The long non-coding RNA ET-20 mediates EMT by impairing desmosomes in breast cancer cells

Saxena, Mohit; Hisano, Mizue; Neutzner, Melanie; Diepenbruck, Maren; Ivánek, Robert; Sharma, Kirti; Kalathur, Ravi Kiran Reddy; Bürglin, Thomas R.; Risoli, Salvatore

doi:10.1242/jcs.258418

Cited by 9 publications

(9 citation statements)

References 80 publications

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“…This process thus results in the impairment of intercellular junctions and enhancement of EMT. [158]. In conclusion, the regulatory activities of miRNAs and lncRNAs as post-transcriptional regulators form a complex regulatory network that controls EMT.…”

Section: Noncoding Rna-mediated Regulationmentioning

confidence: 95%

The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis

2022

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Epithelial–mesenchymal transition (EMT) is an essential process in normal embryonic development and tissue regeneration. However, aberrant reactivation of EMT is associated with malignant properties of tumor cells during cancer progression and metastasis, including promoted migration and invasiveness, increased tumor stemness, and enhanced resistance to chemotherapy and immunotherapy. EMT is tightly regulated by a complex network which is orchestrated with several intrinsic and extrinsic factors, including multiple transcription factors, post-translational control, epigenetic modifications, and noncoding RNA-mediated regulation. In this review, we described the molecular mechanisms, signaling pathways, and the stages of tumorigenesis involved in the EMT process and discussed the dynamic non-binary process of EMT and its role in tumor metastasis. Finally, we summarized the challenges of chemotherapy and immunotherapy in EMT and proposed strategies for tumor therapy targeting EMT.

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Section: Noncoding Rna-mediated Regulationmentioning

confidence: 95%

The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis

2022

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“…154 For example, impaired desmosomes were shown to promote EMT and consequent tumor progression in invasive breast cancer. 155 Besides, loss of desmosomes was observed in invasive pancreatic neuroendocrine tumors (PNET), and genetic deletion of desmoplakin enhanced tumor metastasis in the PNET mouse model. 156 Interestingly, the proper functions of desmosomes require particular posttranslational modifications on several components.…”

Section: Altered Junctional Componentsmentioning

confidence: 99%

“…As tumor suppressors, downregulation of desmosomal components plays vital roles in EMT program and consequent cancer progression 154 . For example, impaired desmosomes were shown to promote EMT and consequent tumor progression in invasive breast cancer 155 . Besides, loss of desmosomes was observed in invasive pancreatic neuroendocrine tumors (PNET), and genetic deletion of desmoplakin enhanced tumor metastasis in the PNET mouse model 156 .…”

Section: Reorganization Of Cell Junctions and Cytoskeleton: Key Chara...mentioning

confidence: 99%

Epithelial–mesenchymal transition: The history, regulatory mechanism, and cancer therapeutic opportunities

Huang

Zhang

Zhou

et al. 2022

MedComm

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Epithelial–mesenchymal transition (EMT) is a program wherein epithelial cells lose their junctions and polarity while acquiring mesenchymal properties and invasive ability. Originally defined as an embryogenesis event, EMT has been recognized as a crucial process in tumor progression. During EMT, cell–cell junctions and cell–matrix attachments are disrupted, and the cytoskeleton is remodeled to enhance mobility of cells. This transition of phenotype is largely driven by a group of key transcription factors, typically Snail, Twist, and ZEB, through epigenetic repression of epithelial markers, transcriptional activation of matrix metalloproteinases, and reorganization of cytoskeleton. Mechanistically, EMT is orchestrated by multiple pathways, especially those involved in embryogenesis such as TGFβ, Wnt, Hedgehog, and Hippo, suggesting EMT as an intrinsic link between embryonic development and cancer progression. In addition, redox signaling has also emerged as critical EMT modulator. EMT confers cancer cells with increased metastatic potential and drug resistant capacity, which accounts for tumor recurrence in most clinic cases. Thus, targeting EMT can be a therapeutic option providing a chance of cure for cancer patients. Here, we introduce a brief history of EMT and summarize recent advances in understanding EMT mechanisms, as well as highlighting the therapeutic opportunities by targeting EMT in cancer treatment.

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“…The vast majority of cancer-related deaths, such as hepatocellular carcinoma and breast cancer (Saxena et al, 2021;Gao et al, 2022), are due to metastatic spread of cancer cells, a process aided by epithelial-mesenchymal transition (EMT) (Atay, 2020;Kitz et al, 2021). EMT refers to the biological process in which epithelial cells are transformed into cells with a mesenchymal phenotype through specific programs (Zhang et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic and immunologic implications of the epithelial–mesenchymal transition model reveal a novel role of SFTA2 in prognosis of non-small-cell lung carcinoma

Zhai

Chen

et al. 2022

Front. Genet.

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Non-small-cell lung cancer (NSCLC) is the second most common cancer worldwide, and most deaths are associated with epithelial–mesenchymal transition (EMT). Therefore, this study aimed to explore the role of EMT-related transcriptomic profiles in NSCLC and the effect of EMT-based signatures on clinical diagnosis, prognosis, and treatment responses for patients with NSCLC. After integrating the transcriptomics and clinicopathological data, we first constructed EMT clusters (C1 and C2) using machine learning algorithms, found the significant relationship between EMT clusters and survival outcomes, and then explored the impact of EMT clusters on the tumor heterogeneity, drug efficiency, and immune microenvironment of NSCLC. Prominently, differential-enriched tumor-infiltrated lymphocytes were found between EMT clusters, especially the macrophages and monocyte. Next, we identified the most significantly down-regulated gene SFTA2 in the EMT clusters C2 with poor prognosis. Using RT-qPCR and RNA-seq data from the public database, we found prominently elevated SFTA2 expression in NSCLC tissues compared with normal lung tissues, and the tumor suppressor role of SFTA2 in 82 Chinese patients with NSCLC. After Cox regression and survival analysis, we demonstrated that higher SFTA2 expression in tumor samples significantly predicts favorable prognosis of NSCLC based on multiple independent cohorts. In addition, the prognostic value of SFTA2 expression differs for patients with lung adenocarcinoma and squamous cell carcinoma. In conclusion, this study demonstrated that the EMT process is involved in the malignant progression and the constructed EMT clusters exerted significant predictive drug resistance and prognostic value for NSCLC patients. In addition, we first identified the high tumoral expression of SFTA2 correlated with better prognosis and could serve as a predictive biomarker for outcomes and treatment response of NSCLC patients.

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The long non-coding RNA ET-20 mediates EMT by impairing desmosomes in breast cancer cells

Cited by 9 publications

References 80 publications

The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis

The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis

Epithelial–mesenchymal transition: The history, regulatory mechanism, and cancer therapeutic opportunities

Transcriptomic and immunologic implications of the epithelial–mesenchymal transition model reveal a novel role of SFTA2 in prognosis of non-small-cell lung carcinoma

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