Epigenetic Activation of TWIST1 by MTDH Promotes Cancer Stem–like Cell Traits in Breast Cancer

Liang, Yajun; Hu, Jing; Li, Jiatao; Liu, Yingjie; Yu, Jun; Zhuang, Xincun; Mu, Lili; Kong, Xiangyin; Hong, Dengli; Yang, Qifeng; Hu, Guohong

doi:10.1158/0008-5472.can-15-0930

Cited by 78 publications

(48 citation statements)

References 49 publications

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“…Yoo et al (20) reported that MTDH is an interaction partner of p100 protein, a component of the RNA-induced silencing complex (RISC). MTDH also facilitates transcription by modulating transcription factors, such as TWIST1 and HIF1A, thereby controlling cancer cell migration, invasion, and angiogenesis during tumorigenesis (21,22). Because of the importance of MTDH in cancer development, novel regulators that modulate MTDH expression need to be further defined.…”

mentioning

confidence: 99%

Long noncoding RNASNHG1promotes non‐small cell lung cancer progression by up‐regulatingMTDH viasponging miR‐145–5p

Shan

et al. 2018

FASEB j.

127

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Long noncoding RNAs participate in the progression and initiation of non-small cell lung cancer (NSCLC), although the mechanism remains unknown. The lncRNA identified as small nucleolar RNA host gene 1 ( SNHG1) is a novel lncRNA that is increased in multiple human cancers; however, the regulatory mechanism requires further investigation. In this study, we discovered that SNHG1 was markedly up-regulated in NSCLC tissues and cells and that SNHG1 silencing decreased tumor volumes. Moreover, we explored its regulatory mechanism and found that SNHG1 directly bound to microRNA (miRNA)-145-5p, isolating miR-145-5p from its target gene MTDH. Inhibition of SNHG1 suppressed NSCLC cell viability, proliferation, migration, and invasion in vitro, but its effect was rescued by miR-145-5p inhibition. These results demonstrate that SNHG1 contributes to NSCLC progression by modulating the miR-145-5p/ MTDH axis, and it could potentially be a therapeutic target as well as a diagnostic marker.-Lu, Q., Shan, S., Li, Y., Zhu, D., Jin, W., Ren, T. Long noncoding RNA SNHG1 promotes non-small cell lung cancer progression by up-regulating MTDH via sponging miR-145-5p.

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mentioning

confidence: 99%

Long noncoding RNASNHG1promotes non‐small cell lung cancer progression by up‐regulatingMTDH viasponging miR‐145–5p

Shan

et al. 2018

FASEB j.

127

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“…In breast cancer cells, MTDH overexpression promoted cancer cells to undergo EMT, while MTDH knockdown reversed EMT changes [16]. In addition, MTDH could regulate TWIST expression in breast cancer cells [17]. MTDH promoted EMT of tongue squamous cell carcinoma (TSCC) through activating Wnt/PCP signaling pathway [6].…”

Section: Discussionmentioning

confidence: 99%

“…However, we could not exclude other mechanisms responsible for MTDH stimulated miR-130b expression, such as epigenetic mechanism. MTDH has been involved in epigenetic activation of TWIST1 [17]. In addition, numerous studies have indicated that epigenetic modifications such as aberrant DNA methylation and histone modification affect miRNA expression in cancer cells [25].…”

Section: Discussionmentioning

confidence: 99%

MTDH promotes glioma invasion through regulating miR-130b-ceRNAs

et al. 2017

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Cell invasion is crucial for high mortality and recurrence rate in glioma. Epithelial-mesenchymal transition (EMT) is an important step in cancer invasion. Metadherin (MTDH) contributes to EMT in several cancers, but the role and mechanism of MTDH in EMT-like process of glioma remain unknown. Here we demonstrate that MTDH was overexpressed in glioma tissues and cells and induced EMT-like change and invasion of glioma cells. Interestingly, MTDH could modulate the expression of a group of glioma-related miRNAs. In particular, MTDH upregulated miR-130b transcription via acting as a coactivator of NF-kB. MiR-130b promoted EMT-like change and invasion of glioma cells through targeting multiple EMT-related genes, including PTEN, PPP2CA and SMAD7. In addition, PTEN acted as the competing endogenous RNA (ceRNA) to affect PPP2CA and SMAD7 expression, and inhibited EMT-like change in glioma cells. Furthermore, miR-130b mediated EMT-like change induced by MTDH, and MTDH inhibited the expression levels of PTEN, PPP2CA and SMAD7. Taken together, we reveal a novel mechanism that MTDH induces EMT-like change and invasion of glioma via the regulation of miR-130b-ceRNAs, providing the first direct link between MTDH and miRNAs in cancer cells.

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“…These results suggest a putative correlation between p300 and Twist1 in the modulation of urothelial cancer invasiveness [11]. Epigenetic activation of Twist1 was confirmed by histone acetyltransferase CBP, which cooperated with metadherin to increase Twist1 expression in breast cancer [12]. Next, in an attempt to investigate the underlying role of Twist1 in progression of human gastric cancer, Qian et al identified the interaction of p300 with Twist1 by co-immunoprecipitation.…”

Section: Acetylation Of Twistmentioning

confidence: 99%

Post-translational modifications of EMT transcriptional factors in cancer metastasis

2016

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Metastasis is an important reason for death of cancer patients which characterized as the formation of secondary cancers at distant sites. Epithelial– mesenchymal transition (EMT) is a dynamic process that appear to facilitate tumor metastasis in various cancers by switching epithelial cells into mesenchymal properties. Although previous investigation suggested a key role of EMT transcriptional factors in suppression of E-cadherin, the association of these factors with other cellular regulators in cancer metastasis need to be fully elucidated. Post-translational modifications (PTMs), such as acetylation and phosphorylation, have emerged as an important mechanism to modulate biological behavior of substrate proteins. In this review, we summarized protein modification and subsequent function changes of Snail, Twist and ZEB, as well as their influence on tumor progression. Acetylation of EMT transcriptional factors usually cause nuclear localization and/or protein stabilization thus contribute to E-cadherin repression. Besides, Twist and ZEB were phosphorylated by diverse kinases to promote metastasis in many cancers, while Snail was negatively regulated by phosphorylation to degradation. Then, the potential of therapy for metastasis by targeting PTMs-involved regulation of EMT transcriptional factors were discussed.

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Epigenetic Activation of TWIST1 by MTDH Promotes Cancer Stem–like Cell Traits in Breast Cancer

Cited by 78 publications

References 49 publications

Long noncoding RNASNHG1promotes non‐small cell lung cancer progression by up‐regulatingMTDH viasponging miR‐145–5p

Long noncoding RNASNHG1promotes non‐small cell lung cancer progression by up‐regulatingMTDH viasponging miR‐145–5p

MTDH promotes glioma invasion through regulating miR-130b-ceRNAs

Post-translational modifications of EMT transcriptional factors in cancer metastasis

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