Targeting deubiquitinating enzyme USP26 by microRNA-203 regulates Snail1’s pro-metastatic functions in esophageal cancer

Li, Gang; Qi, Hong-wei; Dong, He-gui; Bai, Ping; Sun, Mei; Liu, Haiyan

doi:10.1186/s12935-020-01441-2

Cited by 10 publications

(10 citation statements)

References 39 publications

(57 reference statements)

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“…In this case, using RT-qPCR, we studied the expression of the EMT-TFs Snail and Slug, seeing they were increased in glioblastoma. This overexpression has also been detected in other tumor types, such as breast [28], thyroid [29], esophagus [30], and colon [31] cancer, among others. At the protein level, we were able to confirm again the overexpression of the mesenchymal marker N-cadherin in glioblastoma.…”

Section: Expression Of Hdac6 and Mesenchymal And Autophagic Markers In Glioblastoma Samples And Cell Linesmentioning

confidence: 70%

Silencing of Histone Deacetylase 6 Decreases Cellular Malignancy and Contributes to Primary Cilium Restoration, Epithelial-to-Mesenchymal Transition Reversion, and Autophagy Inhibition in Glioblastoma Cell Lines

Urdiciain

Erausquin

Zelaya

et al. 2021

Biology

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Glioblastoma multiforme, the most common type of malignant brain tumor as well as the most aggressive one, lacks an effective therapy. Glioblastoma presents overexpression of mesenchymal markers Snail, Slug, and N-Cadherin and of the autophagic marker p62. Glioblastoma cell lines also present increased autophagy, overexpression of mesenchymal markers, Shh pathway activation, and lack of primary cilia. In this study, we aimed to evaluate the role of HDAC6 in the pathogenesis of glioblastoma, as HDAC6 is the most overexpressed of all HDACs isoforms in this tumor. We treated glioblastoma cell lines with siHDAC6. HDAC6 silencing inhibited proliferation, migration, and clonogenicity of glioblastoma cell lines. They also reversed the mesenchymal phenotype, decreased autophagy, inhibited Shh pathway, and recovered the expression of primary cilia in glioblastoma cell lines. These results demonstrate that HDAC6 might be a good target for glioblastoma treatment.

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Section: Expression Of Hdac6 and Mesenchymal And Autophagic Markers In Glioblastoma Samples And Cell Linesmentioning

confidence: 70%

Silencing of Histone Deacetylase 6 Decreases Cellular Malignancy and Contributes to Primary Cilium Restoration, Epithelial-to-Mesenchymal Transition Reversion, and Autophagy Inhibition in Glioblastoma Cell Lines

Urdiciain

Erausquin

Zelaya

et al. 2021

Biology

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“…. miR-203-5p was significantly down-regulated in esophageal tumor tissue (173). Overexpression of miR-203a-5p inhibited invasion and migration of KYSE150 and TE-1 ESCCs (173).…”

Section: Mir-203a-5p [Targeting Ubiquitin-specific Peptidase 26 (Usp26)]mentioning

confidence: 96%

“…miR-203-5p was significantly down-regulated in esophageal tumor tissue (173). Overexpression of miR-203a-5p inhibited invasion and migration of KYSE150 and TE-1 ESCCs (173). Nude mice injected with a miR-203-5p mimic showed reduced lung metastasis of KYSE150 cells after tail vein injection (173).…”

Section: Mir-203a-5p [Targeting Ubiquitin-specific Peptidase 26 (Usp26)]mentioning

confidence: 99%

MicroRNAs and Corresponding Targets in Esophageal Cancer as ShownIn VitroandIn Vivoin Preclinical Models

Weidle

Nopora

2022

Cancer Genomics Proteomics

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Squamous cell carcinoma of the esophagus is associated with a dismal prognosis. Therefore, identification of new targets and implementation of new treatment modalities are issues of paramount importance. Based on a survey of the literature, we identified microRNAs conferring antitumoral activity in preclinical in vivo experiments. In the category of miRs targeting secreted factors and transmembrane receptors, four miRs were up-regulated and 10 were down-regulated compared with five out of nine in the category transcription factors, and six miRs were down-regulated in the category enzymes, including metabolic enzymes. The down-regulated miRs have targets which can be inhibited by small molecules or antibody-related entities, or re-expressed by reconstitution therapy. Up-regulated miRs have targets which can be reconstituted with small molecules or inhibited with antagomirs.

