Investigating cyclooxygenase-2 signaling in breast cancer-initiating cells.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e21107-e21107
Author(s):  
Carolyn S. Hall ◽  
Andrew Walker ◽  
Barbara A. Laubacher ◽  
Balraj Singh ◽  
Anthony Lucci
Keyword(s):  
Breast Cancer ◽  
Cyclooxygenase 2 ◽  
Receptor Expression ◽  
Prostaglandin E ◽  
Spheroid Formation ◽  
Western Blots ◽  
Ic50 Values ◽  
Cox 2 ◽  
Mcf 7

e21107 Investigating cyclooxygenase-2 signaling in breast cancer-initiating cells Background: Only a small fraction of breast tumor cells, breast cancer-initiating cells (CSC), have the ability to initiate tumor growth and metastasis. Some characteristics of breast CSCs have been described in vitro by employing non-adherent CSC-enriching culture conditions, however, little is known regarding prostanoid signaling or prostaglandin E2 (PgE2) production in CSCs. In this study we measured cyclooxygenase-2 (COX-2) and prostaglandin E2 receptor expression in CSCs and assessed the effects of COX-2 and Ep4 inhibition on in vitro CSC spheroid formation and PgE2 production. Methods: CSCs were cultured in serum-free medium using ultra low attachment plates. Cells were treated with vehicle, a COX-2 inhibitor (Celecoxib), or an EP4 inhibitor (GW627368X) at concentrations of 0.1, 1, 5, 10, 50, or 100uM for 10 days. Spheroids were quantified using a Gelcount machine. Non-linear regression was used to calculate IC50 values. Western blots were performed using anti-COX-2, anti- EP1, 2, 3 and 4 receptor antibodies. Prostaglandin E2 production was measured using a PgE2 immunoassay kit. Results: COX-2 protein expression was observed for MDA-MB-231 and SUM149 CSCs. EP2 and EP4 protein was detected for MCF-7, MDA-MB-231, and SUM149 CSCs. The Celecoxib IC50 values for MCF-7 and SUM149 CSC spheroid formation were 0.5 and 2.2 uM, respectively; GW627386X IC50 values for MCF-7 and SUM149 CSC spheroid formation were 1.2 and 0.3uM, respectively. No significant differences in PGE2 production were observed for MCF-7 CSCs compared to adherent MCF-7 cells (11.5 ± 4.4 vs. 8.7 ± 2.1 pg/mL/106 cells; p=0.88). However, PgE2 production in MDA-MB-231 CSCs was significantly higher than adherent MDA-MB-231 cells (1507.0 ± 329.0 vs. 13.8 ± 5.7 pg/mL/106 cells; p≤0.001) and SUM149 CSC PgE2 production was significantly higher than SUM149 adherent cells (4932.9 ± 501.7 vs. 194.5 ± 31.0 pg/mL/106 cells; p≤0.001). 10uM Celecoxib treatment inhibited PGE2 production in MDA-MB-231 and MDA-MB-231 CSCs. Conclusions: MDA-MB-231 and SUM149 CSCs express COX-2, EP2 and Ep4 and produce high levels of PGE2. CSC spheroid formation is significantly decreased with COX-2 and EP4 inhibition.

scholarly journals A Nitrocarbazole as a New Microtubule-Targeting Agent in Breast Cancer Treatment

2021 ◽  
Vol 11 (19) ◽  
pp. 9139
Author(s):  
Maria Stefania Sinicropi ◽  
Cinzia Tavani ◽  
Camillo Rosano ◽  
Jessica Ceramella ◽  
Domenico Iacopetta ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Anticancer Activity ◽  
Breast Cancer Cell Lines ◽  
Cellular Functions ◽  
Anticancer Properties ◽  
Cycle Arrest ◽  
In Silico Studies ◽  
Ic50 Values ◽  
Mcf 7

Breast cancer is still considered a high-incidence disease, and numerous are the research efforts for the development of new useful and effective therapies. Among anticancer drugs, carbazole compounds are largely studied for their anticancer properties and their ability to interfere with specific targets, such as microtubule components. The latter are involved in vital cellular functions, and the perturbation of their dynamics leads to cell cycle arrest and subsequent apoptosis. In this context, we report the anticancer activity of a series of carbazole analogues 1–8. Among them, 2-nitrocarbazole 1 exhibited the best cytotoxic profile, showing good anticancer activity against two breast cancer cell lines, namely MCF-7 and MDA-MB-231, with IC50 values of 7 ± 1.0 and 11.6 ± 0.8 μM, respectively. Furthermore, compound 1 did not interfere with the growth of the normal cell line MCF-10A, contrarily to Ellipticine, a well-known carbazole derivative used as a reference molecule. Finally, in vitro immunofluorescence analysis and in silico studies allowed us to demonstrate the ability of compound 1 to interfere with tubulin organization, similarly to vinblastine: a feature that results in triggering MCF-7 cell death by apoptosis, as demonstrated using a TUNEL assay.

