Sahapat Barusrux

Melatonin potentiates cisplatin-induced apoptosis and cell cycle arrest in human lung adenocarcinoma cells.

Melatonin produces anti‐cancer effects via several mechanisms, including by induction of apoptosis. In this way, it has been shown to be of use, in combination with chemotherapeutic drugs, for cancer treatment. The study described here has evaluated effects of melatonin on cytotoxicity, apoptosis and cell cycle arrest induced with the chemotherapeutic agent cisplatin, in human lung adenocarcinoma cisplatin‐sensitive cell line (SK‐LU‐1), which previously had only limit data.

FTIR microspectroscopy discriminates anticancer action on human leukemic cells by extracts of Pinus kesiya; Cratoxylum formosum ssp. pruniflorum and melphalan

Apoptosis is the principal molecular goal of chemotherapeutics for effective anticancer action. We studied the effect of 50% ethanolic-water extracts of Pinus kesiya, Cratoxylum formosum ssp. pruniflorum and melphalan on cytotoxicity and apoptosis induction for human leukemic U937 cells, and explored the mode of action using FTIR microspectroscopy. The number of viable U937 cells in vitro was decreased in a concentration-dependent manner by all tested compounds, although potency differed between the U937 and Vero cells. Melphalan and the extract of C. formosum exhibited relatively lower IC(50) values (15.0 ± 1.0 and 82.7 ± 3.2 μg/mL respectively) and higher selectivity (selective index>3) than the extract of P. kesiya (299.0 ± 5.2 μg/mL; selective index<3) on the U937 cells. All three compounds significantly induced apoptosis through the late stage - seen by the indicative DNA ladder - with the most effective being melphalan, then the P. kesiya and C. formosum extracts. FTIR microspectroscopy revealed that all three compounds raised the intensity of the β-pleated sheet - higher than that of the untreated U937 cells - corresponding to a shift in the α-helix band associated with an alteration in the secondary structure of the protein band, confirming induction of apoptosis via pro-apoptotic proteins. The differences in intensity of the FTIR bands associated with lipids, proteins and nucleic acids were responsible for discrimination of the anticancer mode of action of each of the three compounds. The FTIR data suggest that the two plant extracts possessed anticancer activity with a different mode of action than melphalan.

Synergistic anticancer effect of the extracts from Polyalthia evecta caused apoptosis in human hepatoma(HepG2)cells

OBJECTIVE To evaluate the anticancer activity of the extract fraction of Polyalthia evecta (P. evecta) (Pierre) Finet & Gagnep and the synergistic anticancer effect of the extracts from P. evecta by using the ATR/FT-IR spectroscopy. METHODS The 50% ethanol-water crude leaf extract of P. evecta (EW-L) was prepared and was further fractionated to isolate various fractions. The anticancer activity was investigated from cytotoxicity against HepG2 using a neutral red assay and apoptosis induction by evaluation of nuclei morphological changes after DAPI staining. Synergistic anticancer effects of the extracts from P. evecta were performed using the ATR/FT-IR spectroscopy. RESULTS The result showed that the EW-L showed higher cytotoxicity and apoptosis induction in HepG2 cells than its fractionated extracts. The hexane extract exhibited higher cytotoxicity and apoptosis induction than the water extracts, but less than the EW-L. The combined water and hexane extracts apparently increased cytotoxicity and apoptosis induction. The %apoptotic cells induced by the extract mixture were increased about 2-fold compared to the single hexane extract. CONCLUSIONS The polar extract fraction is necessary for the anticancer activity of the non-polar extract fraction. The ATR/FT-IR spectra illustrates the physical interaction among the constituents in the extract mixture and reveals the presence of polyphenolic constituents in the EW-L, which might play a role for the synergistic anticancer effect.

Anticancer effect of the extracts from Polyalthia evecta against human hepatoma cell line (HepG2)

OBJECTIVE To investigate the anticancer activity of Polyalthia evecta (P. evecta) (Pierre) Finet & Gagnep against human hepatoma cell line (HepG2). METHODS The anticancer activity was based on (a) the cytotoxicity against human hepatoma cells (HepG2) assessed using a neutral red assay and (b) apoptosis induction determined by evaluation of nuclei morphological changes after DAPI staining. Preliminary phytochemical analysis of the crude extract was assessed by HPLC analysis. RESULTS The 50% ethanol-water crude leaf extract of P. evecta (EW-L) showed greater potential anticancer activity with high cytotoxicity [IC50 = (62.8 ± 7.3)µg/mL] and higher selectivity in HepG2 cells than normal Vero cells [selective index (SI) = 7.9]. The SI of EW-L was higher than the positive control, melphalan (SI = 1.6) and the apoptotic cells (46.4 ± 2.6) % induced by EW-L was higher than the melphalan (41.6 ± 2.1)% (P<0.05). The HPLC chromatogram of the EW-L revealed the presence of various kinds of polyphenolics and flavonoids in it. CONCLUSIONS P. evecta is a potential plant with anticancer activity. The isolation of pure compounds and determination of the bioactivity of individual compounds will be further performed.

