Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Cho, Anne Arah; Bonavida, Benjamin

doi:10.1615/critrevoncog.2017020473

Cited by 44 publications

(28 citation statements)

References 66 publications

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“…Tumor metastasis involves many tumor processes and EMT is a key initial step for tumor cells to acquire the potential of metastasis and invasion [ 16 , 17 ]. EMT is an evolutionary process in which cells lose epithelial properties and acquire mesenchymal properties.…”

Section: Discussionmentioning

confidence: 99%

Inhibin subunit beta A promotes cell proliferation and metastasis of breast cancer through Wnt/β-catenin signaling pathway

2021

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Emerging evidence has demonstrated that inhibin subunit beta A (INHBA) is dysregulated and plays a critical role in various cancers. With the development of sequencing technology, studies have discovered that INHBA is overexpressed in breast cancer tissues. However, the biological roles of INHBA in breast cancer are still far to clear. In the present study, we analyzed the INHBA expression in the Cancer Genome Atlas (TCGA) database. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to assess the expression of INHBA in breast cancer cell lines. Cell proliferation, invasion and epithelial–mesenchymal transition (EMT) were determined by using CCK-8, EdU, Transwell and western blot assays. The result showed that INHBA was highly expressed in breast cancer cell lines. Functional analysis revealed that silence or elevation of INHBA inhibited or promoted the proliferation, migration, invasion and EMT and Wnt/β-catenin signaling pathway-related markers of MCF-7 cells. Mechanically, blocking of Wnt/β-catenin pathway by XAV939 reversed the promotion effect of INHBA overexpression on breast cancer cells’ proliferation, migration and invasion. Our findings emphasized that INHBA may act as an oncogene via activating the Wnt/β-catenin pathway, which may provide a potential therapeutic target for the treatment of breast cancer.

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Section: Discussionmentioning

confidence: 99%

Inhibin subunit beta A promotes cell proliferation and metastasis of breast cancer through Wnt/β-catenin signaling pathway

2021

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“…YY1 belongs to the polycomb group of proteins; this type of protein may cause epigenetic remodeling of the chromatin and therefore dynamically regulate expressions of their target genes (81). YY1 overexpression observed in the majority of cancers has been correlated with poor prognosis of patients (82). Previous studies have demonstrated that YY1 is implicated in HCC (83–88).…”

Section: Discussionmentioning

confidence: 99%

In silico identification of EP400 and TIA1 as critical transcription factors involved in human hepatocellular carcinoma relapse

Hong

Fan

et al. 2019

Oncol Lett

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Hepatocellular carcinoma (HCC) is the second leading cause of cancer-associated mortality worldwide. Transcription factors (TFs) are crucial proteins that regulate gene expression during cancer progression; however, the roles of TFs in HCC relapse remain unclear. To identify the TFs that drive HCC relapse, the present study constructed co-expression network and identified the Tan module the most relevant to HCC relapse. Numerous hub TFs (highly connected) were subsequently obtained from the Tan module according to the intra-module connectivity and the protein-protein interaction network connectivity. Next, E1A-binding protein p400 (EP400) and TIA1 cytotoxic granule associated RNA binding protein (TIA1) were identified as hub TFs differentially connected between the relapsed and non-relapsed subnetworks. In addition, zinc finger protein 143 (ZNF143) and Yin Yang 1 (YY1) were also identified by using the plugin iRegulon in Cytoscape as master upstream regulatory elements, which could potentially regulate expression of the genes and TFs of the Tan module, respectively. The Kaplan-Meier (KM) curves obtained from KMplot and Gene Expression Profiling Interactive Analysis tools confirmed that the high expression of EP400 and TIA1 were significantly associated with shorter relapse-free survival and disease-free survival of patients with HCC. Furthermore, the KM curves from the UALCAN database demonstrated that high EP400 expression significantly reduced the overall survival of patients with HCC. EP400 and TIA1 may therefore serve as potential prognostic and therapeutic biomarkers.

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“…Tumor metastasis involves many tumor processes and EMT is a key initial step for tumor cells to acquire the potential of metastasis and invasion (18,19). EMT is an evolutionary process in which cells lose epithelial properties and acquire mesenchymal properties.…”

Section: Discussionmentioning

confidence: 99%

UBE2T knockdown inhibits cell growth and metastasis of breast cancer through Wnt/β-catenin pathway

Xueqin¹,

Mei²,

Yuping³

2021

Preprint

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Background: Emerging evidences have demonstrated that Ubiquitin-conjugating enzyme E2T (UBE2T) is dysregulated and play critical roles in various cancers. With the development of sequencing technology, studies have discovered that UBE2T is overexpressed in breast cancer tissues. However, the biological roles of UBE2T in breast cancer are still far to clear. In the present study, Methods: We analyzed the UBE2T expression in the Cancer Genome Atlas (TCGA) database. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to assess the expression of UBE2T in breast cancer cell lines. Cell proliferation, invasion and epithelial-mesenchymal transition (EMT) were determined by using CCK-8, EdU, Transwell and western blot assays.Results: UBE2T was highly expressed in breast cancer cell lines. Functional analysis revealed that silence or elevation of UBE2T inhibited or promoted the proliferation, migration, invasion and EMT and Wnt/β-catenin signaling pathway related markers of MCF-7 cells. Mechanically, blocking of Wnt/β-catenin pathway by XAV939 reversed the promotion effect of UBE2T overexpression on breast cancer cells’ proliferation, migration and invasion.Conclusion: Our findings emphasized that UBE2T may act as an oncogene via activating the Wnt/β-catenin pathway, which may provide a potential therapeutic target for the treatment of breast cancer.

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Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Cited by 44 publications

References 66 publications

Inhibin subunit beta A promotes cell proliferation and metastasis of breast cancer through Wnt/β-catenin signaling pathway

Inhibin subunit beta A promotes cell proliferation and metastasis of breast cancer through Wnt/β-catenin signaling pathway

In silico identification of EP400 and TIA1 as critical transcription factors involved in human hepatocellular carcinoma relapse

UBE2T knockdown inhibits cell growth and metastasis of breast cancer through Wnt/β-catenin pathway

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