Sulforaphane, a Chemopreventive Compound, Inhibits Cyclooxygenase-2 and Microsomal Prostaglandin E Synthase-1 Expression in Human HT-29 Colon Cancer Cells

2018 ◽  
Vol 206 (1-2) ◽  
pp. 46-53 ◽  
Author(s):  
Maryam Sadat Tafakh ◽  
Massoud Saidijam ◽  
Tayebeh Ranjbarnejad ◽  
Sara Malih ◽  
Solmaz Mirzamohammadi ◽  
...  
Keyword(s):  
Anticancer Agents ◽  
Caspase 3 ◽  
Mrna Level ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Prostaglandin E Synthase ◽  
Cox 2 ◽  
Ht 29 ◽  
Microsomal Prostaglandin E Synthase

Background: A high expression of prostaglandin E2 (PGE2) is found in colorectal cancer. Therefore, blocking of PGE2 generation has been identified as a promising approach for anticancer therapy. Sulforaphane (SFN), an isothiocyanate derived from glucosinolate, is used as the antioxidant and anticancer agents. Methods: HT-29 cells were treated with various concentrations of SFN and compared to untreated cells for the expression of microsomal prostaglandin E synthase-1 (mPGES-1), cyclooxygenase 2 (COX-2), hypoxia-inducible factor-1 (HIF-1), C-X-C chemokine receptor type 4 (CXCR4), vascular endothelial growth factor (VEGF), and matrix metalloproteinase (MMP)-2 and MMP-9 at the mRNA level. The PGE2 level was measured by ELISA assay. Apoptosis was evaluated by the proportion of sub-G1 cells. The activity of caspase-3 was determined using an enzymatic assay. HT-29 cell migration was assessed using a scratch test. Results: SFN preconditioning decreased the expression of COX-2, mPGES-1, HIF-1, VEGF, CXCR4, MMP-2, and MMP-9. An apoptotic effect of SFN was preceded by the activation of caspase-3 as well as accumulation of cells in the sub-G1 phase of the cell cycle. SFN decreased PGE2 generation and inhibited the in vitro motility/wound-healing activity of HT-29 cells. Conclusions: SFN anticancer effects are associated with antiproliferative, antiangiogenic, and antimetastatic activities arising from the downregulation of the COX-2/ mPGES-1 axis.

Cyclosporin A impairs dendritic cell migration by regulating chemokine receptor expression and inhibiting cyclooxygenase-2 expression

Blood ◽  
2004 ◽  
Vol 103 (2) ◽  
pp. 413-421 ◽  
Author(s):  
Taoyong Chen ◽  
Jun Guo ◽  
Mingjin Yang ◽  
Chaofeng Han ◽  
Minghui Zhang ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Chemokine Receptor ◽  
Cyclooxygenase 2 ◽  
Lymphoid Organs ◽  
Receptor Expression ◽  
Chemokine Receptor Expression ◽  
Cox 2 ◽  
Secondary Lymphoid Organs

Abstract Migration of dendritic cells (DCs) into tissues and secondary lymphoid organs plays a crucial role in the initiation of innate and adaptive immunity. In this article, we show that cyclosporin A (CsA) impairs the migration of DCs both in vitro and in vivo. Exposure of DCs to clinical concentrations of CsA neither induces apoptosis nor alters development but does impair cytokine secretion, chemokine receptor expression, and migration. In vitro, CsA impairs the migration of mouse bone marrow–derived DCs toward macrophage inflammatory protein-3β (MIP-3β) and induces them to retain responsiveness to MIP-1α after lipopolysaccharide (LPS)–stimulated DC maturation, while in vivo administration of CsA inhibits the migration of DCs out of skin and into the secondary lymphoid organs. CsA impairs chemokine receptor and cyclooxygenase-2 (COX-2) expression normally triggered in LPS-stimulated DCs; administration of exogenous prostaglandin E2 (PGE2) reverses the effects of CsA on chemokine receptor expression and DC migration. Inhibition of nuclear factor–κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathway signaling by CsA may be responsible for the CsA-mediated effects on the regulation of chemokine receptor and cyclooxygenase-2 (COX-2) expression. Impairment of DC migration due to inhibition of PGE2 production and regulation of chemokine receptor expression may contribute, in part, to CsA-mediated immunosuppression.