Melatonin induces apoptosis through biomolecular changes, in SK‐LU‐1 human lung adenocarcinoma cells

Anti‐cancer effects of melatonin (N‐acetyl‐5‐methoxytryptamine, an indole‐amine), have been widely reported, however, little has been known, regarding its mechanism(s) of action in lung cancer. Thus, we investigated its induction of apoptosis through biomolecular changes (lipid, protein and nucleic acid/DNA) in the SK‐LU‐1 human lung cancer cell line.

Evaluation of the anticancer potential of six herbs against a hepatoma cell line

BackgroundSix herbs in the Plant Genetics Conservation Project that have been used as complementary medicines were chosen on the basis of their medicinal value, namely Terminalia mucronata, Diospyros winitii, Bridelia insulana, Artabotrys harmandii, Terminallia triptera, and Croton oblongifolius. This study aims to evaluate the potential anticancer activity of 50% ethanol-water extracts of these six herbs.MethodsFifty percent ethanol-water crude extracts of the six herbs were prepared. The cytotoxicity of the herbal extracts relative to that of melphalan was evaluated using a hepatoma cell line (HepG2), and examined by neutral red assays and apoptosis induction by gel electrophoresis and flow cytometry after 24 h.ResultsA significant difference was found between the cytotoxicity of the 50% ethanol-water crude extracts and melphalan (P = 0.000). The 50% ethanol-water crude extracts of all six herbs exhibited cytotoxicity against HepG2 cells, with IC50 values ranging from 100 to 500 μg/mL. The extract of T. triptera showed the highest cytotoxicity with an IC50 of 148.7 ± 12.3 μg/mL, while melphalan had an IC50 of 39.79 ± 7.62 μg/mL. The 50% ethanol-water crude extracts of D. winitii and T. triptera, but not A. harmandii, produced a DNA ladder. The 50% ethanol-water crude extracts of D. winitii, T. triptera, and A. harmandii induced apoptosis detected by flow cytometry.ConclusionThe 50% ethanol-water crude extracts of D. winitii, T. triptera, and A. harmandii showed anticancer activity in vitro.

Abstract 2344: Soluble MICA in cervical cancer is in a deglycosylated form: Implication for soluble MICA detection

Background: Major histocompatibility complex class I chain related A (MICA/PERB11.1) molecules are expressed as transmembrane proteins. They are ligands recognized by the natural killer cell receptor group (NKG)2D, an activating receptor on NK cells, gamma delta T cells and activated CD8 T cells. Up-regulated MICA expression was reported in many tumors. Shedding of MICA from tumor cells as soluble MICA (sMICA) is a mechanism for immune evasion. MICA proteins could be presented in various sizes from 43 to 75 kDa depending on degree of glycosylation. Eight potential N-glycosylation sites in a MICA molecule were reported. This study aimed to investigate the size of sMICA in sera of cervical cancer patients and women blood donors by western blot technique. Methods: The sMICA*009 plasmid DNA was transfected to COS7 cells for recombinant sMICA protein production in culture supernatant. The recombinant sMICA protein was harvested and validated with mouse monoclonal anti-MICA antibody (WW6B7) by indirect ELISA and immunobloting. Molecular weight of deglycosylated recombinant sMICA protein treated with N-glycosidase F enzyme and sMICA in cervical cancer and healthy sera was determined. Results: The recombinant sMICA and serum sMICA showed 62 kDa and 45 kDa in molecular weight, respectively. The molecular weight of recombinant sMICA treated with N-glycosidase F enzyme was reduced to 45 kDa which equal to serum sMICA indicating that sMICA in sera of patients and blood donor controls was in a deglycosylated form. Conclusion: Recombinant sMICA produced in COS7 had a molecular weight of 62 kDa. In contrast, sMICA in sera was in a deglycosylated form and had a molecular weight of 45 kDa equal to in vitro deglycosylation with N-glycosidase F enzyme of produced recombinant sMICA. The mechanism and kinetic of deglycosylation of sMICA in sera await further investigation. It would be interesting to see whether this form of sMICA would affect sMICA detection in sera. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2344.