Assessment of anti-cancer effects of koenimbine on colon cancer cells

2020 ◽  
Vol 28 (3) ◽  
pp. 185-190
Author(s):  
Maliheh Astaneh ◽  
Soudeh Ghafouri-Fard ◽  
Zahra Fazeli ◽  
Zahra Taherian-Esfahani ◽  
Sepideh Dashti ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Annexin V ◽  
Colon Cancer Cells ◽  
Cytotoxic Effects ◽  
Anti Cancer ◽  
Ht 29

BACKGROUND: Recent studies have highlighted the role of natural elements in reduction of cancer cell growth and apoptosis. Koenimbine, a natural product isolated from Murraya koenigii (L) Spreng is a substance with cytotoxic effects on cancer cells. AIM: The effects of koenimbine on HT-29 and SW48 colon cancer cells were evaluated by MTT and Annexin V assays. Expression levels of Wnt/β-catenin pathway genes were quantified by real time PCR. RESULTS: The IC50 values of koenimbine in HT-29 and SW48 was calculated to be 50 μg/ml based on the results of MTT assay. This value was 75 μg/ml in IEC-18 cells which were used as normal control. Annexin V assays revealed induction of cell apoptosis and necrosis in HT-29 and SW48 cells but not IEG18 cells by koenimbine. Koenimbin treatment resulted in significant down-regulation of CYCLD1 expression in SW48 cell line, but up-regulation of this gene in HT29 cell line. Expression of TBLR1, DKK1, GSK3B and β-catenin was significantly decreased after koenimbin treatment in HT-19 cell line. Moreover, expression of DKK1 and GSK3B was significantly decreased after koenimbin treatment in SW-40 cell line. TCF4 expression was not detected in any of cell lines either before or after treatment with koenimbin. CONCLUSION: The current in vitro study showed the cytotoxic effects of koenimbin on two colon cancer cell lines and the effects of this substance on expression of selected genes from Wnt-β catenin pathway. Future in vivo studies are needed before suggestion of this substance as an anti-cancer drug.

scholarly journals Piperidone Analogue of Curcumin-loaded HPβ-cyclodextrin liposomes as delivery system for human cancer therapy

2017 ◽  
Vol 1 (3) ◽  
Author(s):  
S. Alhabardi, A. Aboussekhra, A. Alshamsan, A. Alomrani
Keyword(s):  
Breast Cancer ◽  
Colon Cancer ◽  
Particle Size ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Delivery System ◽  
Annexin V ◽  
Aqueous Solubility ◽  
Anti Cancer

Cancer is a broad term used to describe different types of tumors affecting various parts of the human body. The resistance to multiple therapeutic agents, toxicity to healthy tissues, and lack of effective therapies obligate scientists to keep looking for new agents. Curcumin (diferuloylmethane) is a natural product. It has been reported that curcumin has anti-inflammatory, anti-diabetic, and anti-cancer effects. However, clinical use of curcumin is limited due to its poor aqueous solubility. Recently, a curcumin analogue, 5-Bis (4-hydroxy-3-methoxybenzylidene)-N-methyl-4-piperidone of curcumin (PAC), was synthesized to overcome this limitation. This compound showed significantly higher anticancer activity on breast cancer cell lines and colon cancer cell lines as compared to native curcumin. However, aqueous solubility of this new chemical compound limited its use and application. Liposomes were found to be the most promising system to use to overcome aqueous solubility and delivery limitations. Liposomes are a self-assembly of phospholipid molecules. They are biodegradable, biocompatible, and nontoxic carrier systems. These features make liposomes an ideal carrier system for anticancer agents. In this study liposomes were utilized to overcome PAC limitations. This project was designed to develop liposomal delivery system for PAC for cancer treatment and evaluate the anti-cancer properties of this system. Liposomal PAC formulae were prepared by the film hydration method and were optimized by adding hydroxypropyl-beta-cyclodextrin (HPβCD) and characterized in term of particle size, entrapment efficiency, release profile and cytotoxic activity. Liposomes with an average size below 150 nm and zwitterionic charge were obtained. Indeed, no major differences were seen in particle size and surface charge. However, HPβCD inclusion gave satisfied incorporation capacity reaching 68.1%. In addition, HPβCD inclusion in the liposomes resulted in increased in vitro release rate compared to conventional liposomes. On colon cancer cells, Annexin V/PI- Flow Cytometery cytotoxicity results revealed that the PAC-loaded HPβ-cyclodextrin liposomes trigger apoptosis by 75% in response (10 µM), whereas it was only 43% in response to the same concentration of PAC conventional liposomes, which confirmed their potential anti-cancer activity. On breast cancer cells, Annexin V/PI- Flow Cytometery cytotoxicity results showed that while PAC conventional liposomes have only minor cytotoxic effect (22-25%), PAC-loaded HPβCD liposomes induced 53% and 70% apoptosis in response to 5 µM and 10 µM, respectively. The cytotoxicity of PAC-loaded HPβ-cyclodextrin liposomes was more pronounced than PAC conventional liposomes in both cells, suggesting the benefits of using HPβ-cyclodextrin. Therefore, PAC-loaded HPβ-cyclodextrin liposomes indicate significant potential as delivery vehicles for the treatment of cancers.

