Liquidambar orientalis Mill. var. orientalis (Hammamelidaceae) commonly known as oriental sweet gum is a medicinal plant endemic to Turkey, and used for treatment of wounds such as ulcers, gastritis and skin diseases. However, there are only a limited number of studies on the anticancer properties of this plant. The aim of this study is to investigate the cellular and molecular mechanisms of L. orientalis in colorectal cancer cell lines and to reveal the active therapeutic components. Antioxidant, anti-proliferative, anti-invasive and apoptotic effects were investigated for determining biological activities. The phytochemical profile and quantitation assays were carried out by using HPLC-ESI-Q-TOF-MS. The results demonstrated that leaf methanol extract (LM) of L. orientalis has the highest cytotoxic activity in HCT-116 (IC₅₀ 27.80 μg/mL) and HT-29 (IC₅₀ 43.13 μg/mL) cell lines as compared to the other extracts tested. Regarding chemical composition, quercetin 3-glucoside (61.005 ± 1.527 mg/g extract), chlorogenic acid (31.627 ± 0.970 mg/g extract), pyrogallol (9.950 ± 0.001 mg/g extract), epigallocatechin gallate (9.671 ± 0.004 mg/g extract), apigenin 7-O-glucoside (2.687 ± 0.027 mg/g extract), gallic acid (2.137 ± 0.012 mg/g extract), genistin (1.270 ± 0.027 mg/g extract), luteolin (0.055 ± 0.0005 mg/g extract) and kaempferol (0.506 ± 0.007 mg/g extract) were identified as the major phytochemical compounds. Our results showed that LM extract exhibited In Vitro cytotoxic and apoptotic properties.

Background: In the treatment of Colorectal Cancer (CRC), the search for new antineoplastic drugs with fewer side effects and more effectiveness continues. A significant part of these pursuits and efforts focus on medicinal herbs and plant components derived from these plants. A. ketenoglui is one of these medicinal plants, and its anticancer potential has never been studied before. Methods: The phenolic and flavonoid content, and antioxidant activity of A. ketenoglui extracts were determined. The phytochemical profiling and quantification analysis of major components were performed by HPLC-ESI-Q-TOF-MS. Cytotoxicity, proliferation, apoptosis and cell cycle were evaluated to reveal the anticancer activity of the extract on CRC cells (HCT 116 and HT-29). The determined anticancer activity was confirmed by mRNA (RT-qPCR) and protein (Western blotting) analyzes. Results: A. ketenoglui methanol extract was found to have high phenolic (281.89±0.23) and flavonoid (33.80±0.15) content and antioxidant activity (IC₅₀ 40.03±0.38). According to the XTT assay, the extract has strong cytotoxic activity (IC50 350 μM in HCT 116 and IC₅₀ 263 μM in HT-29 cell line). The compounds most commonly found in the plant are, in descending order, chlorogenic acid, apigenin, genistin, baicalin, eupatorin, casticin, and luteolin. In flowcytometric analysis, the extract was found to induce greater apoptosis and cell cycle arrest in both cell lines than in both control and positive control (casticin). According to the results of the mRNA expression analysis, the extract treatment upregulated the expression of the critical genes of the cell cycle and apoptosis, such as p53, p21, caspase-3, and caspase-9. In protein expression analysis, an increase in caspase-3 and p53 expression was observed in both cell lines treated with the extract. In addition, caspase-9 expression was increased in HT-29 cells. Conclusion: The findings show that A. ketenoglui has an anticancer potential by inducing apoptosis and arresting the cancer cell cycle and may be promising for CRC therapy. This potential of the plant is realized through the synergistic effects of its newly identified components.

