Aqueous extracts from Tenebrio molitor larval and pupal stages inhibit early hepatocarcinogenesis in vivo

• Published in: Journal of Zhejiang University. B. Science Vol. 22; no. 12; pp. 1045 - 1052
• Main Authors: Zepeda-Bastida, Armando, Ocampo-López, Juan, Alarcón-Sánchez, Brisa Rodope, Idelfonso-García, Osiris Germán, Rosas-Madrigal, Sandra, Aparicio-Bautista, Diana Ivette, Pérez-Carreón, Julio Isael, Villa-Treviño, Saúl, Arellanes-Robledo, Jaime
• Format: Journal Article
• Language: English
• Published: Hangzhou Zhejiang University Press 15.12.2021; Springer Nature B.V; Institute of Agricultural Sciences,Autonomous University of Hidalgo State-ICAP-UAEH,Hidalgo 43600,Mexico%Laboratory of Liver Diseases,National Institute of Genomic Medicine-INMEGEN,CDMX 14610,Mexico; Department of Cell Biology,Center for Research and Advanced Studies of the National Polytechnic Institute-CINVESTAV-IPN,CDMX 07360,Mexico%Laboratory of Liver Diseases,National Institute of Genomic Medicine-INMEGEN,CDMX 14610,Mexico%Laboratory of Cardiovascular Diseases,National Institute of Genomic Medicine-INMEGEN,CDMX 14610,Mexico%Proteomics Unit,National Institute of Genomic Medicine-INMEGEN,CDMX 14610,Mexico%Department of Cell Biology,Center for Research and Advanced Studies of the National Polytechnic Institute-CINVESTAV-IPN,CDMX 07360,Mexico%Laboratory of Liver Diseases,National Institute of Genomic Medicine-INMEGEN,CDMX 14610,Mexico; Directorate of Cátedras,National Council of Science and Technology-CONACYT,CDMX 03940,Mexico
• Subjects: Animals; beta Catenin - analysis; beta Catenin - genetics; Biomedical and Life Sciences; Biomedicine; Correspondence; Diethylnitrosamine; Ki-67 Antigen - analysis; Larva; Liver Neoplasms, Experimental - pathology; Liver Neoplasms, Experimental - prevention & control; Male; Mice; Mice, Inbred C57BL; Pupa; Tenebrio; 二乙基亚硝胺; 肝癌预防; 肝细胞癌; 增殖抑制; Liver cancer prevention; Hepatocellular carcinoma; Proliferation inhibition; Diethylnitrosamine
• ISSN: 1673-1581; 1862-1783
• DOI: 10.1631/jzus.B2100201

Hepatocellular carcinoma (HCC), which is the most frequent primary liver malignancy, is ranked as the sixth most common cancer and the third leading cause of cancer-related deaths worldwide, with its incidence expected to continue rising. One of the reasons is that most patients are diagnosed at an advanced stage when therapeutic options are ineffective. The development of HCC is attributed to a chronic exposition to either one or a combination of low amounts of different hepatotoxins, such as in hepatitis virus infection, alcohol consumption, aflatoxin from contaminated foods, metabolic factors, and exposure to chemical carcinogens from tobacco smoke (Forner et al., 2018). Integrative studies combining exome sequencing, transcriptome analysis, and the genomic characterization of HCC have shown that these etiological factors may raise the frequency of particular genetic alterations, resulting in intra-tumor heterogeneity that presents a huge challenge for treatment. For example, mutations in the catenin β-1 (CTNNB1) gene (a proto-oncogene in the WNT signaling pathway that encodes the β‍-catenin transcription factor) are strongly associated with alcohol-related HCC, whereas mutations in the telomerase reverse transcriptase (TERT) promoter and tumor protein p53 (TP53) genes are the most commonly observed in hepatitis B virus (HBV)‍-associated HCC (Calderaro et al., 2017; Cancer Genome Atlas Research Network, 2017). The above findings emphasize the molecular diversity of HCC and the associations of different etiologies with distinct mechanisms in HCC progression. Consequently, prevention strategies are still attractive for HCC management.