scholarly journals Synthesis of 3-Trifluoromethyl-5,6-dihydro-[1,2,4]triazolo Pyrazine Derivatives and Their Anti-Cancer Studies

Molbank ◽  
10.3390/m1173 ◽  
2020 ◽  
Vol 2020 (4) ◽  
pp. M1173
Author(s):  
Rajaiah Raveesha ◽  
Malavalli Guruswamy Dileep Kumar ◽  
Salekoppal Boregowda Benaka Prasad
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Apoptotic Pathway ◽  
Mitochondrial Apoptotic Pathway ◽  
Colon Cancer Cell Lines ◽  
Anti Cancer ◽  
Ht 29

The synthesis of a wide variety of 3-trifluoromethyl-5,6-dihydro-[1,2,4]triazolo pyrazine derivatives, by the treatment of 3-trifluoromethyl-5,6,7,8-tetrahydro-[1,2,4]triazolo[4,3-α]pyrazine hydrochloride with an array of isocyanates in the presence of triethylamine, is reported. All the target compounds were synthesized in excellent yields under mild reaction conditions. The target molecules were effectively screened for their anti-cancer properties and the results are promising. The resultant compounds were assessed for their antiproliferative action against two human colon cancer cell lines (HCT-116 and HT-29 colon cancer cell lines). The IC50 range was estimated at 6.587 to 11.10 µM showing that compound RB7 had remarkable anticancer movement on HT-29. Additionally, it was discovered that RB7 incited the mitochondrial apoptotic pathway by up-regulating Bax and down-regulating Bcl2, eventually leading to the activation of Caspase 3 in HT-29 cells and initiation of cell death via the mitochondrial apoptotic pathway.

Incomplete processing of progastrin expressed by human colon cancer cells: role of noncarboxyamidated gastrins

1994 ◽  
Vol 266 (3) ◽  
pp. G459-G468 ◽  
Author(s):  
P. Singh ◽  
Z. Xu ◽  
B. Dai ◽  
S. Rajaraman ◽  
N. Rubin ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Colon ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Colon Cancer Cell Lines

Gastrin is mitogenic for several colon cancers. To assess a possible autocrine role of gastrin in colon cancers, we examined human colon cancer cell lines for expression of gastrin mRNA and various forms of gastrin. Gastrin mRNA was not detected in the majority of colon cancer cell lines by Northern hybridization but was detected in all human colon cancer lines by the sensitive method of reverse transcriptase-polymerase chain reaction (PCR). Gastrin mRNA was quantitated by the competitive PCR method. The majority of cell lines expressed very low levels of gastrin mRNA (< 1-5 copies/cell); only one cell line expressed > 20 copies/cell. The mature carboxyamidated form of gastrin was not detected in any of the cell lines by radioimmunoassay or immunocytochemistry. Results suggested that either gastrin mRNA expressed by colon cancer cells was altered (mutated) or posttranslational processing of progastrin was incomplete. Gastrin cDNA from all the colon cancer cell lines had an identical sequence to the published sequence of human gastrin cDNA. Specific antibodies against precursor forms of gastrin were used, and significant concentrations of nonamidated (glycine-extended) and prepro forms of gastrin were measured in tumor extracts of representative colon cancer cell lines. The presence of precursor forms of gastrin suggested a lack of one or more of the processing enzymes and/or cofactors. Significant concentrations of the processing enzyme (peptidylglycine alpha-amidating monooxygenase) were detected in colon cancer cells by immunocytochemistry. Therefore, lack of other cofactors or enzymes may be contributing to incomplete processing of precursor forms of gastrin, which merits further investigation. Since low levels of gastrin mRNA were expressed by the majority of human colon cancer cell lines and progastrin was incompletely processed, it seems unlikely that gastrin can function as a viable autocrine growth factor for colon cancer cells. High concentrations of glycine-extended gastrin-17 (GG) (> 10(-6) M) were mitogenic for a gastrin-responsive human colon cancer (DLD-1) cell line in vitro. It remains to be seen if GG or other precursor forms of gastrin are similarly mitogenic in vivo, which may then lend credibility to a possible autocrine role of gastrinlike peptides in colon cancers.

