EZH2-mediated α-actin methylation needs lncRNA TUG1, and promotes the cortex cytoskeleton formation in VSMCs

Chen, Rong; Kong, Pengfei; Zhang, Fan; Shu, Ya-Nan; Nie, Xi; Dong, Lihua; Lin, Yan-Ling; Xie, Xing; Zhao, Lili; Zhang, Xiangjian; Han, Mei

doi:10.1016/j.gene.2017.03.028

Cited by 32 publications

(23 citation statements)

References 21 publications

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“…In addition, lncRNAs and DNA methylation already interact with each other during the process of epigenetic regulation, which can be achieved via direct physical connection between lncRNAs and DNA methyltransferases . For instance, downregulation of lncRNA TUG1 was observed to inhibit the EZH2‐mediated methylation of α‐actin . In addition, diminished expressions of lncRNA H19 reduced cellular DNA methylation levels through the aid of DNMT1 .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA ADAMTS9‐AS2 suppresses the progression of esophageal cancer by mediating CDH3 promoter methylation

Yang

Zhu

et al. 2019

Molecular Carcinogenesis

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Long noncoding RNAs (lncRNAs) have been implicated in the biology of esophageal cancer via mRNA degradation or translational inhibition. CDH3 is also aberrantly expressed in numerous cancers. This study was conducted with the hypothesis that ADAMTS9-AS2 or CDH3 methylation plays a role in esophageal cancer cell activity and in vivo development. Firstly, mRNA levels of ADAMTS9-AS2 and CDH3 in esophageal cancer tissues and cells were detected by reverse-transcription quantitative polymerase chain reaction. Afterward, esophageal cancer OE21 cells were treated with overexpression of ADAMTS9-AS2, siRNA against ADAMTS9-AS2, overexpression of CDH3 and demethylating agent 5-aza-dc. The biological functions of esophageal cancer OE21 cells were assayed to define the regulatory mechanisms of ADAMTS9-AS2 in esophageal cancer. The interactions among ADAMTS9-AS2, DNMT1/DNMT3 (A/B) and CDH3 were detected by MSP, RNA pull-down, RIP, and ChIP assays. The in vitro findings were reproduced in nude mice to explore the role of ADAMTS9-AS2 in the development of esophageal cancer in vivo. Esophageal cancers expressed low levels of ADAMTS9-AS2 and high levels of CDH3. Methylation of CDH3 promoter was induced by ADAMTS9-AS2 via DNMT1/DNMT3 (A/B). Furthermore, proliferation, invasion, and migration of esophageal cancer cells were inhibited by ADAMTS9-AS2 via downregulation of CDH3. Suppressed esophageal cancer development in vivo was also detected after ADAMTS9-AS2 overexpression. Overexpressed ADAMTS9-AS2 aids in the suppression of esophageal cancer development, which is achieved via inducing CDH3 promoter methylation. K E Y W O R D S ADAMTS9-AS2, CDH3, esophageal cancer, invasion, methylation, migration, proliferation

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA ADAMTS9‐AS2 suppresses the progression of esophageal cancer by mediating CDH3 promoter methylation

Yang

Zhu

et al. 2019

Molecular Carcinogenesis

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“…It is still unclear how EZH2 contributes to cDDP‐induced CTR1 degradation and whether the ribosome‐related genes influenced by EZH2 play a role in acquired cDDP resistance. Although it is well recognized that EZH2 mainly located in the nuclei, several lines of evidence show that cytoplasmic EZH2 retains its methyl transfer activity and is involved in cellular skeleton movement, ubiquitin‐mediated protein degradation, cytoskeleton formation, cell adhesion, and migration . We examined the EZH2 location using immunofluorescence in several cell lines, including cDDP‐sensitive/resistant cell lines and those with EZH2 depletion.…”

