019-10-14) Eskiler, Gamze Güney; Çeçener, Gülşah; Takanlou, Leila Sabour; Takanlou, Maryam Sabour; Egeli, Ünal; Aksoy, Seçil; Ünal, Ufuk; Tezcan, Havva; Eryılmaz, Işıl Ezgi; Gökgöz, Mustafa Şehsuvar; Tunca, Berrin; Çubukçu, Erdem; Evrensel, Türkkan; Çetintaş, Sibel; Taşdelen, İsmet; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji ve Genetik Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Genel Cerrahi Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Onkoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Radyasyon Onkolojisi Anabilim Dalı.; 0000-0002-3820-424X; 0000-0001-7904-883X; 0000-0002-3760-9755; 0000-0003-4913-3616; 0000-0002-3316-316X; 0000-0002-1619-6680; 0000-0002-9732-5340; GGI-6227-2022; EAS-6830-2022; GYU-0252-2022; EWY-5692-2022; ETP-1691-2022; EOI-5652-2022; EBN-1186-2022; 6508156530; 57211585974; 57211582304; 55665145000; 57193933334; 57211584917; 57211580953; 57189380840; 57203870909; 6602965754; 53986153800; 6603942124; 6505881756; 9637821500
The aim of this study was to identify the frequency and spectrum of germline BRCA1/2 pathogenic alterations in a cohort of patients with breast carcinoma. In this study, a total of 603 breast cancer subjects from Turkey were screened for BRCA1/BRCA2 mutations using HDA and Sanger sequencing. In the present study, 21 BRCA1 and BRCA2 pathogenic variants were detected in 30 patients and BRCA1/2 mutations were significantly associated with a family history of breast/ovarian cancer. Analysis of overall survival for BRCA1/BRCA2 mutation carriers showed a trend for poor overall survival only in BRCA1 carriers, although this was not statistically significant in BRCA1 and BRCA2 mutation carriers. The c.5266dupC mutation is one of the most frequently reported mutations in BRCA1 and was identified in five breast cancer patients in our study. The most common BRCA2 gene mutations in the present study were c.8940delA and c.9097dupA, which were found in seven patients. We found mostly BRCA1 and BRCA2 mutation carriers in those patients who showed hormone-positive features. In conclusion, our data showed differences in the distribution of the mutation spectrum of BRCA1 and BRCA2 in Turkey.
In vitro cytotoxic and antiproliferative effects of usnic acid on hormone-dependent breast and prostate cancer cells
(Wiley, 2018-10) Eskiler, Gamze Güney; Eryılmaz, Işıl Ezgi; Egeli, Ünal; Yurdacan, Beste; Çeçener, Gülşah; Tunca, Berrin; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-3316-316X; 0000-0001-7904-883X; 0000-0002-1619-6680; 0000-0002-3820-424X; GWV-3548-2022; AAH-1656-2021; AAH-1420-2021; ABI-6078-2020; AAP-9988-2020; 57189380840; 55665145000; 57203621058; 6508156530; 6602965754
The aim of the current study was first to investigate cytotoxic activity of usnic acid (UA) on hormone-dependent breast and prostate cancer, and normal cells. Cells were treated with increasing concentrations (25 to 150 mu M) of UA for 48hours and cell viability, quantitative and morphological analysis of cell death, and cell cycle analysis were performed. UA was shown to have selective cytotoxicity on hormone-dependent cancer cells with the IC50 levels of 71.4 and 77.5 mu M for MCF7 and LNCaP cells, respectively. UA induced apoptotic cell death and G0/G1 cell cycle arrest without damaging normal cells. MCF7 cells were more sensitive to UA than LNCaP cells. Our results first revealed that UA is a promising candidate as an alternative agent for hormone-dependent breast and prostate cancers. However, molecular mechanism underlying the UA-mediated cell death in cancer cells should be investigated further.