scholarly journals PRMT1 inhibition induces differentiation of colon cancer cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Alexander Plotnikov ◽  
Noga Kozer ◽  
Galit Cohen ◽  
Silvia Carvalho ◽  
Shirly Duberstein ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Differentiation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Differentiation Therapy ◽  
Human Colon Cancer ◽  
Ht 29

AbstractDifferentiation therapy has been recently revisited as a prospective approach in cancer therapy by targeting the aberrant growth, and repairing the differentiation and cell death programs of cancer cells. However, differentiation therapy of solid tumors is a challenging issue and progress in this field is limited. We performed High Throughput Screening (HTS) using a novel dual multiplex assay to discover compounds, which induce differentiation of human colon cancer cells. Here we show that the protein arginine methyl transferase (PRMT) type 1 inhibitor, MS023, is a potent inducer of colon cancer cell differentiation with a large therapeutic window. Differentiation changes in the highly aggressive human colon cancer cell line (HT-29) were proved by proteomic and genomic approaches. Growth of HT-29 xenograft in nude mice was significantly delayed upon MS023 treatment and immunohistochemistry of tumor indicated differentiation changes. These findings may lead to development of clinically effective anti-cancer drugs based on the mechanism of cancer cell differentiation.

scholarly journals 725 Immunomodulation by targeting PDL-1 in colon cancer using nuclear receptor 4A1 (NR4A1) antagonists

2021 ◽  
Vol 9 (Suppl 3) ◽  
pp. A754-A755
Author(s):  
Maen Abdelrahim ◽  
Kumaravel Mohankumar ◽  
Keshav Karki ◽  
Stephen Safe
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Western Blots ◽  
Colon Cancer Cell Lines

