Oncogenic functions of ZEB1 in pediatric solid cancers: interplays with microRNAs and long noncoding RNAs

Fratini, Lívia; Jaeger, Mariane da Cunha; Farias, Caroline Brunetto de; Brunetto, André T.; Brunetto, Algemir Lunardi; Shaw, Lisa; Roesler, Rafaël

doi:10.1007/s11010-021-04226-x

Cited by 5 publications

(4 citation statements)

References 108 publications

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“…Previous research suggests that ZEB1 acts as a transcription factor to induce EMT in cancer cells to promote tumor progression [ 18 ]. The oncogenicity of ZEB1 has been demonstrated in multiple solid tumors such as osteosarcoma, retinoblastoma, and neuroblastoma, which plays a positive regulatory role in the malignant progression of these tumors [ 19 ]. ZEB1 also plays a carcinogenic role in CC and regulates the malignant development of CC by mediating the colorectal neoplasia differentially expressed (CRNDE)/miR-4262/ZEB1 signaling pathway [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Analysis of the Role and Mechanism of ZEB1 in Regulating Cervical Carcinoma Progression via Modulating PD-1/PD-L1 Checkpoint

Lin

Wang

2022

Computational and Mathematical Methods in Medicine

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Background. Cervical carcinoma (CC) is a common and highly malignant tumor in women. The involvement of zinc finger E-box binding homeobox 1 (ZEB1) in many kinds of tumors has been well-documented; however, its role and mechanism in CC remain to be clarified. Objective. This study investigated the mechanism of ZEB1 in modulating the growth and metastasis of CC cells. Methods. The expression of ZEB1 in CC tissues and adjacent normal counterparts was determined by reverse transcription-polymerase chain reaction (RT-PCR). The correlation between ZEB1 and patient clinicopathological indexes was analyzed. In vitro, gain and loss functions of ZEB1 were performed in C-33A and HeLa cell lines. The proliferation, migration, and invasion of CC cells were detected by Cell Counting Kit-8 (CCK-8) assay and transwell assay, respectively. The expression levels of apoptosis-related proteins such as BCL2-associated X (Bax), B-cell lymphoma-2 (Bcl2), and Caspase-3, as well as epithelial-mesenchymal transition (EMT)-associated proteins including E-cadherin, Vimentin, and Snail, were measured by Western blotting. In addition, the targeting relationship between ZEB1 and programmed death 1 (PD-1)/programmed cell death-ligand 1 (PD-L1) was predicted by bioinformatics and further verified by dual-luciferase reporter assay. Results. ZEB1 was significantly up-regulated in CC tissues compared with normal counterparts. ZEB1 overexpression promoted the migration, proliferation, and invasion of CC cells and inhibited apoptosis, while knocking down ZEB1 contributed to the opposite effects. In addition, experiments on related mechanisms confirmed that ZEB1 targeted the 3’EUTR terminal of PD-1/PD-L1 and negatively regulated its expression. And an interaction between ZEB1 and PD-1/PD-L1 was identified. Conclusion. ZEB1 can promote the proliferation and metastasis of CC cells via modulating the PD-1/PD-L1 checkpoint.

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Section: Discussionmentioning

confidence: 99%

Analysis of the Role and Mechanism of ZEB1 in Regulating Cervical Carcinoma Progression via Modulating PD-1/PD-L1 Checkpoint

Lin

Wang

2022

Computational and Mathematical Methods in Medicine

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“…ZEB1, the member of the ZHF family, could regulate the expression of multiple oncogenes, thereby promoting the initiation and development of cancer [ 32 , 33 ]. ZEB1 also was the common and important target of a range of signaling pathways (including miRNA signaling) which can regulate cell differentiation, proliferation, plasticity, and survival [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

microRNA-569 inhibits tumor metastasis in pancreatic cancer by directly targeting NUSAP1

