SOX13/TRIM11/YAP axis promotes the proliferation, migration and chemoresistance of anaplastic thyroid cancer

Tang, Jianing; Tian, Zelin; Liao, Xing

doi:10.7150/ijbs.54194

Cited by 30 publications

(21 citation statements)

References 54 publications

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“…Small interfering RNAs targeting MINDY1(siG000055793A-1-5, siG000055793B-1-5) were obtained from Ruibo Biotechnology Co., Ltd. (Guangzhou, China). The YAP full- and its deletion constructs were gifted from Dr. Gaosong Wu and were described in the previous study [ 19 ]. Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA) was used for plasmid transfection according to the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

MINDY1 promotes bladder cancer progression by stabilizing YAP

et al. 2021

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Background Bladder cancer is one of the most commonly diagnosed urological malignant tumor. The Hippo tumor suppressor pathway is highly conserved in mammals and plays an important role in carcinogenesis. YAP is one of major key effectors of the Hippo pathway. However, the mechanism supporting abnormal YAP expression in bladder cancer remains to be characterized. Methods Western blot was used to measure the expression of MINDY1 and YAP, while the YAP target genes were measured by real-time PCR. CCK8 assay was used to detect the cell viability. The xeno-graft tumor model was used for in vivo study. Protein stability assay was used to detect YAP protein degradation. Immuno-precipitation assay was used to detect the interaction domain between MINDY1 and YAP. The ubiquitin-based Immuno-precipitation assays were used to detect the specific ubiquitination manner happened on YAP. Results In the present study, we identified MINDY1, a DUB enzyme in the motif interacting with ubiquitin-containing novel DUB family, as a bona fide deubiquitylase of YAP in bladder cancer. MINDY1 was shown to interact with, deubiquitylate, and stabilize YAP in a deubiquitylation activity-dependent manner. MINDY1 depletion significantly decreased bladder cancer cell proliferation. The effects induced by MINDY1 depletion could be rescued by further YAP overexpression. Depletion of MINDY1 decreased the YAP protein level and the expression of YAP/TEAD target genes in bladder cancer, including CTGF, ANKRD1 and CYR61. Conclusion In general, our findings establish a previously undocumented catalytic role for MINDY1 as a deubiquitinating enzyme of YAP and provides a possible target for the therapy of bladder cancer.

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Section: Methodsmentioning

confidence: 99%

MINDY1 promotes bladder cancer progression by stabilizing YAP

et al. 2021

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“…ATC is one of the most aggressive solid tumors, representing 2–5% of thyroid cancer [ 140 ]. TRIM11, an E3 ligase that belongs to the tripartite motif (TRIM) protein family, has been linked to the malignant phenotypes of ATC [ 141 ]. Mechanistic studies have indicated that TRIM11 can substantially increase the monoubiquitination of YAP, the key downstream effector in the Hippo pathway, while inhibiting K11- and K48-linked polyubiquitination of YAP, leading to elevated ATC cell migration [ 141 ].…”

Section: Roles Of Monoubiquitination In Cancermentioning

confidence: 99%

Monoubiquitination in Homeostasis and Cancer

Chen

Zhou

Yao

et al. 2022

IJMS

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Monoubiquitination is a post-translational modification (PTM), through which a single ubiquitin molecule is covalently conjugated to a lysine residue of the target protein. Monoubiquitination regulates the activity, subcellular localization, protein–protein interactions, or endocytosis of the substrate. In doing so, monoubiquitination is implicated in diverse cellular processes, including gene transcription, endocytosis, signal transduction, cell death, and DNA damage repair, which in turn regulate cell-cycle progression, survival, proliferation, and stress response. In this review, we summarize the functions of monoubiquitination and discuss how this PTM modulates homeostasis and cancer.

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“…High levels of YAP1 were detected in thyroid cancer tissues, and this finding is correlated with advanced tumor progression and poor prognosis 20–22 . The activation of YAP1 accelerates the malignant progression and metastasis and confers chemoresistance of thyroid cancer 21,23–26 . YAP1 silencing downregulates the proliferation and metastasis of thyroid cancer 27 .…”

Section: Introductionmentioning

confidence: 97%

“…[20][21][22] The activation of YAP1 accelerates the malignant progression and metastasis and confers chemoresistance of thyroid cancer. 21,[23][24][25][26] YAP1 silencing downregulates the proliferation and metastasis of thyroid cancer. 27 Various factors and mechanisms contribute to mediation of the Hippo/YAP1 pathway.…”

Section: Introductionmentioning

confidence: 99%

FERM domain‐containing protein 6 exerts a tumor‐inhibiting role in thyroid cancer by antagonizing oncogenic YAP1

et al. 2021

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The emerging role of FERM domain‐containing protein 6 (FRMD6) in cancer progression has been revealed in several malignancies. However, its relevance on thyroid cancer is not well understood. This work evaluated the possible role and mechanism of FRMD6 in thyroid cancer. We demonstrated that FRMD6 expression was downregulated in thyroid cancer by analyzing the Cancer Genome Atlas data. Remarkable reductions in FRMD6 expression were also confirmed in the clinical specimens and cell lines of thyroid cancer. The upregulation of FRMD6 restrained the proliferation, epithelial–mesenchymal transition, and invasion of thyroid cancer. Moreover, FRMD6 overexpression significantly increased the apoptosis and cell cycle arrest. Further molecular research demonstrated that the overexpression of FRMD6 increased the phosphorylation levels of mammalian STE20‐like protein kinase 1, large tumor suppressor 1, and Yes‐associated protein 1 (YAP1) and prohibited the activation of YAP1. The re‐expression of constitutively active YAP1 strikingly reversed FRMD6‐induced tumor‐inhibiting effects. Thyroid cancer cells overexpressing FRMD6 had a weakened ability to form xenograft tumors in vivo in nude mice. Overall, the overexpression of FRMD6 produces remarkable tumor‐inhibiting effects in thyroid cancer by inhibiting oncogenic YAP1.

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SOX13/TRIM11/YAP axis promotes the proliferation, migration and chemoresistance of anaplastic thyroid cancer

Cited by 30 publications

References 54 publications

MINDY1 promotes bladder cancer progression by stabilizing YAP

MINDY1 promotes bladder cancer progression by stabilizing YAP

Monoubiquitination in Homeostasis and Cancer

FERM domain‐containing protein 6 exerts a tumor‐inhibiting role in thyroid cancer by antagonizing oncogenic YAP1

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