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Review
. 2022 Mar-Apr;19(2):113-129.
doi: 10.21873/cgp.20308.

MicroRNAs and Corresponding Targets in Esophageal Cancer as Shown In Vitro and In Vivo in Preclinical Models

Affiliations
Review

MicroRNAs and Corresponding Targets in Esophageal Cancer as Shown In Vitro and In Vivo in Preclinical Models

Ulrich H Weidle et al. Cancer Genomics Proteomics. 2022 Mar-Apr.

Abstract

Squamous cell carcinoma of the esophagus is associated with a dismal prognosis. Therefore, identification of new targets and implementation of new treatment modalities are issues of paramount importance. Based on a survey of the literature, we identified microRNAs conferring antitumoral activity in preclinical in vivo experiments. In the category of miRs targeting secreted factors and transmembrane receptors, four miRs were up-regulated and 10 were down-regulated compared with five out of nine in the category transcription factors, and six miRs were down-regulated in the category enzymes, including metabolic enzymes. The down-regulated miRs have targets which can be inhibited by small molecules or antibody-related entities, or re-expressed by reconstitution therapy. Up-regulated miRs have targets which can be reconstituted with small molecules or inhibited with antagomirs.

Keywords: miR-based target identification; miR-related treatment modalities; preclinical in vivo models; review; squamous cell esophageal cancer.

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Conflict of interest statement

AN is and UHW was an employee of Roche.

Figures

Figure 1
Figure 1. Up-regulated (A) and down-regulated (B) miRs targeting secreted factors and transmembrane receptors in esophageal cancer cells in preclinical in vivo systems. ADAMTS1: A disintegin and metalloprotease with thrombospondin motifs 1; CD44, 47, 133: cluster of differentiation 44, 47, 133; EGFR: epidermal growth factor receptor; EI24: etoposide-induced 2.4 transcript; HER2: human epidermal growth factor receptor 2; IGF1R: insulin growth factor-like receptor 1; INTα6: integrin α6; INTβ6: integrin β6; INV: invasion; MET: metastasis; PROL: proliferation; RAGE: receptor for advanced glycation end-products; SARA: SMAD anchor for receptor activation; TG: tumor growth; TGFβR2: transforming growth factor receptor 2; TNFα: tumor necrosis factor α; VEGFA: vascular endothelial growth factor A.
Figure 2
Figure 2. Up-regulated (A) and down-regulated (B) miRs targeting transcription factors in esophageal cancer cells in preclinical in vivo systems. AKT: Serine-threonine kinase AKT; ARID3A: AT-rich interactive domain-containing protein 3A; CXX5: CCX-type zinc finger protein 5; DDP res: cisplatin resistance; EMT: epithelial–mesenchymal transition; FOXK2: forkhead box protein K2; FOXO31: forkhead-box protein 31; FOXM1: forkhead box protein M1; GSK3β: glycogen synthase kinase 3β; INV: invasion; KLF4: Krüppel-like factor 4; MAPK: mitogen-activated protein kinase; MET: metastasis; MYC: transcription factor MYC; mTOR: mechanistic target of rapamycin; p38: mitogen-activated protein kinase p38; PITX2: paired-like homeodomain transcription factor 2; PPARγ: peroxisome proliferator-activated receptor γ; PROL: proliferation; SMAD4: signaling protein SMAD4; SNAI2: snail family transcriptional repressor 2; SOX4: sex determining region Y-box 4; STAT3: signal transducer and activator of transcription 3; TG: tumor growth; ZEB1: zinc finger E-box binding homeobox 2.
Figure 3
Figure 3. Down-regulated miRs targeting enzymes in esophageal cancer cells mediating efficacy in preclinical in vivo systems DNA polβ: DNA polymerase β; LDHB: lactate dehydrogenase B; MET: metastasis; MTDH1: metadherin 1; OGT: O-linked-N-acetylglucosaminacetylation transferase; PROL: proliferation; PSAT1: phosphoserine aminotransferase 1; INV: invasion; TG: tumor growth; TIGAR: p53-inducible glycolysis and apoptosis regulator; USP26: ubiquitin-specific protease 26.

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References

    1. Hull R, Mbele M, Makhafola T, Hicks C, Wang SM, Reis RM, Mehrotra R, Mkhize-Kwitshana Z, Hussain S, Kibiki G, Bates DO, Dlamini Z. A multinational review: Oesophageal cancer in low to middle-income countries. Oncol Lett. 2020;20(4):42. doi: 10.3892/ol.2020.11902. - DOI - PMC - PubMed
    1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2020. CA Cancer J Clin. 2020;70(1):7–30. doi: 10.3322/caac.21590. - DOI - PubMed
    1. Lordick F, Janjigian YY. Clinical impact of tumour biology in the management of gastroesophageal cancer. Nat Rev Clin Oncol. 2016;13(6):348–360. doi: 10.1038/nrclinonc.2016.15. - DOI - PMC - PubMed
    1. Testa U, Castelli G, Pelosi E. Esophageal cancer: Genomic and molecular characterization, stem cell compartment and clonal evolution. Medicines (Basel) 2017;4(3):67. doi: 10.3390/medicines4030067. - DOI - PMC - PubMed
    1. Bujanda DE, Hachem C. Barrett’s Esophagus. Mo Med. 2018;115(3):211–213. - PMC - PubMed

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