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“…In this study, miRNA-203 was found to be expressed at lower levels in CML patients’ bone marrow, while miRNA-203 upregulation in combination with imatinib could promote apoptosis in CML cells [ 145 ]. This miRNA targets the de-ubiquitinating enzyme USP26, which is responsible for preventing the proteolytic degradation of onco-proteins [ 146 ]. Contrarily, oncogenic miRNA-486 promotes imatinib resistance in CML cells by targeting PTEN and FOXO1 tumor suppressors [ 147 ].…”

Section: Mirna and Alternative Splicing-induced Drug Resistancementioning

confidence: 99%

MicroRNA and Alternative mRNA Splicing Events in Cancer Drug Response/Resistance: Potent Therapeutic Targets

et al. 2021

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Cancer is a multifaceted disease that involves several molecular mechanisms including changes in gene expression. Two important processes altered in cancer that lead to changes in gene expression include altered microRNA (miRNA) expression and aberrant splicing events. MiRNAs are short non-coding RNAs that play a central role in regulating RNA silencing and gene expression. Alternative splicing increases the diversity of the proteome by producing several different spliced mRNAs from a single gene for translation. MiRNA expression and alternative splicing events are rigorously regulated processes. Dysregulation of miRNA and splicing events promote carcinogenesis and drug resistance in cancers including breast, cervical, prostate, colorectal, ovarian and leukemia. Alternative splicing may change the target mRNA 3′UTR binding site. This alteration can affect the produced protein and may ultimately affect the drug affinity of target proteins, eventually leading to drug resistance. Drug resistance can be caused by intrinsic and extrinsic factors. The interplay between miRNA and alternative splicing is largely due to splicing resulting in altered 3′UTR targeted binding of miRNAs. This can result in the altered targeting of these isoforms and altered drug targets and drug resistance. Furthermore, the increasing prevalence of cancer drug resistance poses a substantial challenge in the management of the disease. Henceforth, molecular alterations have become highly attractive drug targets to reverse the aberrant effects of miRNAs and splicing events that promote malignancy and drug resistance. While the miRNA–mRNA splicing interplay in cancer drug resistance remains largely to be elucidated, this review focuses on miRNA and alternative mRNA splicing (AS) events in breast, cervical, prostate, colorectal and ovarian cancer, as well as leukemia, and the role these events play in drug resistance. MiRNA induced cancer drug resistance; alternative mRNA splicing (AS) in cancer drug resistance; the interplay between AS and miRNA in chemoresistance will be discussed. Despite this great potential, the interplay between aberrant splicing events and miRNA is understudied but holds great potential in deciphering miRNA-mediated drug resistance.

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Targeting deubiquitinating enzyme USP26 by microRNA-203 regulates Snail1’s pro-metastatic functions in esophageal cancer

Cited by 10 publications

References 39 publications

Silencing of Histone Deacetylase 6 Decreases Cellular Malignancy and Contributes to Primary Cilium Restoration, Epithelial-to-Mesenchymal Transition Reversion, and Autophagy Inhibition in Glioblastoma Cell Lines

Silencing of Histone Deacetylase 6 Decreases Cellular Malignancy and Contributes to Primary Cilium Restoration, Epithelial-to-Mesenchymal Transition Reversion, and Autophagy Inhibition in Glioblastoma Cell Lines

MicroRNAs and Corresponding Targets in Esophageal Cancer as ShownIn VitroandIn Vivoin Preclinical Models

MicroRNA and Alternative mRNA Splicing Events in Cancer Drug Response/Resistance: Potent Therapeutic Targets

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