Tested Carcinoma Cell Lines Research Articles

Evidence for a novel, effective approach to targeting carcinoma catabolism exploiting the first-in-class, anti-cancer mitochondrial drug, CPI-613.

Clinical targeting of the altered metabolism of tumor cells has long been considered an attractive hypothetical approach. However, this strategy has yet to perform well clinically. Metabolic redundancy is among the limitations on effectiveness of many approaches, engendering intrinsic single-agent resistance or efficient evolution of such resistance. We describe new studies of the multi-target, tumor-preferential inhibition of the mitochondrial tricarboxylic acid (TCA) cycle by the first-in-class drug CPI-613® (devimistat). By suppressing the TCA hub, indispensable to many metabolic pathways, CPI-613 substantially reduces the effective redundancy of tumor catabolism. This TCA cycle suppression also engenders an apparently homeostatic accelerated, inefficient consumption of nutrient stores in carcinoma cells, eroding some sources of drug resistance. Nonetheless, sufficiently abundant, cell line-specific lipid stores in carcinoma cells are among remaining sources of CPI-613 resistance in vitro and during the in vivo pharmacological drug pulse. Specifically, the fatty acid beta-oxidation step delivers electrons directly to the mitochondrial electron transport system (ETC), by-passing the TCA cycle CPI-613 target and producing drug resistance. Strikingly, tested carcinoma cell lines configure much of this fatty acid flow to initially traverse the peroxisome enroute to additional mitochondrial beta-oxidation. This feature facilitates targeting as clinically practical agents disrupting this flow are available. Two such agents significantly sensitize an otherwise fully CPI-613-resistant carcinoma xenograft in vivo. These and related results are strong empirical support for a potentially general class of strategies for enhanced clinical targeting of carcinoma catabolism.

Coordination compounds of pyrazolone‐based ligand: Design, characterization, biological evaluation, antitumor efficiency, and DNA binding evaluation supported by in silico studies

AbstractCu (II), Ni (II), Mn (II), and Cr (III) chelates of the organic ligand named 3‐(furan‐2‐yl)‐5‐oxo‐N,1‐diphenyl‐4,5‐dihydro‐1H‐pyrazole‐4‐carbothioamide ligand (abbreviated as H2L) have been obtained. Successful structure elucidation of the ligand and its chelates has been managed by applying alternative spectral and analytical techniques including elemental analysis, inductively coupled plasma (ICP), NMR, mass, and FTIR spectra in addition to molar conductance and TGA technique which all joint confirmed the formation of the metal complexes in the molar ratio 1:2 (M:L) for Cu (II) and Mn (II) chelates, while 1:1 for the rest of complexes. The applied techniques also confirmed the metal complexes to be formulated as [Cu (HL)2(H2O)2]‧0.5H2O, [Ni (HL)(H2O)Cl]‧0.5H2O, [Mn (HL)2(H2O)2]‧2H2O and [Cr (HL)(H2O)2(CH3COO)2]‧2.5H2O, where HL is the organic ligand. UV–Vis spectra and μeff values of the metal chelates assured the geometry around the metal ion center to be octahedral for both Cu (II), Mn (II), and Cr (III) complexes. For the Ni (II) complex, tetrahedral arrangement has been concluded. The in vitro antimicrobial efficacy applied on several microorganisms and the antioxidant activity showed biological activities in relation to employed standard reported compounds with enhanced activity of the Cr (III) complex compared with the other tested compounds. The antitumor activity was examined upon four carcinoma cell lines that are HePG‐2 MCF‐7, HCT‐116, and HeP‐2 demonstrated that the Cr (III) complex to has the highest activity against the four tested carcinoma cell lines relative to the other tested compounds. The binding mode of the ligand and its complexes with SS‐DNA have been examined applying UV–Vis spectral titration and viscosity measurements, assuring groove binding interactions, which were supported theoretically through the docking studies.