An in vitro model for the development of acquired tamoxifen resistance
(Springer, 2016-07-15) Eskiler, Gamze Güney; Çeçener, Gülşah; Tunca, Berrin; Egeli, Ünal; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-3820-424X; 0000-0001-7904-883X; 0000-0002-1619-6680; 0000-0002-2088-9914; AAP-9988-2020; AAH-1420-2021; AAB-6011-2022; ABI-6078-2020; 6508156530; 6602965754; 57190947987; 55665145000
The development of resistance to tamoxifen (Tam) remains a challenging clinical problem for ER+ breast cancer patients. To understand the mechanisms underlying of resistance, previous studies have driven the acquisition of Tam resistance by exposing cells to varying concentration of drug for varying lengths of time. However, a detailed protocol for the establishment of Tam-resistant cells remains to be clarified. In the present study, we aimed to determine and compare the effect of different in vitro protocols on the degree of resistance to 4-hydroxytamoxifen (4-OH Tam) for MCF7 cells. For this purpose, MCF7-Tam resistance (MCF7-TamR) cells were developed by treated with different concentrations (100, 200, 400, 600, 800 and 1000 nM) of 4-OH Tam over 3 months. The relative resistance was measured by WST-1 analysis. Studies characterizing of the 4-OH Tam resistance of MCF7-TamR cells were performed by 17 beta-oestradiol (E2) and Annexin V/PI analysis. In addition, the expression levels of ABCC1, ABCG2 and ABCG1 were detected by RT-PCR, any changes in morphological of each resistance group were observed at the end of each month and compared with parental MCF7 cells. Consequently, exposure time and concentration can affect the degree of resistance to 4-OH Tam; thus, dose and treatment duration should be chosen according to the desired degree of resistance. This work presents a novel procedure for the generation of MCF7-TamR cells, thus enabling the identification and characterization of MCF7-TamR cells.
Investigation of new treatment option for hepatocellular carcinoma: A combination of sorafenib with usnic acid
(Oxford University, 2019-07) Yurdacan, Beste; Eskiler, Gamze Güney; Egeli, Ünal; Eryılmaz, Işıl Ezgi; Çeçener, Gülşah; Tunca, Berrin; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Temel Tıp Bilimleri/Tıbbi Biyoloji Bölümü.; 0000-0002-1619-6680; 0000-0002-3820-424X; 0000-0002-3316-316X; 0000-0002-3316-316X; 0000-0001-7904-883X; ABI-6078-2020; AAP-9988-2020; GWV-3548-2022; AAH-1656-2021; AAH-1420-2021; 55665145000; 57189380840; 6508156530; 6602965754
Objectives Sorafenib (SOR) is an orally administered molecular targeted agent in the systemic chemotherapy of hepatocellular carcinoma (HCC). However, the partial response of SOR is limited due to its adverse side effect and high heterogeneity and resistant phenotype of HCC. In the current study, we investigated synergistic effects of SOR and usnic acid (UA) on HCC cell lines including HepG2 and SNU-449, and a normal cell line, HUVEC. Methods The antiproliferative and apoptotic effects of combination therapy and SOR alone were analysed by WST-1 and Annexin V analysis, respectively. Furthermore, cell cycle, gene expression analysis of SOR-targeted kinases and acridine orange-ethidium bromide staining were also performed in combined treatments. Key findings Our results demonstrated that SOR and UA combination indicated a strong synergism in HCC cell lines and reduced SOR toxicity in HUVEC cells. Additionally, the combination treatment SOR and UA significantly induced much more apoptotic cell death and G0/G1 arrest through downregulation of SOR-targeted kinases. Conclusions Consequently, SOR and UA combination could be a new therapeutic strategy for HCC treatment.
The matter of clinical sequencing for familial breast cancer: The route from Sanger to next generation
(IEEE, 2017) Eskiler, Gamze Güney; Eryılmaz, Işıl Ezgi; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-3316-316X; 0000-0002-1619-6680; 0000-0002-3820-424X; 0000-0002-3316-316X; 0000-0001-7904-883X; GWV-3548-2022; ABI-6078-2020; AAP-9988-2020; AAH-1656-2021; AAH-1420-2021; 57189380840; 6508156530; 55665145000; 6602965754
We mentioned the importance of clinical sequence analysis in risk determination, diagnostic and therapeutic process of familial breast cancer and we also summarized next generation sequencing applications in this cancer type. In conclusion, BRCA1/2 genes mutations are associated with an increasing the risk of particularly familial breast cancer. However, sequencing of moderate penetrance genes and/or whole exome could also fill large knowledge gaps in explaining genetic predisposition of breast cancer.
