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Background: Litchi seeds possess rich amounts of phenolics and have been shown to inhibit proliferation of several types of cancer cells. However, the suppression of EGFR signaling in non-small cell lung cancer (NSCLC) by litchi seed extract (LCSE) has not been fully understood., Methods: In this study, the effects of LCSE on EGFR signaling, cell proliferation, the cell cycle and apoptosis in A549 adenocarcinoma cells and NCI- H661 large-cell carcinoma cells were examined., Results: The results demonstrated that LCSE potently reduced the number of cancer cells and induced growth inhibition, cell-cycle arrest in the G1 or G2/M phase, and apoptotic death in the cellular experiment. Only low cytotoxicity effect was noted in normal lung MRC-5 cells. LCSE also suppressed cyclins and Bcl-2 and elevated Kip1/p27, Bax and caspase 8, 9 and 3 activities, which are closely associated with the downregulation of EGFR and its downstream Akt and Erk-1/-2 signaling., Conclusion: The results implied that LCSE suppressed EGFR signaling and inhibited NSCLC cell growth. This study provided in vitro evidence that LCSE could serve as a potential agent for the adjuvant treatment of NSCLC.

One newly bred variety of tea cultivar, purple-shoot tea, was selected to evaluate its antiproliferative effects on colorectal carcinoma cells, as well as normal colon cells. The phytochemicals and identified catechins of purple-shoot tea extract (PTE) were significantly higher than that of ordinary tea, especially the anthocyanins (surpassed by 135-fold) and anthocyanidins (surpassed by 3.5-fold). PTE inhibited the proliferation of COLO 320DM (IC(50) = 64.9 μg/mL) and HT-29 (IC(50) = 55.2 μg/mL) by blocking cell cycle progression during the G(0)/G(1) phase and inducing apoptotic death. Western blotting indicated that PTE induced cell cycle arrest by reducing the expression of cyclin E and cyclin D1 in COLO 320DM and the upregulation of p21 and p27 cyclin-dependent kinase inhibitors in HT-29. Two cells treated with PTE also indicated the cleavage of PARP, activation of caspase 3, and an increased Bax/Bcl-2 ratio. Our results showed that PTE is a potential novel dietary agent for colorectal cancer chemoprevention.

Objectives: Grape-seed procyanidins (GSPs) can inhibit cell proliferation and invasiveness in various human cancers. However, the effect of GSP on pancreatic carcinoma cells has not been investigated., Methods: Pancreatic carcinoma cell lines MIA PaCa-2 and BxPC-3 treated with GSP were assessed for viability by trypan blue exclusion, for cell cycle distribution by flow cytometry, for increased apoptosis by annexin V labeling, for their adhesion and invasion potential by evaluating their ability to penetrate through a matrix gel-coated Boyden chamber, and for changes in the levels of proteins involved in cellular events by immunoblotting., Results: Grape-seed procyanidin inhibited MIA PaCa-2 and BxPC-3 proliferation in a dose-dependent manner and induced G1-phase arrest of the cell cycle in BxPC-3 or mitochondria-mediated apoptosis in MIA PaCa-2. Grape-seed procyanidin also inhibited the adhesion and invasion potential of both cell lines in a dose-dependent manner, which are associated with the suppression of metalloproteases matrix metalloproteinase 9 or 2 (MMP-9 or -2) expression., Conclusions: Grape-seed procyanidin inhibited the proliferation of pancreatic carcinoma cells by cell cycle blockage or apoptotic induction. The invasiveness was also suppressed by GSP through down-regulation of MMP-2 or MMP-9 in pancreatic carcinoma cells. Grape-seed procyanidin is a potential chemotherapeutic or preventive agent for pancreatic carcinoma.

To investigate the influence of longan flower extract (LFE) on the sensitization of colorectal cancer (CRC) cells to 5-fluorouracil (5-FU) treatment, HT-29, Colo 320DM and SW480 cells were treated with LFE and 5-FU alone and in combination, and the cell viability was then assessed by trypan blue exclusion, the cell cycle by propidium iodide staining, the mitochondria membrane potential by rhodamine 123 staining, and the expression levels of associated genes by immunoblotting and quantitative real-time polymerase chain reaction. LFE and 5-FU synergistically inhibited cell proliferation of HT-29 and Colo 320DM cells. Combined treatment also elevated the level of loss of mitochondria membrane potential of these two CRC cells and arrested HT-29 cells in the S phase of the cell cycle, in association with down-regulation of cyclin A mRNA expression. LFE synergistically potentiated chemosensitivity to 5-FU in at least two CRC cell lines. The results indicated that LFE has potential as a novel agent for the sensitization of CRC cells to 5-FU. [ABSTRACT FROM AUTHOR]

Aim Of Study: Proanthocyanidin-rich longan flower extract (LFP) has been previously shown to inhibit the proliferation and anchorage-independent growth in soft agar of two colorectal carcinoma (CRC) cells in vitro. In this report, we further examined the effects of LFP in a CRC spheroid model.Materials and Methods: A liquid-overlay assay employing HT-29 spheroids was used to evaluate the effects of LFP on cancer cell tumorigenesis, viability, and apoptosis. Associated effects on signaling path ways (epidermal growth factor receptor [EGFR], Akt) and apoptotic regulators were measured using Western blot.Results: Treatment with LFP up to 200 μg/ml inhibited tumor growth in a dose-dependent manner and induced prominent apoptosis as measured by annexin V staining. Cells treated with LFP showed decreased EGFR and Akt phosphorylation with decreased expression of B-cell lymphoma 2.Conclusion: The ability of LFP to induce apoptosis in CRC spheroids warrants further investigation of its composition and identification of tumor-active components. [ABSTRACT FROM AUTHOR]