scholarly journals Cross-talk between SIM2s and NFκB regulates cyclooxygenase 2 expression in breast cancer

2019 ◽  
Vol 21 (1) ◽  
Author(s):  
Garhett L. Wyatt ◽  
Lyndsey S. Crump ◽  
Chloe M. Young ◽  
Veronica M. Wessells ◽  
Cole M. McQueen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cyclooxygenase 2 ◽  
Luciferase Reporter ◽  
Signaling Proteins ◽  
Dependent Manner ◽  
Mcf7 Cells ◽  
Human Breast Carcinomas ◽  
Cox 2

Abstract Background Breast cancer is a leading cause of cancer-related death for women in the USA. Thus, there is an increasing need to investigate novel prognostic markers and therapeutic methods. Inflammation raises challenges in treating and preventing the spread of breast cancer. Specifically, the nuclear factor kappa b (NFκB) pathway contributes to cancer progression by stimulating proliferation and preventing apoptosis. One target gene of this pathway is PTGS2, which encodes for cyclooxygenase 2 (COX-2) and is upregulated in 40% of human breast carcinomas. COX-2 is an enzyme involved in the production of prostaglandins, which mediate inflammation. Here, we investigate the effect of Singleminded-2s (SIM2s), a transcriptional tumor suppressor that is implicated in inhibition of tumor growth and metastasis, in regulating NFκB signaling and COX-2. Methods For in vitro experiments, reporter luciferase assays were utilized in MCF7 cells to investigate promoter activity of NFκB and SIM2. Real-time PCR, immunoblotting, immunohistochemistry, and chromatin immunoprecipitation assays were performed in SUM159 and MCF7 cells. For in vivo experiments, MCF10DCIS.COM cells stably expressing SIM2s-FLAG or shPTGS2 were injected into SCID mice and subsequent tumors harvested for immunostaining and analysis. Results Our results reveal that SIM2 attenuates the activation of NFκB as measured using NFκB-luciferase reporter assay. Furthermore, immunostaining of lysates from breast cancer cells overexpressing SIM2s showed reduction in various NFκB signaling proteins, as well as pAkt, whereas knockdown of SIM2 revealed increases in NFκB signaling proteins and pAkt. Additionally, we show that NFκB signaling can act in a reciprocal manner to decrease expression of SIM2s. Likewise, suppressing NFκB translocation in DCIS.COM cells increased SIM2s expression. We also found that NFκB/p65 represses SIM2 in a dose-dependent manner, and when NFκB is suppressed, the effect on the SIM2 is negated. Additionally, our ChIP analysis confirms that NFκB/p65 binds directly to SIM2 promoter site and that the NFκB sites in the SIM2 promoter are required for NFκB-mediated suppression of SIM2s. Finally, overexpression of SIM2s decreases PTGS2 in vitro, and COX-2 staining in vivo while decreasing PTGS2 and/or COX-2 activity results in re-expression of SIM2. Conclusion Our findings identify a novel role for SIM2s in NFκB signaling and COX-2 expression.

scholarly journals Biotinylated xanthohumol: synthesis and in vitro biological evaluation for anticancer therapy

2018 ◽  
Author(s):  
Monika Stompor ◽  
Rafał Podgórski ◽  
Marta Świtalska ◽  
Joanna Wietrzyk
Keyword(s):  
Breast Cancer ◽  
Antioxidant Activity ◽  
Cancer Cells ◽  
Cell Lines ◽  
Biological Evaluation ◽  
Breast Cancer Cell Lines ◽  
Dpph Method ◽  
Ic50 Values ◽  
Mcf 7