Potential role of solid lipid nanoparticles in overcoming the acquired tamoxifen resistance of breast cancer
(Elsevier, 2017) Eskiler, Gamze Güney; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-3820-424X; 0000-0001-7904-883X; 0000-0002-1619-6680; AAP-9988-2020; AAH-1420-2021; ABI-6078-2020
Solid lipid nanoparticles in reversing the acquired tamoxifen-resistance
(IEEE, 2017) Eskiler, Gamze Güney; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-3820-424X; 0000-0001-7904-883X; 0000-0002-1619-6680; AAP-9988-2020; AAH-1420-2021; ABI-6078-2020; 6508156530; 55665145000; 6602965754
The anti-estrogen tamoxifen (Tam) is the most preferred option for patients with estrogen-receptor (ER)-positive breast cancer. However, multi-drug resistance (MDR) is a considerable clinical problem in the successful chemotherapeutic treatment. Members of the ATP-binding cassette (ABC) transporter family proteins play an important role in acquired drug resistance. Many studies have focused primarily on the clinical significance of P-gp (MDR1), BCRP and MRP1 members belong to ABC transporter superfamily on anticancer-drug resistance. Consequently, several strategies have been improved to overcome drug resistance. Nanoparticle drug delivery systems provide an increase in the intracellular concentration of the drugs as well as a reduction in toxicity of free-drug on healthy cells thanks to unique physical and biological properties. Solid lipid nanoparticles (SLNs) have been improved as an alternative colloidal drug delivery systems due to successful incorporation of both hydrophilic and hydrophobic compounds and their related benefits (controlled drug release, high entrapment efficiency and small size etc.) For this purpose, the aim of this study was to discuss the role of Tam-loaded solid lipid nanoparticles (SLNs) to overcome MDR and determine the ability of Tam-SLNs to induce apoptosis.
Synthetic lethal effects of BMN 673 loaded solid lipid nanoparticles on triple-negative breast cancer
(Elsevier, 2018) Eskiler, Gamze Güney; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0001-7904-883X; 0000-0002-1619-6680; 0000-0002-3820-424X; AAH-1420-2021; ABI-6078-2020
Synthetically lethal BMN 673 (Talazoparib) loaded solid lipid nanoparticles for BRCA1 mutant triple negative breast cancer
(Springer, 2018-11-15) Eskiler, Gamze Güney; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-3820-424X; 0000-0001-7904-883X; 0000-0002-1619-6680; AAP-9988-2020; AAH-1420-2021; ABI-6078-2020; 6508156530; 55665145000; 6602965754
Purpose The purpose of the study was to produce BMN 673 loaded solid lipid nanoparticles (SLNs) to improve its therapeutic index, to minimize toxicity and to overcome homologous recombination (HR)-mediated resistance.MethodsFirstly, BMN 673-SLNs were characterized using Nano Zeta Sizer. After treatment with different concentrations of BMN 673 and BMN 673-SLNs, cell viability of HCC1937((BRCA1-/-)), HCC1937-R (BMN 673-resistant) TNBC and MCF-10A normal human mammary breast epithelial cell line was analyzed by WST-1 assay. In an attempt to assess the therapeutic synthetic lethality efficacy of SLNs formulation, cell cycle arrest, DNA damage, mRNA expression levels of PARP1, H2AFX, RAD51 and BRCA1 gene were investigated. Then, PARP, ?H2AX, RAD51 and BRCA1 protein expression and nuclear localization were analyzed by western blot and immunofluorescence analysis.ResultsWhen compared with BMN 673, BMN 673-SLNs showed remarkably a decrease in HCC1937 and HCC1937-R cells with less damage to MCF-10A cells. BMN 673-SLNs significantly induced toxicity through double-stranded DNA breaks, G2/M cell cycle arrest and PARP cleavage in TNBC cells. Additionally, BMN 673-resistance was mediated by miR-107, miR-193b and miR-1255b targeting BRCA1 and RAD51 in HCC1937 and HCC1937-R cells. However, BMN 673-SLNs treatment could overcome HR-mediated resistance in TNBC cells.Conclusions As a result, our findings suggest that SLNs formulation strongly provides a synthetic lethal therapeutic potential in BRCA1 mutated sensitive and resistant TNBC cells.
