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Functional Benefits of Ficus Hispida L.
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
D. Suma, A. Vysakh, R. N. Raji, Ninan Jisha, M. S. Latha
A variety of Thai traditional remedies use stems of the Ficus hispida L. to prescribe for cancer therapy. The antineoplastic result of FH stem was illustrated during sequential extraction with methanol, water-crude ethanol, water-methanol-ethyl acetate fractions on SKBR3, MCF7, T47D, and MDA-MB435 cell lines in vitro by Pratumvinit et al. [24]. Anti-neoplastic activity against T47D cells was shown by only ethanol fraction [24]. MTT assay, cell cycle analysis, and colony-forming assay were also analyzed. According to MTT assay, the IC50 of this extract against T47D cell was 110.3+/-9.63 µg/ml and cell growth inhibition in a dose-dependent manner was confirmed by colony-forming assay. The percentage increase of apoptotic cell population in herbal treated cells was confirmed by cell-cycle analysis. Therefore, F. hispida L. has valuable role in the healing of breast cancer by traditional medicine.
Anti-Cancer Agents from Natural Sources
Published in Rohit Dutt, Anil K. Sharma, Raj K. Keservani, Vandana Garg, Promising Drug Molecules of Natural Origin, 2020
Debasish Bandyopadhyay, Felipe Gonzalez
Colicins are class III bacteriocins, originated from specific strains of the bacterium Escherichia coli or other similar Enterobacteriaceae (Feldgarden et al., 1999). The mechanism of action in bacterial cells has been studied, revealing that colicins have the potential to cause cell death through membrane translocation and cell binding. If colicins could kill bacterial cells, do they have the potential to destroy cancerous cells? A study conducted by Chumchalová (2003)to validate the effectiveness of four types of colicins viz. A, E1, E3, and U, on eleven types of malignant (human) cells and also in fibroblast cells that carried P53 gene mutations. The cell lines of interest were MRC5 (standard fibroblast, wild-type p53), MCF7, and ZR75 (breast carcinoma, wild-type p53). The following cell types had a detection of p53: breast carcinoma: BT549, BT474, MDA-MD-231, SKBR3, and T47D, colon carcinoma: HT29, osteosarcoma: HOS, leiomyosarcoma: SKUT-1, and fibrosarcoma: HS913T. The most promising colicins were colicin A and E1, as both showed inhibition of cellular growth to most of the tested cell lines. Colicine A showed 16–56% inhibition, while colicin E1 showed an inhibition of 17–40%. One problem with colicine A was that it also inhibited 36% of the normal MRC5 fibroblast cells. Colicine E3 and U showed no significant changes in cell cycles. Cell cycle was altered notably in cell lines HS913T and MRC5 produced by Colicin A.
Preclinical and clinical development of new progesterone receptor antagonists with high receptor specificity for breast cancer treatment
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
J. Hoffmann, H. Hess-Stumpp, R. B. Lichtner, U. Fuhrmann, G. Siemeister, M. R. Schneider
Depending on the tissue, progesterone is classified as a proliferative or a differentiative hormone. This has been extensively studied in cultured human T47D breast cancer cells. Treatment of progesterone receptor-positive T47D cells with a progestin produces biphasic effects. Studies focusing on the initial growth-stimulatory components show that progestin-induced entry of cells into S phase is accompanied by transient increases of cyclin D1 and cyclin-dependent kinase-4 activity8. Growth stimulation by progestins is restricted to one cycle, however, and is followed by growth arrest at the G1/S boundary of the second cycle8,9. Cells then enter a period of resistance to growth-regulatory effects of additional progesterone, accompanied by hypophosphorylation and profound down-regulation of pRb, loss of cyclins D, A and B, and subsequential increases first in the levels of the cyclin-dependent kinase inhibitor p21 followed by increases in the cyclin-dependent kinase inhibitor p278.