A novel inhibitor, 2-cyano-3-(1-phenyl-3-(thiophen-2-yl)-pyrazol-4-yl)acrylamide linked to sulphamethoxazole, blocks anti-apoptotic proteins via molecular docking and strongly induced apoptosis of HCT116 cell line by different molecular tools

A new series of cyanoacrylamides incorporating sulphamethoxazol were prepared and confirmed by different spectral tools. Anticancer screening of the new compounds was done against three different types of carcinoma cell lines involving (A549, HCT116, and MDA) using MTT assay. Compound 7 among all tested derivatives achieved the best cytotoxic effect against all tested carcinoma cell lines. HCT116 revealed the best sensitivity and cytotoxic activity toward compound 7 relative to 5-FU. The target compound offered less toxic effect when tested on normal melanocytes (HFB4). Simulation modeling studies revealed strong binding affinity toward the following domains (1dls, 2c6o, and 2wgj) and moderate binding modes toward (3eyl, 4kmp, 2w3l, and 5lab) domains with different binding energy scores. Gene expression profile outlined that caspase-3, BAX, and P53 genes were strongly upregulated relative to their control, while BCL2, MMP1, and CDK2 were effectively down regulated assuming the activation of the apoptotic pathway. Flow cytometry technique revealed that compound 7 stimulated cell cycle arrests at the G2/M phase. Other extensive molecular diagnostic tools were utilized in this report as ELISA, DPA, SEM, and TEM assays which confirmed that our target novel compound 7 was a very promising and interesting chemotherapeutic agent with less toxic effect. Also, authors herein suggested that additional sulphamethoxazole linked to 3-(1-phenyl-3-(thiophen-2-yl)-1H-pyrazol-4-yl)acrylonitrile in compound 7 was responsible for its promising cytotoxic activity against colorectal carcinoma cell line.

Cytotoxic and Antimicrobial Activity of Dehydrozingerone based Cyclopropyl Derivatives.

A small series of 1-acetyl-2-(4-alkoxy-3-methoxyphenyl)cyclopropanes was prepared, starting from dehydrozingerone (4-(4-hydroxy-3-methoxyphenyl)-3-buten-2-one) and its O-alkyl derivatives. Their microbiological activities toward some strains of bacteria and fungi were tested, as well as their in vitro cytotoxic activity against some cancer cell lines (HeLa, LS174 and A549). All synthesized compounds showed significant antimicrobial activity and expressed cytotoxic activity against tested carcinoma cell lines, but they showed no significant influence on normal cell line (MRC5). Butyl derivative is the most active on HeLa cells (IC50 = 8.63 μm), while benzyl one is active against LS174 and A549 cell lines (IC50 = 10.17 and 12.15 μm, respectively).

Anticancer potential of Hericium erinaceus extracts against particular human cancer cell lines

Cancer is a leading cause of death worldwide. Cancer resulted in 8.2 million human deaths in 2012. It is expected that annual cancer cases will rise from 14 million in 2013 to 22 million within the next two decades. Mushrooms are extensively used as nutritional supplements in many countries. Moreover, mushrooms have many medicinal properties, including anticancer activity. In this study, the anticancer activity of different polar and non-polar extracts of Hericium erinaceus were evaluated against different human cancer cell lines including human liver carcinoma (Hep G2), the human colonic epithelial carcinoma (HCT 116), the human cervical cancer cells (HeLa) and the human breast adenocarcinoma (MCF-7) using 3-(4,5- Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Furthermore, as a control, the cytotoxicity effect of the different extracts were tested against isolated mouse hepatocytes. It was observed that the extracts by water and methanol from fresh and lyophilized fruiting bodies of H. erinaceus had the strongest anticancer effect. In contrast, the extracts by ether and ethyl acetate from mycelia and broth of H. erinaceus showed lower anticancer activity against the tested carcinoma cell lines. The highest anticancer activity was recorded for aqueous extract of lyophilized fruiting bodies with half maximal inhibitory concentration (IC50) values of 6.1±0.2, 5.1±0.1, 5.7±0.2 and 5.8±0.3 μg/ml against Hep G2, HCT 116, HeLa and MCF-7 cells, respectively with non-significant effect on the normal mouse hepatocytes. To summarise, polar extracts of H. erinaceus can be good sources for isolating natural anticancer compounds. I recommend further chemical studies to isolate the active principles of the extract of H. erinaceusevaluated in the present.

Stimulating effect of normal-dosing of fibrates on cell proliferation: word of warning.