BackgroundThe nuclear orphan receptor 4A1 (NR4A1, Nur77, TR3) is overexpressed in multiple solid tumors including colorectal tumors and is a negative prognostic factor for patient survival.1–3 NR4A1 is expressed in colon cancer cells and exhibit pro-oncogenic activity4 and results of examination of several colon cancer cell lines show that PD-L1 expression is limited and NR4A1 and PD-L1 are co-expressed in SW480 and RKO colon cancer cell lines. Previous studies showed that PD-L1 was regulated by NR4A1 which activates transcription factor Sp1 bound to the PD-L1 gene promoter.5–7 Knockdown of NR4A1 or Sp1 by RNA interference or treatment with mithramycin an inhibitor of Sp-mediated transcription decreased expression of PD-L1 in RKO and SW480 colon cancer cell lines.MethodsSW480, RKO and MC-38 cells were used in this study. Cells were treated for 24 hrs with DIM series of compounds.ResultsCurrent data coupled with ongoing gene expression and PD-L1 promoter studies demonstrate that PD-L1 expression is regulated by NR4A1/Sp1 in colon cancer cells (figures 1–3). Bis-indole derived NR4A1 ligand that act as receptor antagonists have been developed in this laboratory and these compounds block pro-oncogenic NR4A1-regulated genes/pathways. Treatment of RKO and SW480 colon cancer cell lines with a series of potent 1,1-bis(3′-indolyl)-1-(3,5-disubstitutedphenyl) analogs decreased expression of PD-L1. These results show that bis-indole derived NR4A1 antagonists act as small molecule mimics of immunotherapeutics that target PD-L1. In vivo applications of NR4A1 ligands that target PD-L1 and their effects on tumor growth and immune surveillance are currently being investigated.ConclusionsBis-indole derived NR4A1 antagonists inhibit PD-L1 expression. NR4A1/SP1 regulates PD-L1 and is inhibited by NR4A1 antagonist. NR4A1 ligands such as DIM-3-Br-5-OCF3 were among the most potent of the substituted DIM compounds and ongoing in vivo studies show that this DIM compound also inhibits tumor growth in a syngenic mouse model (data not shown). Data from this study demonstrate the pro-oncogenic activity of NR4A1 and show that the synthetic buttressed analog DIM-3-Br-5-OCF3 acts as an NR4A1 antagonist and inhibits PD-L1 expression. These drugs can be developed for future clinical applications.Referenceswww.cancer.org/cancer/colon-rectal-cancer/about/key-statistics.html.Garcia-Villatoro et al., Effects of high-fat diet and intestinal aryl hydrocarbon receptor deletion on colon carcinogenesis. Am J Physiol Gastrointest Liver Physiol 2020;318(3):G451–G463.Safe S, Jin UH, Hedrick E, et al. Minireview: role of orphan nuclear receptors in cancer and potential as drug targets. Mol Endocrinol 2014;28(2):157–72.Maxwell MA, Muscat GE. The NR4A subgroup: immediate early response genes with pleiotropic physiological roles. Nucl Recept Signal 2006;4:e002.Lee SO, Li X, Hedrick E, et al. Diindolylmethane analogs bind NR4A1 and are NR4A1 antagonists in colon cancer cells. Mol Endocrinol 2014;28(10):1729–39.Safe S, Kim K. Non-classical genomic estrogen receptor (ER)/specificity protein and ER/activating protein-1 signaling pathways. J Mol Endocrinol 2008;41(5):263–75.Tao LH, Zhou XR, Li FC, Chen Q, Meng FY, Mao Y, et al. A polymorphism in the promoter region of PD-L1 serves as a binding-site for SP1 and is associated with PD-L1 overexpression and increased occurrence of gastric cancer. Cancer Immunol Immunother 2017;66(3):309–18.Abstract 725 Figure 1NR4A1 inactivation inhibits PD-L1 expression. SW480, RKO and MC-38 cells were transfected with siCtrl (non-specific oligonucleotide) and two oligonucleotides targeting NR4A1 (siNR4A1(1) and siNR4A1(2)) or PD-L1 (siPD-L1(1) and siPD-L1(2)) for 72 hrss. Protein expression from whole cell lysates were analyzed by western blots and effects on PD-L1 expression were determinedAbstract 725 Figure 2Sp1 inactivation inhibits PD-L1 expression. SW480, RKO and MC-38 cells were transfected with siCtrl and oligonucleotides targeting Sp1 (siSp1(1) and siSp1(2)) for 72 hrs as well as treated with Mithrsamycin (150 and 300 nM) for 24 hrs. Protein expression from was analyzed by western blots and effects on PD-L1 levels were determined.Abstract 725 Figure 3Role of NR4A1/Sp in regulation of PD-L1. SW480, RKO and MC-38 cells were treated with DIM-3-Br-5-OCF3 for 24 hrss and protein interactions with the GC-rich PD-L1 promoter region were analyzed by ChIP using primers encompassing GC-rich region of the promoter

scholarly journals Trolox induces inhibition of cell proliferation and apoptosis in human colon cancer cells

2015 ◽  
Vol 10 (4) ◽  
pp. 931 ◽  
Author(s):  
Li-Guang Yang ◽  
Xiang-An Tian ◽  
Xiao-Yan Li ◽  
Jian-Guo Huang ◽  
Nai-Qing Liu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Colon Cancer Cell Lines

<p class="Abstract">In the present study, the effect of trolox on human colon cancer cell lines was investigated. The results revealed that trolox treatment caused inhibition of cell growth in T84 and HCT-15 colon cancer cell lines in a dose-dependent manner. The inhibition was significant at 50 µM of trolox after 48 hours in both cell lines. Trolox treatment promoted expression of p38 and inhibited expression of survivin and Akt. It also induced cleavage of PARP and caspase-3 and ultimately induced apoptosis in T84 and HCT-15 cells. The tumor growth was inhibited significantly in the xenotransplanted mice on treatment with trolox compared to the control group. Since trolox treatment exhibits inhibitory effect on the proliferation of colon cancer cells and inhibits tumor growth in vivo therefore, can be of therapeutic importance for the treatment of colon cancer.</p><p> </p>

