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Keywords = hepatocellular carcinoma (HCC), lichen

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12 pages, 6379 KiB  
Article
The Comprehensive Roles of ATRANORIN, A Secondary Metabolite from the Antarctic Lichen Stereocaulon caespitosum, in HCC Tumorigenesis
by Young-Jun Jeon, Sanghee Kim, Ji Hee Kim, Ui Joung Youn and Sung-Suk Suh
Molecules 2019, 24(7), 1414; https://doi.org/10.3390/molecules24071414 - 10 Apr 2019
Cited by 24 | Viewed by 4535
Abstract
Hepatocellular carcinoma (HCC) is one of the most deadly genetic diseases, but surprisingly chemotherapeutic approaches against HCC are only limited to a few targets. In particular, considering the difficulty of a chemotherapeutic drug development in terms of cost and time enforces searching for [...] Read more.
Hepatocellular carcinoma (HCC) is one of the most deadly genetic diseases, but surprisingly chemotherapeutic approaches against HCC are only limited to a few targets. In particular, considering the difficulty of a chemotherapeutic drug development in terms of cost and time enforces searching for surrogates to minimize effort and maximize efficiency in anti-cancer therapy. In spite of the report that approximately one thousand lichen-derived metabolites have been isolated, the knowledge about their functions and consequences in cancer development is relatively limited. Moreover, one of the major second metabolites from lichens, Atranorin has never been studied in HCC. Regarding this, we comprehensively analyze the effect of Atranorin by employing representative HCC cell lines and experimental approaches. Cell proliferation and cell cycle analysis using the compound consistently show the inhibitory effects of Atranorin. Moreover, cell death determination using Annexin-V and (Propidium Iodide) PI staining suggests that it induces cell death through necrosis. Lastly, the metastatic potential of HCC cell lines is significantly inhibited by the drug. Taken these together, we claim a novel functional finding that Atranorin comprehensively suppresses HCC tumorigenesis and metastatic potential, which could provide an important basis for anti-cancer therapeutics. Full article
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2 pages, 1039 KiB  
Abstract
Investigation of Apoptotic Effects of Usnic Acid on Hepatocellular Carcinoma
by Beste Yurdacan, Ünal Egeli, Gamze Güney Eskiler, Işıl Ezgi Eryılmaz, Gülşah Çeçener and Berrin Tunca
Proceedings 2017, 1(10), 1010; https://doi.org/10.3390/proceedings1101010 - 15 Nov 2017
Cited by 1 | Viewed by 2001
Abstract
Hepatocellular carcinoma (HCC) ranks the sixth among common cancers in the world due to limited treatment option. In recent years, fungicides and lichen metabolites have gained importance in development of new generation chemotherapeutics. For this purpose, we aimed to investigate the cytotoxic and [...] Read more.
Hepatocellular carcinoma (HCC) ranks the sixth among common cancers in the world due to limited treatment option. In recent years, fungicides and lichen metabolites have gained importance in development of new generation chemotherapeutics. For this purpose, we aimed to investigate the cytotoxic and apoptotic effects of a lichen metabolite, usnic acid (UA), on HCC cells in the present study. After treatment with different concentrations (6.25–100 µM) of UA for 48 h, a significant decrease in the number of viable cells was determined in HCC cells. The HepG2 and SNU-449 cell viability decreased to 21.8% and 15.6% at the maximum concentration, respectively (p < 0.05). However cell viability ratio was 104.3% in HUVEC cells. Additionally, UA induced particularly late apoptosis in HCC cells in a dose-dependent manner. The percentage of apoptotic cells was significantly increased to 86.67% and 81.36% at 100 µM UA in HepG2 and SNU-449 cells, respectively. To confirm the apoptosis-inducing effect of UA, cells were stained with AO/EB and the morphological characteristic of apoptotic cell death were observed. In conclusion, UA displayed cytotoxic and apoptotic activity against human HCC cells without damaging control cells. Thus, we think that UA may be a suitable candidate as therapeutic agent for treatment of HCC. Full article
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