Delayed cytotoxic effects of methyl jasmonate and cis-jasmone induced apoptosis in prostate cancer cells.

Advanced prostate cancer cells are typically hormone independent, resistant to apoptosis and do not respond to chemotherapeutic agents. The ability of methyl jasmonate (MJ) and cis-jasmone (CJ) to inhibit growth in hormone independent prostate cancer cell lines, PC-3 and DU-145, was evaluated. CJ and MJ inhibited cell growth, induced cell cycle arrest and apoptosis.

Methyl jasmonate induced apoptosis in human prostate carcinoma cells via 5-lipoxygenase dependent pathway.

Methyl jasmonate--a plant stress hormone with striking resemblance to lipoxygenase products have been reported to induce apoptosis in several cancers. However, 5-HETE--a product of the lipoxygenase pathway has been implicated in human prostate cancer progression and yet possible interaction between methyl jasmonate and the lipoxygenase pathway has not been reported, thus, leaving some unanswered questions on the mechanism(s) of action by methyl jasmonate. Using cytotoxicity and flow cytometry assays (BrdU assay) as well as fluorescence microscopy, we investigated the effects of the methyl jasmonate on the proliferation of human prostate adenocarcinoma cell lines (DU-145, PC-3) in vitro and the potential interaction between methyl jasmonate and the lipoxygenase pathway.

Perillyl alcohol and perillic acid induced cell cycle arrest and apoptosis in non small cell lung cancer cells.

Plant products such as perillyl alcohol have been reported to possess anti-tumor activities against a number of human cancers though the mechanism of action has not yet been elucidated. The effects of perillyl alcohol (POH) and its metabolite perillic acid (PA) on the proliferation of non small cell lung cancer (NSCLC, A549, and H520) cells were investigated. Both POH and PA elicited dose-dependent cytotoxicity, induced cell cycle arrest and apoptosis with increasing expression of bax, p21 and caspase-3 activity in both the cell lines.

Jasmonates induce apoptosis and cell cycle arrest in non-small cell lung cancer lines.

The jasmonates, cis-jasmone (CJ) and methyl jasmonate (MJ), were investigated for their effects against NSCLC cell lines A549 and H520. CJ or MJ inhibited the proliferation of both cell lines in a dose-dependent manner as well as induced cell cycle arrest in the G2/M phase. Apoptosis was observed following treatment with CJ or MJ as indicated by Hoechst staining and confirmed by dual annexin V-fluorescein isothiocyanate (FITC)/prodium iodide (PI) and DAPI (4',6-diamidine-2'-phenylindole dihydrochloride) staining.

Monoterpenes enhanced the sensitivity of head and neck cancer cells to radiation treatment in vitro.

Background: Perillyl alcohol (POH) elicited anticarcinogenic effects in a number of cancer models and pharmacokinetic studies in humans revealed that PA is the major circulating metabolite following POH administration.

Materials And Methods: Effects of PA or POH alone, or in combination with radiation, on human head and neck squamous cell carcinoma cell lines (HNSCC), were investigated using cytotoxicity and flow cytometry assays. HNSCC cells were pretreated with 1.

Perillyl alcohol and perillaldehyde induced cell cycle arrest and cell death in BroTo and A549 cells cultured in vitro.

The role of the monoterpenes, especially limonene and perillyl alcohol, in the treatment of certain cancers is currently being evaluated in clinical trials. In this study, the effects of perillyl alcohol (POH) and its analog, perillaldehyde (PALD), on human carcinoma cell lines (BroTo and A549) cultured in vitro were investigated using proliferation assays (MTT and colony formation) and DNA content analysis by flow cytometry. POH and PALD elicited dose- and time-dependent inhibition of proliferation in both cell lines.

Induction of apoptosis and inhibition of papilloma formation may signal a new role for okadaic acid.

Okadaic acid (OA), a tumor promoter in the mouse skin carcinogenesis model, has been shown to induce apoptosis in tumor cell lines that harbor H-ras mutations. We examined the effects of OA on mouse keratinocytes with (308) and without (C50) H-ras mutation in vitro and in an in vivo system. Following exposure to varying concentrations of OA over time, the effects of OA in vitro were assessed using microscopic, biochemical and flow cytometric techniques.