Che

et al. 2022

Aging

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MicroRNAs (miRNAs) are known to be involved in the development and progression of pancreatic cancer (PC). In this study, the prognostic significance and mechanistic role of microRNA-569 in PC were explored. Quantitative real-time PCR was used to detect the expression of microRNA-569 in PC tissues and cell lines. Scratch test and Transwell assay were conducted to detect migration and invasion ability. The xenograft nude mice model was used to determine tumor metastasis in vivo . The direct targets of microRNA-569 were determined by using bioinformatics analysis and a dual-luciferase reporter assay. The expression level of microRNA-569 was down-regulated in PC patients with a poor prognosis. In vitro and in vivo experiments indicated that over-expression of microRNA-569 inhibited the migration and invasion of PC cells. MicroRNA-569 negatively regulated NUSAP1 by directly binding its 3'-untranslated region. Further mechanism research implied that the ZEB1 pathway was involved in microRNA-569/NUSAP1 mediation of the biological behaviors in PC. These data demonstrated that microRNA-569 may exert a tumor-suppressing effect in PC and maybe a potential therapeutic target for PC patients.

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“…The two‐handed zinc‐finger homeodomain transcription factor TCF8 is a zinc finger transcription factor binding to the E‐box motifs (Fratini et al, 2021; Wang et al, 2021). Previous studies have demonstrated that TCF8 plays a regulatory role in epithelial–mesenchymal transition (EMT), a process that is critical for embryogenesis, hematopoietic stem cell differentiation, and tumor development (Goossens et al, 2011; Wang et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Regulation of osteoclast differentiation and inflammatory signaling by TCF8 in periodontitis

et al. 2023

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ObjectivesThe aim of this study was to explore the potential role of zinc‐finger homeodomain transcription factor (TCF8) in osteoclastogenesis and inflammation during periodontitis.Materials and MethodsRats with periodontitis were induced via Porphyromonas gingivalis‐lipopolysaccharide (Pg‐LPS) injection. The recombinant lentivirus delivering short hairpin RNA (shRNA) against TCF8 was used to downregulate TCF8 in vivo. Alveolar bone loss in rats was determined by micro‐computed tomography (Micro‐CT). Typical pathological changes, periodontal tissue inflammation, and osteoclastogenesis were evaluated via histological analyses. The RAW264.7‐derived osteoclasts were induced by RANKL stimulation. TCF8 downregulation in vitro was achieved by lentivirus infection. The osteoclast differentiation and inflammatory signaling in RANKL‐induced cells were measured via immunofluorescence methods and molecular biology approaches.ResultsPorphyromonas gingivalis‐lipopolysaccharide induced rats exhibited overexpressed TCF8 in their periodontal tissues, while TCF8 knockdown attenuated the bone loss, tissue inflammation, and osteoclastogenesis in LPS‐induced rats. Besides, TCF8 silencing inhibited RANKL‐induced osteoclast differentiation in RAW264.7 cells, as evidenced by the reduced numbers of TRAP‐positive osteoclasts, less formation of F‐actin rings, and downregulated expressions of osteoclast‐specific markers. It also exerted an inhibitory effect on the NF‐κB signaling in RANKL‐induced cells via blocking NF‐κB p65 phosphorylation and nuclear translocation.ConclusionsTCF8 silencing inhibited alveolar bone loss, osteoclast differentiation, and inflammation in periodontitis.

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Oncogenic functions of ZEB1 in pediatric solid cancers: interplays with microRNAs and long noncoding RNAs

Cited by 5 publications

References 108 publications

Analysis of the Role and Mechanism of ZEB1 in Regulating Cervical Carcinoma Progression via Modulating PD-1/PD-L1 Checkpoint

Analysis of the Role and Mechanism of ZEB1 in Regulating Cervical Carcinoma Progression via Modulating PD-1/PD-L1 Checkpoint

microRNA-569 inhibits tumor metastasis in pancreatic cancer by directly targeting NUSAP1

Regulation of osteoclast differentiation and inflammatory signaling by TCF8 in periodontitis

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