Say 'No' to Cancer and 'Yes' to Cranberry: The Role of Cranberry Extract in Inhibition of Growth of Lung Adenocarcinoma Cells.

BACKGROUND/AIM: Lung cancer is the leading cause of mortality due to cancer death. Treatment of lung adenocarcinoma (LUAD) is still challenging. Cranberries contain many rich bioactive components that may help fight cancer. The action of cranberry against some cancer types has been reported, however, its role in lung cancer has only been investigated in large-cell lung cancer. In this study, we expanded current research on the role of cranberry in LUAD. MATERIALS AND METHODS: A549 LUAD cancer cells were treated with commercial cranberry extract (CE). Proliferation of A549 cells was measured with a clonogenic survival assay and quick proliferation assay. Caspase-3 activity was used to evaluate apoptosis of A549 cells. Reverse transcriptase-polymerase chain reaction was conducted to investigate the possible molecular mechanisms involved in the action of CE. RESULTS: Treatment of LUAD with CE reduced the percentage of A549 colonies. This was consistent with the decrease in the optic density of cancer cells after treatment with CE. Caspase-3 activity increased after treatment with CE. The anti-proliferative effect of CE on A549 cells correlated with reduced expression of pro-proliferation molecules cyclin E, cyclin-dependent kinase 2 (CDK2) and CDK4. The pro-apoptotic effect of CE on A549 cells correlated with the reduced expression of the anti-apoptotic molecule caspase 8 and FADD-like apoptosis regulator (FLIP). CONCLUSION: CE had an inhibitory effect on the growth of LUAD cells by modulation of both pro-proliferative and anti-apoptotic molecules. Our research hopes to guide future treatment options for LUAD.

Harnessing the Power of Kiwifruit for Radiosensitization of Melanoma.

BACKGROUND: Melanoma is the deadliest variant of skin cancer and its incidence continues to increase. There are limited treatment options for advanced and metastatic cases of melanoma, despite advances in immunotherapy and chemotherapy. Melanoma is notorious as a radioresistant tumor. Previous studies found that phytochemicals, such as resveratrol and those found in green tea and blueberry, can sensitize various cancer cells, including melanoma, to radiotherapy. Our previous study also revealed that kiwifruit extract (KE) has antitumor activity to melanoma cells. This study was designed to expand upon our previous investigation and determine KE's potential as a radiosensitizer on CRL-11147 melanoma cancer cells and elucidate the possible mechanisms behind its potential. MATERIALS AND METHODS: Proliferation and apoptosis of CRL-11147 melanoma cells under radiation therapy (RT) plus KE versus RT alone were investigated using Proliferative cell nuclear antigen (PCNA) staining, quick cell proliferation assay, clonogenic assay, and caspase-3 activity assay. Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) were then used to investigate the mechanisms behind the observed results. RESULTS: The percentage of CRL-11147 colonies, PCNA staining intensity, and the optic density value of CRL-11147 cells decreased with RT/KE vs. RT alone. Relative caspase-3 activity was increased with RT/KE vs. RT alone. Increased expression of the anti-proliferative molecule p27 and pro-apoptotic molecule TRAILR1 correlated with the anti-tumor effect seen in the RT/KE group versus the RT alone group. CONCLUSION: KE augments radiosensitivity of CRL-11147 by up-regulating both p27 and TRAILR1 to inhibit proliferation and increase apoptosis, respectively.

Cranberry Extract Is a Potent Radiosensitizer for Glioblastoma.

BACKGROUND/AIM: Glioblastoma, also known as glioblastoma multiforme (GBM), is the most aggressive type of primary brain tumor and a cornerstone in its treatment is radiotherapy (RT). However, RT for GBM is largely ineffective at clinically safe doses, thus, the study of radiosensitizers is of great significance. MATERIALS AND METHODS: With accumulating evidence for the anticancer effect of compounds from cranberry, this study was designed to investigate if cranberry extract (CE) sensitizes GBM to RT in the widely used human glioblastoma cell line U87. We utilized clonogenic survival assays, cell proliferation assays, and caspase-3 activity kits. Potential proliferative and apoptotic molecular mechanisms were evaluated by reverse transcription-polymerase chain reaction. RESULTS: We found that CE alone had little effect on the survival of U87 cells. However, RT supplemented by CE significantly inhibited proliferation and promoted apoptosis of U87 cells when compared with RT alone. The proliferation-inhibitory effect of RT/CE might be attributable to the up-regulation of p21, along with the down-regulation of cyclin B and cyclin-dependent kinase 4. This pro-apoptotic effect might additionally be attributable to the down-regulation of survivin. CONCLUSION: These results warrant further study of the potential radiosensitizing capacity of CE in glioblastoma and other cancer types.

Potential use of kiwifruit extract for treatment of melanoma.

Skin cancers are the most common cancers in the world and among the different types of skin cancers, melanoma is the deadliest and incidence is rising. Previous studies have shown promising in vitro and human evidence of kiwifruit exhibiting anti-cancer effects. This study was designed to investigate if kiwifruit extract (KE) has any effect on CRL-11147 melanoma cancer cells and to investigate the possible mechanisms behind the results. The effects of KE on CRL-11147 melanoma cell survival, proliferation, and apoptosis was investigated using clonogenic survival assay, cell proliferation, and caspase-3 activity kits. Potential anti-tumor molecular mechanisms were elucidated using RT-PCR and IHC. Addition of KE decreased CRL-11147 cell colonies percentages indicated by a decreased optical density value of cancer cells when compared to control. Furthermore, treatment with KE increased relative caspase-3 activity in cancer cells, which indicated increased apoptosis of cancer cells. The anti-proliferative effect of KE on cancer cells corresponded with decreased expression of the pro-proliferative molecule Cyclin E and CDK4, while increased expression of the pro-apoptotic molecule TRAILR1 corresponded with the pro-apoptotic effect. KE decreases CRL-11147 melanoma cell growth via downregulation of Cyclin E and CDK4 and upregulation in TRAILR1. Our study suggests a potential use for KE in treatment of melanoma.