BackgroundFibrates are widely used hypolipidemic drugs, which serve as ligand of peroxisome proliferator-activated receptor α (PPARα). Recently, they have also been considered as potential anticancer agents. We studied effect of fibrates treatment on cell proliferation, expression of CYP2J2 and concomitant changes in expression of cell cycle regulatory proteins in three different human cell lines: HEK293, HepG2, and HT-29.MethodsWe used WST-1 viability test, western blot and immunocytochemistry for detection of proteins of interests and analysis of cell cycle.ResultsOur results showed that at lower concentrations of all tested fibrates, viability of all tested cell lines is increased, whereas at higher concentrations, repression is apparent. Unfortunately, the viability of tested cells is predominantly increased in a range of concentration which is reached in patient plasma. This phenomenon is accompanyed by elevation of CYP2J2, increased number of cyclin E-positive cells and decreased number of Cdc25A-positive cells in all tested cell lines, and elevated cyclin A expression in HepG2 and HT-29. These changes are concentration-dependent. We suppose that increased level of CYP2J2 could explain enhanced cell proliferation in lower concentration of fibrates.ConclusionBased on our results, we suggested there is no anti-cancer effect of fibrates in tested carcinoma cell lines.Electronic supplementary materialThe online version of this article (doi:10.1186/s12944-016-0335-z) contains supplementary material, which is available to authorized users.

Cytotoxicity and Anti–inflammation Profiles of Synthesized Thiazoles‐Based N‐Bisphosphonates and Relevant Bisphosphonic acids

AbstractA series of substituted thiazole‐bisphosphonates and relevant bisphosphonic acid counterparts was synthesized from the reaction of 2‐chloro‐N‐(substituted)thiazole acetamides with tetraethyl methylene‐1,1‐bisphosphonate reagent in the presence of a base. The reactions proceeded smoothly via nucleophilic substitution to give our targets in good to high yields. Among the products, 4 bisphosphonic acids exhibited excellent anticancer activity vs four tested carcinoma cell lines (MCF7, HELA, DU‐145, and HCT‐116) with GI50 values ranging from 1.8 to 4.8 μMmL−1. According to the prediction results (using PASS program), the same acids and their BP‐analogs were also evaluated for their anti‐inflammatory properties. The acute carrageenan induced paw edema in rats model was used and the tested compounds showed notable anti‐inflammatory potency without toxicity side effects.

Resveratrol Treatment Inhibits Proliferation of and Induces Apoptosis in Human Colon Cancer Cells

BackgroundResveratrol, a natural isolate from plant sources, has a long and important history in traditional Chinese medicine. In the present study we investigated the effect of resveratrol on human colon cancer cell lines.Material/MethodsWe used the Cell Counting kit-8 (CCK-8) for determination of colon cancer cell viability. Apoptosis induction was analyzed using the DeadEnd™ Colorimetric TUNEL System (Promega, Madison, WI, USA). The siRNA Transfection Reagent kit (Santa Cruz Biotechnology, Inc.) was used for the administration of COX-2 silencer RNA (siRNA) into the colon cancer cells. Primer Express® software for Real-Time PCR ver. 3.0 (Applied Biosystems, Foster City, CA, USA) was used to prepare the primers for RT-PCR.ResultsThe results revealed that exposure of colon cancer cells to resveratrol inhibited cell viability. Resveratrol exhibited a significant inhibitory effect on cell viability at 30 μM concentration after 48 h of exposure. We observed that 30-μM doses of resveratrol for 72 h led to 18, 29, and 34% reduction in the viability of HCA-17, SW480, and HT29 cells, respectively. It also significantly induced apoptosis in both of the tested carcinoma cell lines. The population of apoptotic cells in HCA-17 and SW480 cell lines after 48 h of resveratrol treatment was 59.8±4 and 67.2±4%, respectively, compared to 2.3±1% in the control cells. The colon cancer cells exposed to resveratrol showed significantly lower cyclooxygenase-2 and prostaglandin receptor expression. Treatment of colon cancer cells with the inhibitor of cyclooxygenase-2, indomethacin, and administration of silencer RNA for cyclooxygenase-2 also produced similar results.ConclusionsThese findings suggest that resveratrol treatment can be a promising strategy for the treatment of colon cancer.

Chemical Composition and Antibacterial Activity of Volatile Oil of Sequoia sempervirens (Lamb.) Grown in Egypt

The hydrodistilled essential oil of leaves of Sequoia sempervirens (Lamb.) belonging to family Cupressaceae was analyzed by GC/MS. Thirty six compounds were identified representing 95.62% of the total oil containing α-phellandrene (29.60%), dl-limonene (15.60%), α-pinene (8.65%) and terpinene-4-ol (3.5%) as major components. The studied essential oil showed a dose-dependent antioxidant activity using 2, 2-diphenyl-1-picrylhydrazyl assay (IC50: 32.2 μg/mL). The antimicrobial activity of S. sempervirens leaves oil was screened against Gram-positive and Gram-negative bacteria and fungi. The strongest antibacterial effects of oil were on Bacillus subtilis, Trichophyton mentagrophytes and Staphylococcus aureus. S. sempervirens oil showed potent cytotoxic activity against the tested carcinoma cell lines; hepatocellular (HEPG2), colon adenocarcinoma (HCT-116) and breast (MCF7) comparing to doxorubicin.

