The cytotoxicity of the cyclopalladated compounds has been evaluated against a panel of murine {mammary carcinoma (4T1) and melanoma (B16F10-Nex2)} and human {melanoma (A2058, SK-MEL-110 and SK-MEL-5) tumor cell lines.
Among them, Il, with the solubility of 0.107 mg/mL, demonstrated favorable cellular activity against vemurafenib-resistant carcinoma cells including BRaf<sup>WT</sup> phenotypic melanoma SK-MEL-2 and BRaf<sup>V600E</sup> phenotypic colorectal cancer HT-29 cell lines.
SK-MEL-5 is a human melanoma cell line that has been used in various studies to explore new therapies against melanoma in different <i>in vitro</i> experiments.
Among them, compound <b>29</b> showed GI<sub>50</sub> (50% growth inhibition) values ranging from 0.3 to 0.9 μM against 26 different tumor cell lines and selectivity for one colon (COLO 205) and two melanoma (SK-MEL-5 and UACC-257) cell lines at the TGI (total growth inhibition) level.
Five cell lines, including one normal human primary epidermal melanocytes and two human malignant melanoma (A375, G361) and two human metastatic melanoma (A2058, SK-MEL-3) cell lines, were chosen for this research.
The expression of tissue factor was investigated after the treatment with the BRAF inhibitor Dabrafenib and the MEK inhibitor Trametinib in the BRAF<sup>v600e</sup> mutated melanoma cell lines A-375 and SK-MEL-28, together with its ability to activate the coagulation cascade.
We found that doxorubicin (0.5-5 μmol/L) induced pyroptosis in melanoma cell lines SK-MEL-5, SK-MEL-28, and A-375 with high expression of DFNA5, but not in human breast cancer cell line MCF-7 with little expression of DFNA5.
FEPS inhibited mushroom tyrosinase with the half maximal inhibitory concentration (IC<sub>50</sub>) of 16.5 mg/ml and dose-dependently inhibited cellular tyrosinase activity (63.9% at 50 μg/ml, and 83.3% at 100 μg/ml) in the cell-free extract of SK-MEL-5 human melanoma cell and α-melanocytestimulating hormone (α-MSH)-stimulated melanin formation in intact SK-MEL-5 human melanoma cell.
In this study, we found that overexpression of snail significantly increased the mRNA and protein expression levels of FAPα in malignant melanoma B16 and SK-MEL-28 cells.
The cancer cell lines used in this research work are SK-MEL-2 (melanoma), MCF-7 (breast cancer), IMR-32 (neuroblastoma) MG-63 (human osteosarcoma), HT-29 (human colon cancer) and Hep-G2 (human hepatoma).
The synthesized compounds 6(a-j) were appraised for their in vitro anticancer activity against human cancer cell lines such as SK-MEL-2 (melanoma), IMR-32 (Neuroblastoma), HT-29(Colon) and also on normal murine embryonic fibroblast NIH/3T3 by Sulforhodamine B (SRB) assay, using Adriamycin as a standard drug.
Analogs bearing substituted phenyl ring attached to oxadiazole ring 14a showed the greatest inhibitory activities against non-small-cell lung cancer NCI-H522 and melanoma SK-MEL-2 with inhibition percent of 48.70 and 42.62, respectively.
We demonstrated that QS-13 binds to SK-MEL-28 melanoma cells through the α<sub>v</sub>β<sub>3</sub> integrin using blocking antibody and β3 integrin subunit siRNAs strategies.
All withanolides were evaluated for their cytotoxic activity against a panel of tumor cell lines including LNCaP (androgen-sensitive human prostate adenocarcinoma), 22Rv1 (androgen-resistant human prostate adenocarcinoma), ACHN (human renal adenocarcinoma), M14 (human melanoma), SK-MEL-28 (human melanoma), and normal human foreskin fibroblast cells.
TCGA-RNAseq data obtained from 341 melanoma patient samples as well as a panel of melanoma cell lines were used in an expression correlation analysis between PHB1 and predicted miRNAs. miR-195 impact on PHB1 mRNA and protein levels and relevance of this regulation were investigated in UACC-62 and SK-MEL-5 melanoma lines by RT-qPCR and western blot, luciferase reporter and genetic rescue experiments.
We demonstrated that the DPS from P. pacifica KMM 9010<sup>T</sup> non-toxic for normal mouse epidermal cells (JB6 Cl41 cell line) and inhibited colony formation of human colorectal carcinoma HT-29, breast adenocarcinoma MCF-7 and melanoma SK-MEL-5 cells in a dose-dependent manner.
SK-MEL-2 (melanoma), HL-60 (leukemia), HeLa (cervical cancer), MCF-7 (breast cancer) and normal breast epithelial cell (MCF-10A) using 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay method.
Treatment with a demethylating agent resulted in transcriptional induction of MT1A in the melanoma cell lines SK-MEL-5 and G-361 with high methylation levels prior to treatment.
Three cell lines, non-small cell lung cancer Hop-92, ovarian cancer IGROV1, and melanoma SK-MEL-2, exhibited some sensitivity against most of the tested compounds.
It showed GI<sub>50</sub> values of 0.36, 0.66, 0.68, and 0.60 μM against the breast MDA-MB-468, renal A498, and melanoma SK-MEL-5 and UACC-62 cell lines, respectively.