Section: Discussionmentioning

confidence: 99%

“…Although it is well recognized that EZH2 mainly located in the nuclei, several lines of evidence show that cytoplasmic EZH2 retains its methyl transfer activity and is involved in cellular skeleton movement, ubiquitinmediated protein degradation, cytoskeleton formation, cell adhesion, and migration. [42][43][44] We examined the EZH2 location using immunofluorescence in several cell lines, including cDDP-sensitive/ resistant cell lines and those with EZH2 depletion. We observed both nuclear and cytoplasmic EZH2 expression while EZH2 mainly remained in the nuclei.…”

Section: Discussionmentioning

confidence: 99%

Enhancer of zeste homolog 2 promotes cisplatin resistance by reducing cellular platinum accumulation

et al. 2018

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Enhancer of zeste homolog 2 (EZH2), which is overexpressed in a wide range of tumors, contributes to ovarian cancer malignancy in several different ways. We aimed to illustrate the role of EZH2 in ovarian cancer cisplatin resistance and to identify possible underlying mechanisms of this role that may provide a rationale for targeting EZH2 in cancer treatment. Here, we present data indicating that EZH2 overexpression is associated with cisplatin resistance and intracellular platinum drug accumulation. Measurements of EZH2 in 84 ovarian cancer patients suggested that patients with high EZH2 levels tend to have poor responses to cisplatin. The EZH2 level progressively increased in cells receiving repeated cisplatin exposure. Downregulation of EZH2 not only sensitized cellular reactions to cisplatin and increased cellular platinum accumulation when cells were exposed to both cisplatin and BODIPY‐Pt (a fluorescent cisplatin complex) but also protected copper transporter 1, a high‐affinity copper transporter closely related to cisplatin resistance, from cisplatin‐induced proteasomal degradation. Overall, these findings identify a new mechanism that expands the unrecognized role of EZH2 in ovarian cancer cisplatin resistance.

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“…lncRNAs can affect the migration of tumor cells by regulating the cytoskeleton or related proteins [ 50 – 52 ]. The most direct evidence comes from the function of a lncRNA called “downregulated in hepatocellular carcinoma” (Dreh).…”

Section: Lncrnas Regulate the Cytoskeleton In Cancermentioning

confidence: 99%

LncRNAs regulate the cytoskeleton and related Rho/ROCK signaling in cancer metastasis

et al. 2018

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Some of the key steps in cancer metastasis are the migration and invasion of tumor cells; these processes require rearrangement of the cytoskeleton. Actin filaments, microtubules, and intermediate filaments involved in the formation of cytoskeletal structures, such as stress fibers and pseudopodia, promote the invasion and metastasis of tumor cells. Therefore, it is important to explore the mechanisms underlying cytoskeletal regulation. The ras homolog family (Rho) and Rho-associated coiled-coil containing protein serine/threonine kinase (ROCK) signaling pathway is involved in the regulation of the cytoskeleton. Moreover, long noncoding RNAs (lncRNAs) have essential roles in tumor migration and guide gene regulation during cancer progression. LncRNAs can regulate the cytoskeleton directly or may influence the cytoskeleton via Rho/ROCK signaling during tumor migration. In this review, we focus on the regulatory association between lncRNAs and the cytoskeleton and discuss the pathways and mechanisms involved in the regulation of cancer metastasis.

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EZH2-mediated α-actin methylation needs lncRNA TUG1, and promotes the cortex cytoskeleton formation in VSMCs

Cited by 32 publications

References 21 publications

Long noncoding RNA ADAMTS9‐AS2 suppresses the progression of esophageal cancer by mediating CDH3 promoter methylation

Long noncoding RNA ADAMTS9‐AS2 suppresses the progression of esophageal cancer by mediating CDH3 promoter methylation

Enhancer of zeste homolog 2 promotes cisplatin resistance by reducing cellular platinum accumulation

LncRNAs regulate the cytoskeleton and related Rho/ROCK signaling in cancer metastasis

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