Chondroitin sulfate proteoglycan CSPG4 as a novel hypoxia-sensitive marker in pancreatic tumors.

CSPG4 marks pericytes, undifferentiated precursors and tumor cells. We assessed whether the shed ectodomain of CSPG4 (sCSPG4) might circulate and reflect potential changes in CSPG4 tissue expression (pCSPG4) due to desmoplastic and malignant aberrations occurring in pancreatic tumors. Serum sCSPG4 was measured using ELISA in test (n = 83) and validation (n = 221) cohorts comprising donors (n = 11+26) and patients with chronic pancreatitis (n = 11+20) or neoplasms: benign (serous cystadenoma SCA, n = 13+20), premalignant (intraductal dysplastic IPMNs, n = 9+55), and malignant (IPMN-associated invasive carcinomas, n = 4+14; ductal adenocarcinomas, n = 35+86). Pancreatic pCSPG4 expression was evaluated using qRT-PCR (n = 139), western blot analysis and immunohistochemistry. sCSPG4 was found in circulation, but its level was significantly lower in pancreatic patients than in donors. Selective maintenance was observed in advanced IPMNs and PDACs and showed a nodal association while lacking prognostic relevance. Pancreatic pCSPG4 expression was preserved or elevated, whereby neoplastic cells lacked pCSPG4 or tended to overexpress without shedding. Extreme pancreatic overexpression, membranous exposure and tissuehigh/seralow-discordance highlighted stroma-poor benign cystic neoplasm. SCA is known to display hypoxic markers and coincide with von-Hippel-Lindau and Peutz-Jeghers syndromes, in which pVHL and LBK1 mutations affect hypoxic signaling pathways. In vitro testing confined pCSPG4 overexpression to normal mesenchymal but not epithelial cells, and a third of tested carcinoma cell lines; however, only the latter showed pCSPG4-responsiveness to chronic hypoxia. siRNA-based knockdowns failed to reduce the malignant potential of either normoxic or hypoxic cells. Thus, overexpression of the newly established conditional hypoxic indicator, CSPG4, is apparently non-pathogenic in pancreatic malignancies but might mark distinct epithelial lineage and contribute to cell polarity disorders. Surficial retention on tumor cells renders CSPG4 an attractive therapeutic target. Systemic ‘drop and restoration’ alterations accompanying IPMN and PDAC progression indicate that the interference of pancreatic diseases with local and remote shedding/release of sCSPG4 into circulation deserves broad diagnostic exploration.

Inhibitory effect of novel S,N-bisphosphonates on some carcinoma cell lines, osteoarthritis, and chronic inflammation

A new series of S,N-bisphosphonate derivatives was synthesized and evaluated as antitumor agents against breast-, cervix-, liver, and colon cancer diseases. Antiarthritic and antichronic inflammatory properties of the new bisphosphonates (BPs) were also investigated. The studies demonstrated an efficient site selective method for making condensation products of BP-derivatives in high yields from thiazinethiones and tetraethyl methylenebisphosphonate reagent. The bioscreening evaluation showed that one of the tested BPs exhibited remarkable antitumor activity against the four tested carcinoma cell lines; nevertheless, all tested S,N-BP-derivatives (11 compounds) showed significant to moderate anti-inflammatory activity and capable of inhibiting polyarthritis.

Synthesis, characterization and cytotoxicity of mixed-ligand complexes of palladium(II) with 2, 2′-biquinoline/1, 4-diaminobutane and 4-toluenesulfonyl-L-amino acid dianion

Seven new palladium(II) complexes (1–7) with 4-toluenesulfonyl-L-amino acid dianion and 2, 2′-biquinoline (bqu)/1,4-diaminobutane (dab) have been synthesized and characterized by elemental analysis, IR, 1H NMR, and mass spectra techniques. Crystal structure of the complex (7) has been determined by X-ray diffraction analysis. The cytotoxicity was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and sulforhodamine B (SRB) assays. The results indicate that the complexes exert cytotoxic effects with selectivity against tested carcinoma cell lines, but their cytotoxicity is less than that of cisplatin. It suggests that all the amino acids, N-containing ligands and metal ions have important effect on cytotoxicity, but the IC50 values do not show definite correlation with variation of amino acids, N-containing ligands and metal ions, the cytotoxicity of complexes is related to tumor cell species.