Cedrus deodara (Bark) Essential Oil Induces Apoptosis in Human Colon Cancer Cells by Inhibiting Nuclear Factor kappa B

2020 ◽  
Vol 20 (22) ◽  
pp. 1981-1992
Author(s):  
Madhulika Bhagat ◽  
Ajay Kumar ◽  
Renuka Suravajhala
Keyword(s):  
Colon Cancer ◽  
Essential Oil ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Anticancer Agent ◽  
Octadecenoic Acid ◽  
Colon Cancer Cells ◽  
Cedrus Deodara

Aims: The aim of this study is to explore essential oil from the bark of Cedrus deodara (CDEO) as an potential anticancer agent. Background: The frontline drugs against cancer in clinical settings are posing challenges of resistance and other detrimental side-effects. This has led to the exploration of new anticancer chemical entities from natural sources, particularly plant-based products such as essential oils that serve as vast repositories of pharmacologically active substances for combating cancer. Objective: The objective is to isolate and characterize the essential oil from the bark of Cedrus deodara (CDEO) and evaluate its potential as an anticancer agent and delineate the possible underlying mechanism of action. Methods: Cedrus deodara essential oil from bark (CDEO) was obtained by hydro-distillation and analyzed by GC/MS for vital constituents. Further, in vitro cytotoxic potential was measured by MTT assay against a panel of cancer cell lines. The apoptosis-inducing potential of CDEO was analyzed by mitochondrial membrane potential loss (ΔΨm) and nuclear fragmentation assay. Besides, wound healing assay and colonogenic assay were employed to check the anti-metastatic potential of CDEO. Molecular docking approaches were employed for target identification, while immuno-blotting was carried out for target validation. Results and Discussion: The major components identified were 2-(tert-Buyl)-6-methyl-3-(2- (trifluoromethyl) benzyl)imidazo [1,2-a]pyridine (26.32 %);9- Octadecenoic acid (8.015 %); Copaene (5.181 %);2-(4-Methoxy-2,6-dimethylphenyl) -3-methyl-2H- benzo[g]indazole(4.36 %) and 9(E),11(E)- Conjugated linoleic acid (4.299 %). Further, potent in vitro cytotoxic activity with IC50 values of 11.88 μg/ ml and 14.63 μg/ ml in colon cancer cell lines of HCT-116 and SW-620, respectively. Further, a significant and dose-dependent decrease in colony formation, cell migration, induction of ROS formation and loss in ΔΨm was observed. Additionally, major compounds identified were chosen for ligandprotein binding interaction studies to predict the molecular targets in colon cancer. It was observed that compounds such as 9-Octadecenoic acid;4H-1- Benzopyran-4-one, 3-(3,4-dimethoxyphenyl)-6,7- dimethoxy; 2-(4-Methoxy-2,6-dimethylphenyl) -3-methyl-2H-benzo [g]indazole and 2-Bornanol,5-(2,4- dinitro phenyl) hydrazono have a prominent binding affinity with NF-κB. This was also further validated by immuno-blotting results wherein CDEO treatment in colon cancer cells led to the abrogation of NFκB, and the Bcl-2-associated X protein (Bax): B-cell lymphoma (Bcl)-2 ratio was up-regulated leading to enhanced cleaved caspase 3 formation and subsequent apoptosis. Conclusion: These results unveil CDEO inhibits cell proliferation and induces apoptosis in colon cancer cells, which can be attributed to the abrogation of the NFκB signaling pathway.

