Data on cytotoxic pattern of cholesterol analogs for lung adenocarcinoma cells

Abstract

Cholesterol (Cho) is a sterol that plays an essential role in the maintenance of biologic cell membranes, and various lipoproteins are its carriers through blood circulation [1]. Some FDA-approved anticancer drugs (i.e., Lipoplatin and Myocet) are conjugated to Cho moieties to improve their pharmacokinetic properties, cellular uptake and target specificity [2]. Recently natural and synthetic sterol compounds have shown a broad spectrum of pharmacological activities [3,4]. Herein, we investigated the anticancer activity of various natural Cho analogs, ie. asiatic acid (AsA), betulinic acid (BeA), oleanolic acid (OleA), ursolic Acid (UrA), lupeol (Lupe) and β-sitosterol (β-Sito) against non-small cell lung adenocarcinoma (A549). We performed theoretical calculations of the biophysicochemical properties, and viability assays in a range of 5–100 μM in A549 cells of these Cho analogs. We used ChemSketch and ChemSpider to determine physical properties, and GraphPad Prism 8 software for the data analysis to determine the inhibitory concentrations at 50% (IC 50 ) of each compound.

Unraveling the Influence of Six Lupane-, Oleanane-, and Ursane- type Pentacyclic Triterpenes' Structure-Activity Relationship on Non-Small Lung Adenocarcinoma Cells

“…A549 and MRC5 IC50 and TI for each pentacyclic triterpene under study. These results were previously published by us[10]. # TI = MRC5 IC50 / A549 IC50, where >1 means higher selectivi.ty…”

“…The 50% inhibitory concentration (IC50) of some of these triterpenes in A549 NSCLC cells were previously determined by us [10]. A similar procedure was done to determine the IC50 of the triterpenes in a normal lung fibroblast cell line (MRC5).…”

Unraveling the Impact of Six Pentacyclic Triterpenes Regulating Metabolic Pathways on Lung Carcinoma Cells

“…* These results have already been obtained by the authors[10]. # TI = MRC5 IC 50 /A549 IC 50 , where >1 means higher selectivity.…”

“…We selected pentacyclic triterpenes because, in our previous study, we found that the fifth ring of the structure is essential for the cytotoxic activity in NSCLC A549 cells. For instance, even at the highest concentration of 100 μM, β-sitosterol and cholesterol (tetracyclic triterpenes) did not kill A549 cells [ 10 ]. Thus, this study explored the underlying mechanistic principles ( Figure 7 ) with a particular emphasis on key pathways to induce cell death (i.e., cell cycle arrest, expression of RR, DNA damage, activation of caspase 3, and oxidative stress) but also in chemoresistance-related processes (i.e., inhibition of autophagy; MAPK, PI3K, STAT3, and PDL1 expression).…”

“…The 50% inhibitory concentration (IC 50 ) of some of these triterpenes in A549 NSCLC cells were previously determined by us [ 10 ]. A similar procedure was performed to determine the IC 50 of the triterpenes in a normal lung fibroblast cell line (MRC5).…”