Synthesis, characterization, and cytotoxicity of mixed-ligand complexes of platinum(II) with 2,2′-bipyridine and 4-toluenesulfonyl-L-amino acid dianion

Five new platinum(II) complexes (1–5) with 4-toluenesulfonyl-L-amino acid dianion and 2,2′-bipyridine (bipy) have been synthesized and characterized by elemental analysis, IR, UV, 1H-NMR, 13C-NMR, and mass spectra. The crystal structure of 1 has been determined by X-ray diffraction analysis. Cytotoxicity was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and sulforhodamine B (SRB) assays. The results indicate that 1–5 exert cytotoxic effects with selectivity against tested carcinoma cell lines; 5 displays better cytotoxicity against BGC-823, Bel-7402, and KB cell lines, while 1 has better cytotoxicity against KB cell line. The 4-toluenesulfonyl- L-amino acid dianions have important effects on cytotoxicity; when 4-toluenesulfonyl-L-amino acid dianions are 4-toluenesulfonyl-L-glycine and 4-toluenesulfonyl-L-phenylalanine, the complexes show better cytotoxicity.

Synthesis, Characterization, and Cytotoxicity of New Types of Binuclear Platinum(II) Complexes

Four new types of iodo-bridged binuclear platinum complexes [Pt2AI5] (A = dimethylamine, pyridine, 2-methylpyridine, and o-toluidine) (a-d) have been synthesized and characterized by elemental analysis, conductivity, thermal analysis, IR, 1H NMR, and mass spectra techniques. The cytotoxicity was investigated by MTT assay. The results indicate that complexes (a-d) have certain cytotoxicity against Bel-7402, HCT-8 and Hela cell lines. The complex a, c, and d display increased cytotoxicity than cisplatin against HCT-8, Bel-7402 and Hela cell lines, respectively. The results suggest that these complexes have selectivity against the tested carcinoma cell lines, with the amine ligand having an important effect on the cytotoxicity.

Synthesis, characterization and cytotoxicity of mixed-ligand complexes of palladium(II) with aromatic diimine and 4-toluenesulfonyl- l-amino acid dianion

Eight new palladium(II) complexes ( 1a– 2d) with 4-toluenesulfonyl- l-amino acid dianion and diimine (bipy and phen) have been synthesized and characterized by elemental analysis, IR, UV, 1H NMR, 13C NMR and mass spectra techniques. Crystal structure of the complex ( 2d) has been determined by X-ray diffraction analysis. The cytotoxicity was tested by MTT and SRB assays. The results indicate that the complexes ( 1a– 2d) have selectivity against tested carcinoma cell lines. The complex ( 2c) has the best cytotoxicity among the eight complexes, moreover its cytotoxicity is better than that of cisplatin against BGC-823, Bel-7402 and KB cell lines. It suggests that both aromatic diimine and 4-toluenesulfonyl- l-amino acid have important effect on cytotoxicity.

Synthesis, characterization and cytotoxicity of iodo-bridged binuclear platinum(II) complexes

Seven new iodo-bridged binuclear platinum(II) complexes [Pt(L)I 2] 2 ( 1– 7) (L = n-butylamine, isopropylamine, m-toluidine, p-toluidine, diethylamine, N-methylaniline and aniline) have been synthesized and characterized by elemental analysis, conductivity, thermal analysis, IR, 1H NMR and mass spectra techniques. The cytotoxicity was tested by MTT assay. The results indicate that they have selectivity against tested carcinoma cell lines. For example, the complexes ( 3 and 7) have better cytotoxicity than cisplatin against Bel-7402 cell line, the complexes ( 2– 5 and 7) have better cytotoxicity than cisplatin against Hela cell line. The results suggest that the species of amine has important effect on cytotoxicity, when L = m-toluidine, p-toluidine and aniline, the complexes have better cytotoxicity against tested carcinoma cell lines.

