human hepatocellular carcinoma
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2022 ◽  
Vol 18 ◽  
Vivian Cordeiro Rodrigues ◽  
William Queiroz Felippe ◽  
Carla Marins Goulart ◽  
Aurea Echevarria ◽  
Ana Paula Pereira da Silva

Background: Chalcones are open-chain flavonoids especially attractive to medicinal chemistry due to their easy synthesis and the possibility of structural modifications. Objective: Evaluate the in vitro anticancer activity of a series of hybrids chalcones-thiosemicarbazones against the human hepatocellular carcinoma cell line, HepG2. Methods: Seven hybrid chalcones-thiosemicarbazones (CTs), 3-(4’-X-phenyl)-1-phenylprop-2-en-1-one thiosemicarbazone, where X=H (CT-H), CH3 (CT-CH3), NO2 (CT-NO2), Cl (CT-Cl), CN (CT-CN), F (CT-F) and Br (CT-Br), were synthesized and their effects on cells viability and mitochondrial oxygen consumption were accessed. Results: Incubation with CTs caused a decrease in HepG2 cells viability in a time-concentration-dependent manner. The most effective compounds in inhibiting cell viability, after 24 hours of treatment, were CT-Cl and CT-CH3 (IC50 20.9 and 23.63 μM, respectively). In addition, using 10 M and only 1 hour of pre-incubation, CT-CH3 caused a reduction in basal respiration (-37%), oxygen consumption coupled with ATP synthesis (-60%) and maximum oxygen consumption (-54%). These alterations in respiratory parameters may be involved with the inhibitory effects of CT-CH3, since significant changes in oxygen consumption rates were observed in a condition that anticipates more significant losses of cell viability. The ADME parameters and the no violation of Lipinski Rule of Five showed that all compounds are safe. Conclusion: These results may contribute to the knowledge about the effects of CTs on these cells and the development of new treatments against HCCs.

Xiaoyu Li ◽  
Yingju Qin ◽  
Long Kong ◽  
Xiliang Yan ◽  
Wei Zhang ◽  

Copper hydroxide (Cu(OH)2) nanopesticide formulas are becoming more frequently used in agriculture, however human exposure risks are not completely characterized. Here, the effect of Cu(OH)2 nanopesticide exposure on cell metabolism...

2021 ◽  
Andreia P Alves ◽  
Sandra M Rocha ◽  
Ana C Mamede ◽  
Marco G Alves ◽  
Pedro F Oliveira ◽  

Abstract Background: The human Amniotic Membrane (hAM) has been studied as a potential therapeutic option in cancer, namely in hepatocellular carcinoma. Previously, our research group evaluated the effect of human Amniotic Membrane Protein Extracts (hAMPE) in cancer therapy, demonstrating that hAMPE inhibit the metabolic activity of human hepatocellular carcinoma cell lines: Hep3B2.1-7, HepG2 and Huh7. Therefore, the aim of this study was to evaluate the effect of hAMPE treatment in glucose metabolism of hepatocellular carcinoma. Methods and Results: Glucose uptake and lactate production was assessed by 1H-NMR, and the expression of several mediators of the glycolytic pathway was evaluated by Western blot or fluorescence. Our results showed that hAMPE treatment increased glucose consumption on Hep3B2.1-7, HepG2, and Huh7 through the increase of GLUT1 in Hep3B2.1-7 and Huh7, and GLUT3 in HepG2 cells. It was observed increased expression of 6-phosphofrutokinase (PFK-1L) in all cell lines, indicating that glucose can be converted to pyruvate. Also, it was verified that glucose seems not to be converted to lactate on HepG2 and Huh7 cells, suggesting that hAMPE treatment may contradict the Warburg effect observed in carcinogenesis. In Hep3B2.1-7, the hAMPE treatment induced an increase in expression of lactate dehydrogenase (LDH) and monocarboxylate transporter isoform 4 (MCT4). Conclusions: Overall, this work highlighted the potential usefulness of hAMPE as anticancer therapy through the modulation of the glycolytic metabolism in human hepatocellular carcinoma.

2021 ◽  
Vol 23 (1) ◽  
Marcone Dos Santos ◽  
Andressa França ◽  
Antônio Lima Filho ◽  
Rodrigo Florentino ◽  
Paulo Diniz ◽  

2021 ◽  
Vol 12 (1) ◽  
Eva G. Álvarez ◽  
Jonas Demeulemeester ◽  
Paula Otero ◽  
Clemency Jolly ◽  
Daniel García-Souto ◽  

AbstractMost cancers are characterized by the somatic acquisition of genomic rearrangements during tumour evolution that eventually drive the oncogenesis. Here, using multiplatform sequencing technologies, we identify and characterize a remarkable mutational mechanism in human hepatocellular carcinoma caused by Hepatitis B virus, by which DNA molecules from the virus are inserted into the tumour genome causing dramatic changes in its configuration, including non-homologous chromosomal fusions, dicentric chromosomes and megabase-size telomeric deletions. This aberrant mutational mechanism, present in at least 8% of all HCC tumours, can provide the driver rearrangements that a cancer clone requires to survive and grow, including loss of relevant tumour suppressor genes. Most of these events are clonal and occur early during liver cancer evolution. Real-time timing estimation reveals some HBV-mediated rearrangements occur as early as two decades before cancer diagnosis. Overall, these data underscore the importance of characterising liver cancer genomes for patterns of HBV integration.

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