Two biotinylated derivatives of the main hop chalcone xanthohumol (1) were prepared by a one-step synthesis via esterification using biotin and 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride (EDC HCl) and 4-dimethylaminopyridine (DMAP) as coupling reagents. The products were characterized spectroscopically and their antiproliferative activity toward MCF-7, MCF-10A, HepG2, MDA-MB-231, 4T1 and Balb/3T3 cell lines was investigated using the SRB assay. For all three tested compounds the best activity was noted in the case of human (MCF-7) and mice (4T1) breast cancer cell lines (IC50 values < 9 μM). Both biotinylated derivatives showed higher anticancer activity than xanthohumol (1) towards all types of tested breast cancer cells. Double biotinylated xanthohumol (3) proved to be the most active in inhibiting cell growth, with IC50 values equal to 5.35 ± 1.5 μM for 4T1 and 8.03 ± 0.53 µM for MCF-7 cell lines. Compound 3 was also more active than 1 and 2 against liver cancer cells HepG2 (IC50 = 17.37 ± 5.1 μM), while the IC50 values for 1 and 2 were equal to 21.5 ± 2.7 and 22.1 ± 3.9 µM, respectively. 4‑O‑biotinylxanthohumol (2) was the second most active growth inhibitor, particularly with respect to MCF-7 (IC50 = 6.19 ± 1.7 μM) and 4T1 (IC50 = 6.64 ± 0.4 μM) cell lines. The antioxidant activity was evaluated using the 1.1-diphenyl-2-picrylhydrazyl radical (DPPH) method. All tested compounds (1-3) have antioxidant activity between 2.73 and 3.38 mM. It was reported for the first time that new prenylated chalcones containing the biotin moiety effectively inhibited proliferation of cancer cells in vitro.

scholarly journals Cross-talk between SIM2s and NFkB regulates cyclooxygenase 2 expression in breast cancer

2019 ◽  
Author(s):  
Garhett Wyatt ◽  
Chloe Young ◽  
Lyndsey Crump ◽  
Veronica Wessells ◽  
Tanya Gustafson ◽  
...  
Keyword(s):  
Breast Cancer ◽  
The United States ◽  
Cyclooxygenase 2 ◽  
Luciferase Reporter ◽  
Signaling Proteins ◽  
Dependent Manner ◽  
Human Breast Carcinomas ◽  
Reporter Assays ◽  
Cox 2

AbstractBackgroundBreast cancer is a leading cause of cancer-related death for women in the United States. Thus, there a need to investigate novel prognostic markers and therapeutic strategies. Inflammation raises challenges to both treating and preventing the spread of breast cancer. Specifically, the nuclear factor kappa b (NFkB) pathway contributes to cancer progression by stimulating proliferation and preventing apoptosis. One target gene of this pathway is PTGS2, the gene that encodes for cyclooxygenase 2 (COX-2), which is upregulated in 40% of human breast carcinomas. COX-2 is an enzyme involved in inflammation. Here we investigate the effect of Singleminded 2s, a transcriptional tumor suppressor that is implicated in inhibition of tumor growth and metastasis, in regulating NFkB and COX-2.MethodsWe utilized in vitro reporter assays, immunoblot analyses, qPCR and immunohistochemical analysis to dissect the relationship between NFκB, SIM2s, and COX-2. Furthermore, we utilized COX-2 targeting strategies to determine tumor suppressive activities.ResultsOur results reveal that SIM2s attenuates the activation of a NFκB via luciferase reporter assays. Furthermore, immunostaining of lysates from breast cancer cells over expressing SIM2s showed reduction in various NFκB signaling proteins, whereas knockdown of SIM2 revealed increases in the same NFκB signaling proteins. Additionally, by increasing NFκB translocation to the nucleus in DCIS.COM cells, we show that NFκB signaling can act in a reciprocal manner to decrease expression of SIM2s. Likewise, suppressing NFκB translocation in DCIS.COM cells increases SIM2s expression. We also found that NFκB/p65 represses SIM2 in via dose-dependent manner and when NFκB is suppressed the effect on the SIM2 is negated. Additionally, our CHIP analysis confirms that NFκB/p65 binds directly to SIM2 promoter site and that the NFκB sites in the SIM2 promoter are required for NFkB-mediated suppression of SIM2s. Finally, over expression of SIM2s decreases PTGS2 in vitro and COX-2 staining in vivo while decreasing PTGS2 and/or Cox-2 activity results in re-expression of SIM2. Our findings identify a novel role for SIM2s in NFκB signaling and COX-2 expression.ConclusionsThese findings provide evidence for a mechanism where SIM2s may represses COX-2 expression to provide an overall better prognosis for breast cancer patients.