Efficacy of telotristat ethyl: A peripheral tryptophan hydroxylase inhibitor that blocks serotonin biosynthesis against cultured liposarcoma, colon cancer, and cholangiocarcinoma cell lines.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15602-e15602
Author(s):  
Harvey J. Kliman ◽  
Ivy S Ling ◽  
Kristin M Milano
Keyword(s):  
Colon Cancer ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tryptophan Hydroxylase ◽  
Tumor Cell Line ◽  
Main Function ◽  
Specific Expression ◽  
Cholangiocarcinoma Cell ◽  
Ht 29

e15602 Background: Serotonin (5-HT) is most often considered a neurotransmitter—but in reality its main function is to promote cell proliferation at the site of wound healing via platelet degranulation. We tested the hypothesis that blocking 5-HT production in cancer cells might lead to their death by exposure to a specific tryptophan hydroxylase (TPH) inhibitor: telotristat ethyl (TE). The advantage of this TPH inhibitor is that it does not cross the blood brain barrier and therefore can be used to treat peripheral cancers without danger of interfering with central nervous system 5-HT production. Methods: Three cancer cell lines were tested: liposarcoma (94T778), colon cancer (HT-29), and cholangiocarcinoma (TFK-1). The cells were grown with 0, 5, 15 and 30 µM TE, plated into four-chambered slides with an initial confluence of at least 30%, and cultured for 24-96 H. At the end of each 24 hour period slides were removed, washed, fixed, and stained with hematoxylin for density assessment. Experiments were performed in triplicate and repeated in at least three separate experiments. Cell confluence was determined under low power microscopic examination. Results: In the absence of TE the three cell lines increased their confluence from approximately 30% to 83±5.8% (94T778), 68±11% (HT-29), and 60±16% (TFK-1) over 96 H. When the 94T778 cells were exposed to increasing concentrations of TE their confluence decreased progressively. At a dose of 30 µM cell confluence at 24 H was 3±0%, at 48 H 0.3±0.6%, at 72 H 0±0%, and at 96 H 0±0%. For the HT-29 cells, cell confluence in the 30 µM TE groups were 12±8%, 3±3%, 7±5% and 2±1% at 24, 48, 72 and 96 H, respectively. For the TFK-1cells, cell confluence in the 30 µM TE groups were 7±3%, 20±14%, 17±14% and 24±16% at 24, 48, 72 and 96 H, respectively. Conclusions: Telotristat ethyl is a potent inhibitor of tumor cell line growth. However, the efficacy of this inhibition varies between cell lines. The liposarcoma cell line was most sensitive to TE, with the cholangiocarcinoma cell line being moderately impacted. The colon cancer cell line was intermediate between these two. The differences in response to TE may be related to the specific expression of TPH in any particular cell line, with cancers that are more dependent on 5-HT production being most impacted by TPH blockade. Just as ER PR positive breast cancers are sensitive to blockade of these receptors, TPH positive cancers may be successfully targeted by specific inhibition of the 5-HT biosynthetic pathway.

scholarly journals Effects of Silymarin-Loaded Nanoparticles on HT-29 Human Colon Cancer Cells

Medicina ◽  
2018 ◽  
Vol 54 (1) ◽  
pp. 1 ◽  
Author(s):  
Maryam Mombeini ◽  
Ghasem Saki ◽  
Layasadat Khorsandi ◽  
Neda Bavarsad
Keyword(s):  
Colon Cancer ◽  
Toxic Effect ◽  
Cancer Cells ◽  
Cancer Cell Line ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Anti Cancer ◽  
Human Colon Cancer Cells ◽  
Ht 29

Background and objective: Previous studies have demonstrated the anti-cancer effects of silymarin (SLM). However, the low bioavailability of SLM has restricted its use. This study investigated the toxic effect of nanostructured SLM encapsulated in micelles (Nano-SLM) on the growth of the HT-29 human colon cancer cell line. Materials and methods: HT-29 cells were treated with 25 μM/mL of SLM or Nano-SLM for 48 h. MTT and colony formation assays were used to assess the cytotoxicity and proliferation of HT-29 cells, respectively. The cells were stained with annexin V/PI for assessment of apoptosis. Results: MTT assays revealed that Nano-SLM treatment was able to exert a more pronounced toxic effect on the HT-29 cells as compared to free SLM treatment (p < 0.01). In the Nano-SLM-treated cells, colony numbers were significantly reduced in comparison to the free SLM-treated cells (p < 0.01). Apoptotic and necrotic indexes of Nano-SLM-treated HT-29 cells were also significantly increased in comparison to those of the free SLM-treated cells (p < 0.01). The viability, proliferation and apoptosis of healthy cells (NIH-3T3 cells) were not changed in response to Nano-SLM or SLM. Conclusions: Our results indicate that Nano-SLM enhances the anti-cancer effects of SLM against human colon cancer cells.

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