Effects of an elemental diet, Elental®, may differ between healthy oral cells and oral cancer cells

2020 ◽  
Vol 45 (2) ◽  
pp. 738-751
Author(s):  
Koji Harada ◽  
Tarannum Ferdous ◽  
Kenji Watanabe ◽  
Yoichi Mizukami ◽  
Katsuaki Mishima
Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2450
Author(s):  
Sheng-Yao Peng ◽  
Jen-Yang Tang ◽  
Ruei-Nian Li ◽  
Hurng-Wern Huang ◽  
Chang-Yi Wu ◽  
...  

Combined treatment is increasingly used to improve cancer therapy. Non-ionizing radiation ultraviolet-C (UVC) and sinularin, a coral Sinularia flexibilis-derived cembranolide, were separately reported to provide an antiproliferation function to some kinds of cancer cells. However, an antiproliferation function using the combined treatment of UVC/sinularin has not been investigated as yet. This study aimed to examine the combined antiproliferation function and explore the combination of UVC/sinularin in oral cancer cells compared to normal oral cells. Regarding cell viability, UVC/sinularin displays the synergistic and selective killing of two oral cancer cell lines, but remains non-effective for normal oral cell lines compared to treatments in terms of MTS and ATP assays. In tests using the flow cytometry, luminescence, and Western blotting methods, UVC/sinularin-treated oral cancer cells exhibited higher reactive oxygen species production, mitochondrial superoxide generation, mitochondrial membrane potential destruction, annexin V, pan-caspase, caspase 3/7, and cleaved-poly (ADP-ribose) polymerase expressions than that in normal oral cells. Accordingly, oxidative stress and apoptosis are highly induced in a combined UVC/sinularin treatment. Moreover, UVC/sinularin treatment provides higher G2/M arrest and γH2AX/8-hydroxyl-2′deoxyguanosine-detected DNA damages in oral cancer cells than in the separate treatments. A pretreatment can revert all of these changes of UVC/sinularin treatment with the antioxidant N-acetylcysteine. Taken together, UVC/sinularin acting upon oral cancer cells exhibits a synergistic and selective antiproliferation ability involving oxidative stress-dependent apoptosis and cellular DNA damage with low toxic side effects on normal oral cells.


2020 ◽  
Vol 19 (18) ◽  
pp. 2223-2230 ◽  
Author(s):  
Poonam Verma ◽  
Sanjukta Naik ◽  
Pranati Nanda ◽  
Silvi Banerjee ◽  
Satyanarayan Naik ◽  
...  

Background: Coconut oil is an edible oil obtained from fresh, mature coconut kernels. Few studies have reported the anticancer role of coconut oil. The fatty acid component of coconut oil directly targets the liver by portal circulation and as chylomicron via lymph. However, the anti-cancer activity of coconut oil against liver cancer cells and oral cancer cells is yet to be tested. The active component of coconut oil, that is responsible for the anticancer activity is not well understood. In this study, three different coconut oils, Virgin Coconut Oil (VCO), Processed Coconut Oil (PCO) and Fractionated Coconut Oil (FCO), were used. Objective: Based on previous studies, it can be hypothesized that fatty acids in coconut oil may have anticancer potential and may trigger cell death in cancer cell lines. Methods: Each cell line was treated with different concentrations of Virgin Coconut Oil (VCO), Processed Coconut Oil (PCO) and Fractionated Coconut Oil (FCO). The treated cells were assayed by MTT after 72 hr of incubation. The fatty acid composition of different coconut oils was analyzed by gas chromatography. Result: Different concentrations of coconut oils were used to treat the cells. Interestingly, the anticancer efficacy of VCO, PCO and FCO was not uniform, rather the efficacy varied from cell line to cell line. Only 20% VCO showed significant anticancer activity in HepG2 cells in comparison to 80% PCO against the KB cell line. Remarkably, 20% of PCO and 5% of FCO showed potential growth inhibition in the KB cell line as compared to 80% PCO in HepG2 cells. Moreover, there was a difference in the efficacy of VCO, PCO and FCO, which might be due to their fatty acid composition. Comparing the anticancer efficacy of VCO, PCO and FCO in this study helped to predict which class of fatty acids and which fatty acid might be associated with the anticancer activity of VCO. Conclusion: This study shows that VCO, PCO and FCO have anticancer efficacy and may be used for the treatment of cancer, especially liver and oral cancer.


2010 ◽  
Vol 71 (4) ◽  
pp. 240-248 ◽  
Author(s):  
Daih-Huang Kuo ◽  
Li-Min Liu ◽  
Hsin-Wei Chen ◽  
Fu-An Chen ◽  
Chung-Ren Jan

2013 ◽  
Vol 35 (2) ◽  
pp. 178-184 ◽  
Author(s):  
Jau-Min Chien ◽  
Chiang-Ting Chou ◽  
Yi-Chau Lu ◽  
Ti Lu ◽  
Chao-Chuan Chi ◽  
...  

2013 ◽  
Vol 20 (8) ◽  
pp. 624-632 ◽  
Author(s):  
Ying-hui Chen ◽  
Lyh-Jyh Hao ◽  
Chih-peng Hung ◽  
Jung-wei Chen ◽  
Sew-fen Leu ◽  
...  

2014 ◽  
Vol 67 (1) ◽  
pp. 126-136 ◽  
Author(s):  
Zhaohu Yuan ◽  
Huili Wang ◽  
Ziyou Hu ◽  
Yanqing Huang ◽  
Fang Yao ◽  
...  

2021 ◽  
Vol 22 (14) ◽  
pp. 7509
Author(s):  
Hai Huang ◽  
Jun-Koo Yi ◽  
Su-Geun Lim ◽  
Sijun Park ◽  
Haibo Zhang ◽  
...  

Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain unclear. This study investigated the potential anticancer ability and underlying mechanisms of CTD in OC in vivo and in vitro. Cell viability and anchorage-independent colony formation assays were performed to examine the antigrowth effects of CTD on OC cells; assessments for migration and invasion of OC cells were conducted by transwell; Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. The results revealed that CTD suppressed the proliferation, migration and invasion of oral cancer cells effectively and induced cell cycle arrest and apoptosis; regarding the mechanism, CTD bound to AKT directly by binding assay and repressed AKT activities through kinase assay, which thereby downregulating the downstream of AKT. Furthermore, CTD remarkably promotes the generation of reactive oxygen species by flow cytometry assay, leading to cell apoptosis. Notably, CTD strongly suppresses cell-derived xenograft OC tumor growth in an in vivo mouse model. In conclusion, our results suggested that costunolide might prevent progression of OC and promise to be a novel AKT inhibitor.


2017 ◽  
Vol 18 (10) ◽  
pp. 783-791 ◽  
Author(s):  
Xiao Huaitong ◽  
Feng Yuanyong ◽  
Tao Yueqin ◽  
Zhao Peng ◽  
Shang Wei ◽  
...  

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