YES1 Is a Targetable Oncogene in Cancers Harboring <i>YES1</i> Gene Amplification

Hamanaka, Natsuki; Nakanishi, Yoshito; Mizuno, Takakazu; Horiguchi-Takei, Kana; Akiyama, Nukinori; Tanimura, Hiromi; Hasegawa, Masami; Satoh, Yasuko; Tachibana, Yukako; Fujii, Toshihiko; Sakata, Kiyoaki; Ogasawara, Kiyomoto; Ebiike, Hirosato; Koyano, Hiroshi; Sato, Haruhiko; Ishii, Nobuya; Mio, Toshiyuki

doi:10.1158/0008-5472.can-18-3376

Cited by 49 publications

(44 citation statements)

References 48 publications

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“…The ability of a specific CDK8/19 kinase inhibitor, CCT251545, inhibits Wnt pathway-induced tumours in mouse models [ 225 ]. Similarly, another kinase, YES1, implicated in YAP dependent β-catenin transcriptional output, can be inhibited by CH6953755 to restrict YES1-YAP1-dependent tumour growth [ 94 , 226 ]. Lastly, NSC48300, a pharmacologic inhibitor for Taspase1, can effectively inactivate breast and brain tumour growth via preventing the formation of a mature MLL1 complex [ 227 ].…”

Section: Therapeutic Strategymentioning

confidence: 99%

Transcriptional Regulation of Wnt/β-Catenin Pathway in Colorectal Cancer

Dannappel

Wan

et al. 2020

Cells

181

111

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The Wnt/β-catenin signaling pathway exerts integral roles in embryogenesis and adult homeostasis. Aberrant activation of the pathway is implicated in growth-associated diseases and cancers, especially as a key driver in the initiation and progression of colorectal cancer (CRC). Loss or inactivation of Adenomatous polyposis coli (APC) results in constitutive activation of Wnt/β-catenin signaling, which is considered as an initiating event in the development of CRC. Increased Wnt/β-catenin signaling is observed in virtually all CRC patients, underscoring the importance of this pathway for therapeutic intervention. Prior studies have deciphered the regulatory networks required for the cytoplasmic stabilisation or degradation of the Wnt pathway effector, β-catenin. However, the mechanism whereby nuclear β-catenin drives or inhibits expression of Wnt target genes is more diverse and less well characterised. Here, we describe a brief synopsis of the core canonical Wnt pathway components, set the spotlight on nuclear mediators and highlight the emerging role of chromatin regulators as modulators of β-catenin-dependent transcription activity and oncogenic output.

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Section: Therapeutic Strategymentioning

confidence: 99%

Transcriptional Regulation of Wnt/β-Catenin Pathway in Colorectal Cancer

Dannappel

Wan

et al. 2020

Cells

181

111

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“…Several lines of evidence indicate that YAP1 is an oncogene. YAP1 was found to act as oncogenic target of 11q22 amplification in multiple cancer subtypes, whereas YAP1 silencing significantly decreases cell proliferation (Lorenzetto et al, 2014, Hamanaka et al, 2019. YAP1 was shown to promote growth of prostate cancer, whereas knock down of its expression or inhibition of YAP1 function significantly suppressed tumor recurrence (Jiang et al, 2017).…”

Section: Yes-associated Protein 1 Encoded By the Yap1 Genementioning

confidence: 99%

Use of signals of positive and negative selection to distinguish cancer genes and passenger genes

Bányai

Trexler

Kerekes

et al. 2021

eLife

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A major goal of cancer genomics is to identify all genes that play critical roles in carcinogenesis. Most approaches focused on genes positively selected for mutations that drive carcinogenesis and neglected the role of negative selection. Some studies have actually concluded that negative selection has no role in cancer evolution. We have re-examined the role of negative selection in tumor evolution through the analysis of the patterns of somatic mutations affecting the coding sequences of human genes. Our analyses have confirmed that tumor suppressor genes are positively selected for inactivating mutations, oncogenes, however, were found to display signals of both negative selection for inactivating mutations and positive selection for activating mutations. Significantly, we have identified numerous human genes that show signs of strong negative selection during tumor evolution, suggesting that their functional integrity is essential for the growth and survival of tumor cells.

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“…YES1, as a member of the SRC family, acts as an oncogene in most tumors 30 and plays an important role in the acquired drug resistance of breast and lung cancer 31,32 . This study found that YES1 is signi cantly overexpressed in HB.…”

Section: Discussionmentioning

confidence: 99%

MiR-125b-5p Inhibited The Progression of Hepatoblastoma As A Shared miRNA of The lncRNA NEAT1 and YES1

Jin

Chen

Mao

et al. 2020

Preprint

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Background: microRNAs have been studied widely in hepatoblastoma. However, the role of miR-125b-5p and its relationship with the lncRNA sNEAT1 and YES1 in hepatoblastoma have not been reported previously. We aimed to reveal the role of NEAT1/miR-125b-5p/YES1 in the progression of hepatoblastoma.Methods: We collected tumor tissues and their adjacent tissues from 12 hepatoblastoma patients. qRT-PCR was applied to detect the expression of miR-125b-5p, and the relationship of miR-125b-5p with clinicopathological characteristics was analyzed. Dual luciferase reporter assays and RNA pull down assays were used to identify the relationships among NEAT1, miR-125b-5p and YES1. CCK8, Transwell assays and wound healing assays were used to examine cell viability, invasion and migration. In vivo experiments were also applied to detect the effect of miR-125b-5p on hepatoblastoma.Results: miR-125b-5p was significantly downregulated in hepatoblastoma tissue and cells. The higher the PRETEXT grade, the lower the miR-125b-5p level. NEAT1 could bind to miR-125b-5p and inhibit its expression. miR-125b-5p could target YES1 and inhibit its expression. Overexpression of miR-125b-5p decreased the proliferation, invasion, and migratory ability of hepatoblastoma cells. YES1 could rescue the above effects. At the same time, overexpression of miR-125b-5p resulted in decreased YES1 and tumor growth inhibition in vivo.Conclusion: miR-125b-5p acted as a shared miRNA of NEAT1 and YES1 in hepatoblastoma. Overexpression of miR-125b-5p could target YES1 and inhibit its expression, therefore inhibiting the progression of hepatoblastoma.

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YES1 Is a Targetable Oncogene in Cancers Harboring YES1 Gene Amplification

Cited by 49 publications

References 48 publications

Transcriptional Regulation of Wnt/β-Catenin Pathway in Colorectal Cancer

Transcriptional Regulation of Wnt/β-Catenin Pathway in Colorectal Cancer

Use of signals of positive and negative selection to distinguish cancer genes and passenger genes

MiR-125b-5p Inhibited The Progression of Hepatoblastoma As A Shared miRNA of The lncRNA NEAT1 and YES1

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