Downregulation of CHIP promotes ovarian cancer metastasis by inducing Snail‐mediated epithelial–mesenchymal transition

Park, Sun Mi; Park, Seung Ho; Ryu, Ki Jun; Kim, In Kyu; Han, Hyeontak; Kim, Hyo Jin; Kim, Seon Hee; Hong, Keun Seok; Kim, Hye-Min; Kim, Min-Ju; Cho, Bok Im; Heo, Jeong‐Doo; Kim, Na Hyun; Hwang, Eun Mi; Park, Jae Yong; Yook, Jong In; Cho, Hee Jun; Hwangbo, Cheol; Kim, Kwang Dong; Song, Hoseok; Yoo, Ji Myong

doi:10.1002/1878-0261.12485

Cited by 18 publications

(12 citation statements)

References 33 publications

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“… 15 STUB1 suppressed stemness and tumorigenicity of oral carcinoma cell, 16 and downregulation of STUB1 promoted epithelial-mesenchymal transition of ovarian cancer. 17 Recent study has shown that STUB1 was aberrantly expressed in breast cancer, 18 and STUB1 promoted ubiquitin/proteasome-dependent degradation of ERBB2-mediated oncogenes in breast cancer. 19 Our results showed that over-expression of STUB1 attenuated TRIM6-induced increase in breast cancer cell proliferation, migration and invasion.…”

Section: Discussionmentioning

confidence: 99%

Tripartite motif-containing protein 6 facilitates growth and migration of breast cancer through degradation of STUB1

Wei

Liu

et al. 2021

Eur J Histochem

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Proteins in the tripartite motif-containing protein (TRIM) family participates in carcinogenesis. However, little attention was focused on the role of TRIM6 on development of breast cancer. Expression level of TRIM6 was found to be markedly enhanced in breast cancer cells and tissues. Functional assays demonstrated that overexpression of TRIM6 promoted breast cancer progression through increase of YAP1 (Yes-associated Protein 1), while knockdown of TRIM6 suppressed in vitro breast cancer progression and in vivo tumor growth through decrease of YAP1. Co-Immunoprecipitation (co-IP) showed that TRIM6 interacted with STUB1 (stress induced phosphoprotein 1 homology and U-box containing protein 1). TRIM6 promoted ubiquitination-mediated degradation of STUB1 to promote YAP1 signaling. Overexpression of STUB1 attenuated TRIM6-induced promotion of breast cancer growth. In conclusion, TRIM6 contributed to breast cancer progression through ubiquitination-dependent proteasomal degradation of STUB1 and provocation of YAP1 pathway, providing potential therapeutic target for breast cancer.

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Section: Discussionmentioning

confidence: 99%

Tripartite motif-containing protein 6 facilitates growth and migration of breast cancer through degradation of STUB1

Wei

Liu

et al. 2021

Eur J Histochem

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“…SPSB3 targets SNAI1 to promote polyubiquitination and degradation in response to GSK3β phosphorylation of SNAI1. Through yeast two-hybrid screening, the carboxyl terminus of Hsc70-interacting protein (CHIP) was identified as a novel SNAI1 ubiquitin ligase that interacts with SNAI1 to induce ubiquitin-mediated proteasomal degradation [49]. Recently, it was reported that SNAI1 was monoubiquitinated by the ubiquitin-editing enzyme A20.…”

Section: Ubiquitination and Deubiquitinationmentioning

confidence: 99%

Epigenetic Regulation and Post-Translational Modifications of SNAI1 in Cancer Metastasis

Dong

2021

IJMS

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SNAI1, a zinc finger transcription factor, not only acts as the master regulator of epithelial-mesenchymal transition (EMT) but also functions as a driver of cancer progression, including cell invasion, survival, immune regulation, stem cell properties, and metabolic regulation. The regulation of SNAI1 occurs at the transcriptional, translational, and predominant post-translational levels including phosphorylation, acetylation, and ubiquitination. Here, we discuss the regulation and role of SNAI1 in cancer metastasis, with a particular emphasis on epigenetic regulation and post-translational modifications. Understanding how signaling networks integrate with SNAI1 in cancer progression will shed new light on the mechanism of tumor metastasis and help develop novel therapeutic strategies against cancer metastasis.

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“…Besides, the expression of SNAIL is associated with cancer metastasis. It has also been observed that SNAIL expression levels are elevated in distant metastasis originating from ovarian cancer [ 175 , 176 ]. A recent study revealed that SNAIL-induced EMT accelerates metastasis through induction of immune suppression [ 161 , 177 ].…”

Section: Myc–the Regulator Of Emt and Metastasismentioning

confidence: 99%

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Meškytė

Keskas

Ciribilli

2020

IJMS

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The Myc family of oncogenes is deregulated in many types of cancer, and their over-expression is often correlated with poor prognosis. The Myc family members are transcription factors that can coordinate the expression of thousands of genes. Among them, c-Myc (MYC) is the gene most strongly associated with cancer, and it is the focus of this review. It regulates the expression of genes involved in cell proliferation, growth, differentiation, self-renewal, survival, metabolism, protein synthesis, and apoptosis. More recently, novel studies have shown that MYC plays a role not only in tumor initiation and growth but also has a broader spectrum of functions in tumor progression. MYC contributes to angiogenesis, immune evasion, invasion, and migration, which all lead to distant metastasis. Moreover, MYC is able to promote tumor growth and aggressiveness by recruiting stromal and tumor-infiltrating cells. In this review, we will dissect all of these novel functions and their involvement in the crosstalk between tumor and host, which have demonstrated that MYC is undoubtedly the master regulator of the tumor microenvironment. In sum, a better understanding of MYC’s role in the tumor microenvironment and metastasis development is crucial in proposing novel and effective cancer treatment strategies.

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Downregulation of CHIP promotes ovarian cancer metastasis by inducing Snail‐mediated epithelial–mesenchymal transition

Cited by 18 publications

References 33 publications

Tripartite motif-containing protein 6 facilitates growth and migration of breast cancer through degradation of STUB1

Tripartite motif-containing protein 6 facilitates growth and migration of breast cancer through degradation of STUB1

Epigenetic Regulation and Post-Translational Modifications of SNAI1 in Cancer Metastasis

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

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