Investigation of the enantioselectivity of acetylcholinesterase and butyrylcholinesterase upon inhibition by tacrine-iminosugar heterodimers
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
I. Caroline Vaaland, Óscar López, Adrián Puerta, Miguel X. Fernandes, José M. Padrón, José G. Fernández-Bolaños, Magne O. Sydnes, Emil Lindbäck
For the antiproliferative tests, we applied our implementation of the National Cancer Institute (NCI) screening protocol39. As a model of human solid tumour cells, we selected the cell lines A549 (non-small cell lung), HBL-100 (breast), HeLa (cervix), SW1573 (non-small cell lung), T-47D (breast), and WiDr (colon). Cell seeding densities, based on the cell line doubling time, were 2500 (A549, HBL-100, HeLa and SW1573) or 5000 (T-47D and WiDr) cells/well. Compounds were initially dissolved in DMSO at 400 times the desired final maximum test concentration. Control cells were exposed to an equivalent concentration of DMSO (0.25% v/v, negative control). Each compound was tested in triplicate at different dilutions ranging from 1 to 100 μM. Drug treatment began on day 1 after sowing. The drug incubation times were 48 h, after which the cells were precipitated with ice-cold TCA (50% w/v) and fixed for 60 min at 4 °C. Then the SRB test was performed. The optical density (OD) of each well was measured at 530 nm using a microplate absorbance reader (PowerWave XS, BioTek Instruments Inc.). Values were corrected for background OD of wells containing medium only39. The results were expressed as GI50, i.e. the dose that causes 50% growth inhibition after 48 h of exposure.
Design, synthesis, and biological evaluation of new thieno[2,3-d] pyrimidine derivatives as targeted therapy for PI3K with molecular modelling study
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Fatma M. Elmenier, Deena S. Lasheen, Khaled A. M. Abouzid
The cytotoxic activity of the most promising synthesised compounds (IIIa, IIIj and VIb) was also evaluated against the breast cancer (T-47D) cell line, by SRB assay (Routine Analysis) (0.01,0.1,1,10,100 μM). T-47D was chosen to perform further cytotoxic activity as it is a tumour cell with the PIK3CA mutation52. PIK3CA gene responses for making (p110α) protein which is a subunit of PI3K53. The PIK3CA mutation overexpresses in breast cancer54–57. T-47D is a Breast Ductal Carcinoma cell line was obtained from Nawah Scientific Inc., (Mokatam, Cairo, Egypt). Cells were maintained in DMEM media supplemented with 100 mg/ml of streptomycin, 100 units/ml of penicillin, and 10% of heat-inactivated foetal bovine serum in humidified, 5% (v/v) CO2 atmosphere at 37 °C. Cytotoxic activity is expressed in terms of IC50 and is provided in (Table 1).
Toll-like receptor (TLR) gene expression and immunostimulatory effect of CpG oligonucleotides in hormone receptor positive cell line T47D and triple negative breast cancer cell line MDA-MB-468
Published in Immunopharmacology and Immunotoxicology, 2020
Sudhakar Natarajan, Mohan Ranganathan
The human breast cancer cell lines T47D and MDA-MB-468 were purchased from National Center for Cell Science (NCCS), Pune, India. T47D represents luminal A subtype (ER+, PR±, HER2-) of breast cancer and MDA-MB-468 cell line is a triple- negative (ER-, PR-, HER2-) breast cancer with basal subtype [13]. T47D cell line was subcultured in RPMI 1640 medium (Himedia, India) and MDA-MB-468 cell line was subcultured in DMEM medium (Himedia, India) . T47D and MDA-MB-468 cell lines were supplemented with 10% fetal bovine serum (Gibco-BRL, USA), 100 U/ml penicillin and 100 µg/ml streptomycin (Gibco-BRL) respectively. The cells were cultured at 37 °C in an atmosphere of 5% CO2 and 95% air in a humidified incubator (VWR). When the cells were 80% confluent, they were sub-cultured in fresh media.