Effect of Rosehip (<i>Rosa Canina</i>) Extracts on Human Brain Tumor Cell Proliferation and Apoptosis

Abstract

Rosehips are blossoms from the wild rose (Rosa canina) and are commonly used as an herbal remedy. Previous reports have shown that extracts made from rosehip plants are able to reduce cell proliferation of cancer cells. In this study, we investigated the efficacy of rosehip extracts in preventing cell proliferation of three human glioblastoma cell lines A-172, U-251 MG and U-1242 MG cell lines. Each of the glioblastoma cell lines treated with rosehip extracts (1 mg/mL -25 ng/mL) demonstrated a significant decrease in cell proliferation. The rosehip extract-mediated decrease in cell proliferation was equal to or better than the decrease of cell proliferation observed when inhibitors of the MAPK (U0126, 10 µM) or AKT (LY294002, 20 µM) signaling pathways were utilized. Additionally, pretreatment of the these cell lines with Rosehip extracts (1 mg/mL -25 ng/mL) selectively decreased AKT, MAPK, and p70S6K phosphorylation suggesting these extracts prevent glioblastoma multiforme cell proliferation by blocking both the MAPK and AKT signaling mechanisms. Results from colorimetric cell death assays, cell cycle analysis by flow cytometry, as well as western blot studies demonstrate that rosehip extracts inhibit cell proliferation but do not promote apoptosis. Moreover, rosehip extracts were able to increase the efficacy of Temozolomide, a chemotherapeutic agent used to treat patients with glioblastomas. Surprisingly, rosehip extracts demonstrated a greater inhibition of cell proliferation than in combination with Temozolomide (100 µM) or Temozolomide as a single agent. Taken together these data suggest that rosehip extracts are capable of decreasing glioblastoma cell proliferation without promoting apoptosis and demonstrate a greater cell proliferation inhibitory effect than Temozolomide. More importantly, rosehip extracts may serve as an alternative or compliment to current chemotherapeutic regimens for glioblastomas.

Synergistic complex from plants Solanaceae exhibits cytotoxicity for the human hepatocellular carcinoma cell line HepG2

“…According to our previous results, there is a difference between response of HepG2 cancer cell line to the plant extract mixture or to individual molecules present in this plant extract in terms of both the time of onset and extent of apoptosis induction [ 13 ]. This was clearly seen in experiments for the identification of rate of apoptosis triggered by plant extract mixture in contrast to individual molecules from the plant extract as also shown by other research groups [ 26 – 30 ]. We demonstrate in this study that when using HPLC fraction 10 containing cellobiose, selenium, sulphur and vitamin C, already at 0.01 mg/ml, it induces 20 % of dead cells and 16 % of apoptotic cells within the first 3 h of treatment (Fig.…”

The antiproliferative and apoptotic effects of apigenin on glioblastoma cells

“…Activation of the PI3K/AKT pathway through phosphorylation induces cell growth, proliferation and inhibits apoptosis possibly by blocking the effects of pro-apoptotic targets such as Bad and activating pro-survival transcription factor NF-jB. [18,30] Apigenin inhibited ERK phosphorylation in the U1242 cell line but did not modulate ERK phosphorylation in U87 cells. Phosphorylated ERK enhances cell growth, proliferation, differentiation and migration.…”

“…Of particularly importance, apigenin inhibited downstream targets of EGFR signalling as demonstrated by inhibition of AKT phosphorylation as well as S6K and mTOR in both cell lines. Activation of the PI3K/AKT pathway through phosphorylation induces cell growth, proliferation and inhibits apoptosis possibly by blocking the effects of pro‐apoptotic targets such as Bad and activating pro‐survival transcription factor NF‐κB …”

Cytotoxic effect of Rosa canina extract on human colon cancer cells through repression of telomerase expression

“…Consistent with our results, Jiménez et al [18] reported that R. canina extracts arrested the cell cycle of Caco-2 cells at the S phase. Cagle et al [33] demonstrated that an 80% methanolic extract of R. canina exhibited antiproliferative effects on human glioblastoma cells by increasing cell cycle arrest at the G 2 /M phase and blocking both the MAPK and AKT signaling mechanisms. No findings were determined concerning apoptosis in that study.…”