## 2 Results and Discussion
### Cytotoxicity of Extracts Toward Selected Cell Lines  
Two extracts, Futu 1 and Futu 2, were selected for the study of their antiproliferative activity against six human cancer cell lines: biphenylpinoThe cannabinoids at concentrations of 0.02-2 \(\upmu\)g/mL and plant extracts at concentrations of 0.2-2.0 \(\upmu\)g/mL strongly stimulated MV4-11 cell growth (the stimulation in Figure 4 is marked as (\(-\)) values; the inhibition of growth is marked as (\(+\)) values). At concentrations of 2 \(\upmu\)g/mL, THC stimulated the growth of MV4-11 cells by 180% (compared to untreated control cells) and CBD, CBN, and CBC by 140%. At the same concentration, Futu1 and Futu2 stimulated growth by 70%. The inhibition of MV4-11 cell growth was observed only at the highest used concentrations. A similar observation was noticed in triple-negative breast cancer model MDA-MB-468 (Figure 4). All compounds at concentrations of 0.063-6.33 \(\upmu\)g/mL stimulated cell growth. The highest stimulation of MDA-MB-468 growth was observed at a concentration of 0.63 \(\upmu\)g/mL. Cannabinoids stimulated cell growth by 30-40% and Futu1 and Futu2 stimulated cell growth by 20-30% compared to untreated control cells (the stimulation in Figure 4 is marked as (\(-\)) values; the inhibition of growth is marked as (\(+\)) values). For concentrations higher than 6.33 \(\upmu\)g/mL, the inhibition of cell proliferation was observed. The effect of cell growth stimulation in some concentrations of the tested compounds was observed only for two of the used cell lines. These compounds stimulated growth only in the case of triple-negative breast cancer MDA-MB-468 cells and not ER+ breast cancer MCF-7 cells. The complex effects of cannabinoids on cancer processes, as influenced by their concentration, molecular mechanisms, and cancer type, are well documented in the literature. Cannabinoidss can both stimulate and inhibit the proliferation of cancer cells. For example, \begin{table}
\begin{tabular}{c c c c c c} \hline \multirow{2}{*}{**Lp**} & \multirow{2}{*}{**Compounds**} & \multicolumn{4}{c}{**Cell Line/Calculated Selectivity Index SI**} \\ \cline{3-6}  & & **A549** & **HT-29** & **AGS** & **MCF-7** \\ \hline
1 & THC & 2.82 & 2.98 & 1.75 & 1.33 \\
2 & CBD & 3.68 & 3.47 & 2.82 & 2.87 \\
3 & CBG & 2.89 & 1.07 & 1.76 & 1.45 \\
4 & CBC & 3.23 & 1.77 & 1.9 & 1.39 \\
5 & CBN & 3.27 & 1.78 & 1.75 & 1.87 \\
6 & CBDV & 1.81 & 3.12 & 1.34 & 1.33 \\
7 & Futu1 & 5.8 & 5.85 & 3.76 & 4.53 \\
8 & Futu2 & 3.4 & 4.45 & 3.08 & 3.53 \\ \hline \end{tabular} The SI index = IC\({}_{50}\) for normal cell line (MCF-10A)/IC\({}_{50}\) for respective cancerous cell line. A beneficial SI \(>1.0\) indicates a drug with efficacy against tumor cells greater than toxicity against normal cells.  
\end{table} 
Table 4: The selectivity index (SI) of tested compounds. Figure 4: Activity of extract against MV4-11 leukemia and breast cancer MDA-MB-468 (TNBC) cell lines. THC at low concentrations (nanomolar) may stimulate the growth of cancer cells, such as glioblastoma (U373-MG) and lung cancer (NCI-H292). This effect is attributed to the activation of CB1 receptor-dependent signaling pathways or receptor-independent mechanisms, such as the activation of TNF-alpha convertase (TACE/ADAM17) and the transactivation of the epidermal growth factor receptor (EGFR) [38]. Conversely, at higher concentrations (micromolar), THC exhibits antiproliferative and pro-apoptotic effects by inducing apoptosis in various cancer cell types. This mechanism often involves the activation of CB1/CB2 receptors and endoplasmic reticulum stress [39]. Cannabidiol (CBD), a non-psychoactive cannabinoid, predominantly exhibits antiproliferative activity through mechanisms independent of CB1 and CB2 receptors. CBD induces endoplasmic reticulum stress, activates TRPV2 receptors, modulates signaling pathways such as ERK and Akt, and promotes autophagy and apoptosis [40; 41]. Additionally, CBD inhibits angiogenesis and the invasive capacity of cancer cells, making it a promising candidate for anticancer therapy.