Synthesis, cytotoxicity and DNA-binding levels of new type binuclear platinum(II) complexes

Six new type binuclear platinum(II) complexes ( a– f) have been synthesized and characterized by elemental analysis, conductivity, thermal analysis, IR, UV, 1H NMR and mass spectra techniques. The cytotoxicity of the complexes was tested by MTT and SRB assays. The cell cycle analysis and the levels of total platinum bound to DNA were measured by flow cytometry and ICP-MS, respectively. The results indicate that the complex ( a) has no cytotoxicity against HL-60, BGC-823, Bel-7402, KB and Hela, the complexes ( b, c, e and f) have weaker cytotoxicity against some tested carcinoma cell lines, the complex ( d) has better cytotoxicity against HL-60, BGC-823, Bel-7402, KB, MCF-7, HCT-8 and Hela with respect to the IC 50 values obtained. The cytotoxicity of the complex ( d) is equal to that of cisplatin against HL-60 and Bel-7402 ( P > 0.05), but it has better cytotoxicity than that of cisplatin against BGC-823 and MCF-7 ( P < 0.05). The complex ( d) causes significant G 2/M arrest and a concomitant decrease of cell population in G 1 and S phases, and the total DNA platination levels of the complex ( d) are higher than those of cisplatin under the same experimental conditions. It suggests that the bridging linker has important effect on their cytotoxicity. Indeed, when the bridging linker is dicarboxylic acid, their cytotoxicity is better than that of platinum complexes with an amino acid as bridging linker. The new type binuclear platinum(II) complexes represent a novel class of anticancer agents, which deserves further attention in search of anticancer lead compounds.

Synthesis, cytotoxicity and DNA binding levels of tri-functional mononuclear platinum(II) complexes

Seven new tri-functional mononuclear platinum(II) complexes ( a– g) have been synthesized and characterized by elemental analysis, conductivity, thermal analysis, IR, UV and 1H NMR spectral techniques. The cytotoxicity of these complexes was tested by MTT and SRB assays. The cell cycle analysis and the levels of total platinum bound to DNA were measured by flow cytometry and ICP-MS. The results indicate that the complexes ( a– g) have selectivity against tested carcinoma cell lines; they have weaker cytotoxicity against HCT-8 and MCF-7. Complexes a, b, d and g also exert weaker cytotoxicity against BGC-823 and complexes a, b, e and f have better cytotoxicity against EJ, but their cytotoxicity is weaker than that of cisplatin. Complexes c, e and f, confer substantially greater cytotoxicity against HL-60 with an IC 50 value of 7.68 ± 0.23, 3.87 ± 0.19 and 2.41 ± 0.18 μM, respectively, moreover, cytotoxicity of complex f is equal to that of cisplatin. Complexes c, e and f cause significant G 2/M arrest and a concomitant decrease of cell population in G 1 and S phases. The total DNA-platination levels of them are higher than that of cisplatin under the same experimental conditions. It suggests that there is no correlation between total DNA-platination levels in HL-60 cells and cytotoxicity of complexes. When leaving groups are aromatic carboxylates, the complexes have better cytotoxicity, moreover, the substituent in benzene ring also influences cytotoxicity. In addition, when leaving groups are dicarboxylates, dicarboxylates coordinating with platinum through oxygen atoms form different chelate cycle and cycle size also affects their cytotoxicity.

Synthesis, cytotoxicity and DNA-binding levels of ammine/propylamine platinum(II) complexes with carboxylates

Seven new mixed ammine/propylamine platinum(II) complexes with carboxylates ( a– g) have been synthesized and characterized by elemental analysis, conductivity, IR, UV, and 1H NMR spectra techniques. The cytotoxicity of these complexes was tested by MTT assay. The levels of total platinum bound to DNA were measured by ICP-MS. The results indicate that the complexes ( a– g) have better cytotoxicity against EJ and HL-60 than other carcinoma cell lines. The cytotoxicity increases in the sequence: g < f < e < d < b < c < a against tested carcinoma cell lines. The cytotoxicity of complexes ( a– c) is equal to that of cisplatin against HL-60. The cytotoxicity of complex a is also equal to that of cisplatin against EJ. However, the complexes ( a– g) are significantly less potent than cisplatin against BGC-823, HCT-8 and MCF-7. The total DNA-platination levels increase in the sequence: cisplatin < g < e < f < d < b < c < a under the same experimental conditions. It suggests that there is no correlation between total DNA-platination levels in HL-60 cells and cytotoxicity of ammine/propylamine platinum complexes. When leaving groups are aromatic carboxylates, the complexes have better cytotoxicity, and moreover, the substituent in benzene ring also influences cytotoxicity.