Talazoparib loaded solid lipid nanoparticles: Preparation, characterization and evaluation of the therapeutic efficacy in vitro
(Bentham Science Publisher, 2019) Eskiler, Gamze Güney; Dikmen, Gökhan; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı; 0000-0002-3820-424X; 0000-0001-7904-883X; 0000-0002-1619-6680; AAP-9988-2020; AAH-1420-2021; ABI-6078-2020; 6508156530; 55665145000; 6602965754
Objective: In the present work, we report for the first time the therapeutic potential of talazoparib (BMN 673)-SLNs for the treatment of BRCA1 deficient Triple Negative Breast Cancer (TNBC). BMN 673-SLNs were produced by hot-homogenization technique and then characterized. Methods: The cytotoxic and apoptotic effects of BMN 673-SLNs compared with BMN 673 were determined on HCC1937BRCA1-/-, HCC1937-R resistant TNBC and MCF-10A control cell lines. BMN 673- SLNs were found to have reduced particle size (219.5 ± 1.45 nm) and thus more stable (-28.4 ± 2.52 mV) than BMN 673 (1652 ± 2.46 nm and -18.6 ± 0.45 mV) at 4ºC. Results: In vitro cell line studies demonstrated that BMN 673-SLNs showed significant cytotoxic effects on HCC1937 (29.8%) and HCC1937-R cells (35.7%) at 10 nM for 12 days compared with BMN 673 (HCC1937 cells: 34.0% and HCC1937-R cells: 93.8% at 10 nM for 12 days) (p<0.05). Additionally, BMN 673-SLNs (40.1%) reduced the toxicity of BMN 673 (53.1%) on MCF-10A control cells thanks to unique physical properties. Conclusion: The apoptotic rates in the 10 nM BMN 673-SLNs treatment (88.78% and 85.56%) for 12 days were significantly higher than those in 10 nM BMN 673 (82.6% and 25.86%) for 12 days in HCC1937 and HCC1937-R cells, respectively (p<0.01). Furthermore, these effects were consistent with the findings of colony formation, wound healing and calcein accumulation analysis. In conclusion, the therapeutic potential of BMN 673-SLNs provides a promising chemotherapeutic strategy for the treatment of drugresistant TNBC.
Talazoparib nanoparticles for overcoming multidrug resistance in triple-negative breast cancer
(Wiley, 2020-02-03) Eskiler, Gamze Güney; Çeçener, Gülşah; Egeli, Ünal; Tunca, Berrin; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; 0000-0002-1619-6680; 0000-0002-2088-9914; 0000-0002-3820-424X; 6508156530; 55665145000; 6602965754
Herein, we investigated efflux pumps-mediated talazoparib-resistance in the treatment of triple-negative breast cancer (TNBC). Furthermore, we produced a novel talazoparib-solid lipid nanoparticles (SLNs) and then explored in vitro therapeutic efficacy of talazoparib-SLNs to overcome talazoparib-resistance in TNBC cells. Talazoparib-SLNs formulation was produced and then characterized. Calcein and Rho-123 were used to analyze the functional activity of drug efflux pumps in these cells. Additionally, RT-PCR, western blot and immunofluorescence analysis were used to detect the messenger RNA, and protein expression level, and cellular localization of the multidrug resistance (MDR1), breast cancer resistance protein (BCRP), and MRP1. We found that talazoparib efflux was mediated by BCRP and MRP1 pumps in TNBC cells. Talazoparib-SLNs could significantly enhance therapeutic efficacy of talazoparib. Furthermore, talazoparib-SLNs were more effective in the suppression of MDR1, BCRP, and MRP1 gene and protein expression levels than talazoparib. Consequently, this study suggests that talazoparib-SLNs formulation represents a promising therapeutic carrier to reverse MDR-mediated resistance in TNBC.