The aim of this study was to evaluate the anticancer effects of piceatannol, a natural stilbenoid, on human neuroblastoma cells. In order to accomplish this goal, we performed various cellular assays, including the XTT cell proliferation assay for cell viability, colony formation assay for colony formation capacity, FITC Annexin V and cell death detection kit for apoptosis, matrigel invasion assay for invasion capacity, intracellular reactive oxygen species (ROS) red dye for intracellular ROS levels, TMRM staining method for mitochondrial membrane potential (MMP), and the CYTO‐ID autophagy detection kit for autophagy. Furthermore, we analyzed the expression levels of genes associated with apoptosis and autophagy using RT‐qPCR. Based on our findings, piceatannol exhibited cytotoxic effects on neuroblastoma cells. Besides, treatment with piceatannol at both 50 and 100 μM concentrations for 72 h decreased colony formation, induced apoptosis and autophagy, inhibited cell invasion, decreased MMP, and increased ROS levels in SH‐SY5Y cells. In addition, we observed significant upregulation in the expression levels of CASP8, BECLIN, ATG5, ATG7, and MAPILC3A genes between the two doses. These results suggest that piceatannol enhances autophagic activity and induces caspase‐dependent apoptosis, indicating its potential as a therapeutic agent against neuroblastoma cells.

Aims: In this study, it was aimed to investigate the possible neuroprotective effect of Apigenin-7-Glycoside (AP7Glu), a natural product with known anticancer and anti-inflammatory activity, against hydrogen proxide (H2O2)-induced oxidative stress in SH-SY5Y cells. Methods: The effect of H2O2 and AP7Glu on cell viability was determined by XTT analysis. SOD and catalase analyzes were performed to determine antioxidant enzyme activities. Expression levels of antioxidant defense system related genes and caspase genes were evaluated by qRT-PCR analysis. Results: After treatment of 300 µM H2O2 to SH-SY5Y cells for 24 hours, cell viability was determined as 63.18% and this dose was used to induce oxidative stress. H2O2 treatment in the presence of different concentrations of AP7Glu increased cell viability compared to H2O2-treated cells. And, H2O2 decreased SOD and catalase enzyme activities compared to control group. With the treatment of H2O2 in the presence of AP7Glu, an increase was observed in these enzymes activities compared to H2O2-treated cells. In addition, H2O2 decreased the expression levels of genes associated with antioxidant defense system and increased expression levels of Caspase genes. And, H2O2 treatment in the presence of AP7Glu increased the expression levels of genes associated with antioxidant defense system and decreased CASP8 expression compared to H2O2-treated cells. Conclusion: AP7Glu has a neuroprotective effect against H2O2-induced oxidative stress and neuronal cell death.

Glioblastoma multiforme (GBM) is one of the most common brain tumors. Chemotherapy, radiotherapy and surgical resection are methods used in GBM treatment, however, the investigation of possible anticancer effects of low-toxicity natural products on various cancer cells, including GBM, leads to promising results. In this study, it was aimed to investigate anticancer effect of tomentosin, which is a sesquiterpene lactone, on U87 human GBM cells. The cytotoxic effect of tomentosin was evaluated by XTT assay. The concentration of tomentosin that inhibits 50% cell viability (IC50) was determined by the results from XTT, and, in further analyzes cells were treated with tomentosin at IC50 concentration. Then, total RNA isolation and cDNA synthesis were performed in control and dose groups, and, the possible anticancer effect of tomentosin was determined by evaluating the expression levels of important genes associated with apoptosis and metastasis by qPCR analysis. In addition, the effect of tomentosin on the colony forming capacity of GBM cells was evaluated by colony formation assay. According to our results, IC50 dose of tomentosin was found to be 28.8 µM in U87 cells for 48 hours. When compared to the control group, tomentosin increased expression of BAX, CASP3, CASP8, CASP9, CYCS, FADD, TNF, TNFR1, TNFR2 and TIMP2 genes. And, tomantosin significantly decreased colony forming capacity of U87 cells. In conclusion, it is thought that tomentosin exerts its anticancer effect by changing the expression levels of genes associated with apoptosis and metastasis in U87 GBM cells.