scholarly journals pH and redox dual-responsive nanoparticles based on disulfide-containing poly(β-amino ester) for combining chemotherapy and COX-2 inhibitor to overcome drug resistance in breast cancer

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Sipei Zhang ◽  
Nan Guo ◽  
Guoyun Wan ◽  
Tao Zhang ◽  
Chunyu Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Synergistic Effects ◽  
Chemotherapeutic Agents ◽  
Common Mechanism ◽  
Drug Resistant ◽  
Dual Responsive ◽  
Cox 2 ◽  
Mcf 7

Abstract Background Multidrug resistance (MDR) generally leads to breast cancer treatment failure. The most common mechanism of MDR is the overexpression of ATP-binding cassette (ABC) efflux transporters such as P-glycoprotein (P-gp) that reduce the intracellular accumulation of various chemotherapeutic agents. Celecoxib (CXB), a selective COX-2 inhibitor, can dramatically enhance the cytotoxicity of doxorubicin (DOX) in breast cancer cells overexpressing P-gp. Thus it can be seen that the combination of DOX and CXB maybe obtain synergistic effects against breast cancer by overcoming drug resistance. Results In this study, we designed a pH and redox dual-responsive nanocarrier system to combine synergistic effects of DOX and CXB against drug resistant breast cancer. This nanocarrier system denoted as HPPDC nanoparticles showed good in vitro stability and significantly accelerated drug releases under the acidic and redox conditions. In drug-resistant human breast cancer MCF-7/ADR cells, HPPDC nanoparticles significantly enhanced the cellular uptake of DOX through the endocytosis mediated by CD44/HA specific binding and the down-regulated P-gp expression induced by COX-2 inhibition, and thus notably increased the cytotoxicity and apoptosis-inducing activity of DOX. In MCF-7/ADR tumor-bearing nude mice, HPPDC nanoparticles showed excellent tumor-targeting ability, remarkably enhanced tumor chemosensitivity and reduced COX-2 and P-gp expressions in tumor tissues. Conclusion All results demonstrated that HPPDC nanoparticles can efficiently overcome drug resistance in breast cancer both in vitro and in vivo by combining chemotherapy and COX-2 inhibitor. In a summary, HPPDC nanoparticles show a great potential for combination treatment of drug resistant breast cancer.

scholarly journals Biomechanical regulation of cyclooxygenase-2 in the renal collecting duct

2014 ◽  
Vol 306 (2) ◽  
pp. F214-F223 ◽  
Author(s):  
Yu Liu ◽  
Daniel Flores ◽  
Rolando Carrisoza-Gaytán ◽  
Rajeev Rohatgi
Keyword(s):  
Fluid Shear Stress ◽  
Collecting Duct ◽  
Isotonic Saline ◽  
Cyclooxygenase 2 ◽  
Dietary Sodium ◽  
Prostaglandin E ◽  
Urinary Flow ◽  
Cox 2 ◽  
Tubular Flow

High-dietary sodium (Na), a feature of the Western diet, requires the kidney to excrete ample Na to maintain homeostasis and prevent hypertension. High urinary flow rate, presumably, leads to an increase in fluid shear stress (FSS) and FSS-mediated release of prostaglandin E2 (PGE2) by the cortical collecting duct (CCD) that enhances renal Na excretion. The pathways by which tubular flow biomechanically regulates PGE2 release and cyclooxygenase-2 (COX-2) expression are limited. We hypothesized that FSS, through stimulation of neutral-sphingomyelinase (N-SM) activity, enhances COX-2 expression to boost Na excretion. To test this, inner medullary CD3 cells were exposed to FSS in vitro and mice were injected with isotonic saline in vivo to induce high tubular flow. In vitro, FSS induced N-SM activity and COX-2 protein expression in cells while inhibition of N-SM activity repressed FSS-induced COX-2 protein abundance. Moreover, the murine CCD expresses N-SM protein and, when mice are injected with isotonic saline to induce high tubular flow, renal immunodetectable COX-2 is induced. Urinary PGE2 (445 ± 91 vs. 205 ± 14 pg/ml; P < 0.05) and microdissected CCDs (135.8 ± 21.7 vs. 65.8 ± 11.0 pg·ml−1·mm−1 CCD; P < 0.05) from saline-injected mice generate more PGE2 than sham-injected controls, respectively. Incubation of CCDs with arachidonic acid and subsequent measurement of secreted PGE2 are a reflection of the PGE2 generating potential of the epithelia. CCDs isolated from polyuric mice doubled their PGE2 generating potential and this was due to induction of COX-2 activity/protein. Thus, high tubular flow and FSS induce COX-2 protein/activity to enhance PGE2 release and, presumably, effectuate Na excretion.

scholarly journals Novel augmentation by bufalin of protein kinase C-induced cyclooxygenase-2 and IL-8 production in human breast cancer cells

2016 ◽  
Vol 23 (1) ◽  
pp. 54-66 ◽  
Author(s):  
Hsiao-Ting Chen ◽  
David Sun ◽  
Yen-Chun Peng ◽  
Pu-Hong Kao ◽  
Yuh-Lin Wu
Keyword(s):  
Breast Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Mrna Levels ◽  
Kinase C ◽  
Cox 2

Cyclooxygenase-2 (COX-2) and IL-8 are two inflammatory mediators induced by protein kinase C (PKC) via various stimuli. Both contribute significantly to cancer progression. Bufalin, a major active component of the traditional Chinese medicine Chan Su, is known to induce apoptosis in various cancer cells. This study clarifies the role and mechanism of bufalin action during PKC regulation of COX-2/IL-8 expression and investigates the associated impact on breast cancer. Using MB-231 breast cancer cells, bufalin augments PKC induction of COX-2/IL-8 at both the protein and mRNA levels, and the production of prostaglandin E2 (PGE2) and IL-8. The MAPK and NF-κB pathways are involved in both the PKC-mediated and bufalin-promoted PKC regulation of COX-2/IL-8 production. Bufalin increases PKC-induced MAPKs phosphorylation and NF-κB nuclear translocation. PGE2 stimulates the proliferation/migration of breast cancer cells. Furthermore, PKC-induced matrix metalloproteinase 3 expression is enhanced by bufalin. Bufalin significantly enhances breast cancer xenograft growth, which is accompanied by an elevation in COX-2/IL-8 expression. In conclusion, bufalin seems to promote the inflammatory response in vitro and in vivo, and this occurs, at least in part, by targeting the MAPK and NF-κB pathways, which then enhances the growth of breast cancer cells.

scholarly journals IN VITRO CYTOTOXIC ACTIVITY OF RODENT TUBER MUTANT PLANT (TYPHONIUM FLAGELLIFORME LODD.) AGAINST TO MCF-7 BREAST CANCER CELL LINE

2019 ◽  
pp. 185-189 ◽  
Author(s):  
NESTI FRONIKA SIANIPAR ◽  
KHOIRUNNISA ASSIDQI ◽  
RAGAPADMI PURNAMANINGSIH ◽  
TATI HERLINA
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Bioactive Compounds ◽  
Acid Methyl Ester ◽  
Cancer Cell Line ◽  
Octadecanoic Acid ◽  
Acid Methyl ◽  
Ic50 Values ◽  
Mcf 7

Objective: The objective of this study was to determine the new bioactive compounds through gas chromatography–mass spectrometry analysis and the cytotoxic activity of two rodent tuber mutant plants against breast cancer cells (MCF-7). Methods: The bioactive compounds in rodent tuber mutant plants were successfully increased by somaclonal variation using gamma rays irradiation technique. Further, the cytotoxicity activity of rodent tuber mutant plants was tested on breast cancer cell line (MCF-7) performed by 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide assay method. Results: This results study confirmed that the presence of phytochemical composition in the tuber of rodent tuber mutant plants KB 6–1–3–4 and KB 6–9–5 was found six bioactive compounds from fatty acid groups which have the potential as an anticancer compound, such as octadecanoic acid, hexadecanoic acid, hexadecanoic acid methyl ester, 9-octadecanoic acid, linolelaidic acid methyl ester, and butanoic acid. The results showed that extracts from rodent tuber mutant plants had a cytotoxicity effect on MCF-7 cancer cells with half maximal inhibitory concentration (IC50) values that were lower than the control (mother plant). In vitro tests of KB 6–1–3–4 and KB 6–9–5 against MCF-7 cancer cell lines have IC50 values of 12.482 μg/mL and 7.043 μg/mL, respectively, while it had a lower cytotoxicity effect with the IC50 value of control plant was 19.113 μg/mL. The mutant plants of KB 6-9-5 have 3 times more effective than control. Conclusion: The results of this study clearly indicated that rodent tuber mutant plants have shown promising as an anticancer drug on breast cancer.

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