Downregulation of miR-22 Contributes to Epithelial-Mesenchymal Transition in Osteosarcoma by Targeting Twist1

Zhu, Shutao; Wang, Xiao; Wang, Junyi; Xi, Guanghui; Liu, Yang

doi:10.3389/fonc.2020.00406

Cited by 13 publications

(9 citation statements)

References 39 publications

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“…EMT is a crucial process that participated in the metastasis of OS. 27,29 And in the present study, we found that EMT markers E-cadherin and N-cadherin were associated with the expression of CASC15/miR-338-3p/RAB14 axis, indicating that CASC15/miR-338-3p/RAB14 axis can regulate the invasion and metastasis of OS via EMT.…”

Section: Dovepresssupporting

confidence: 62%

<p>LncRNA CASC15 is Upregulated in Osteosarcoma Plasma Exosomes and CASC15 Knockdown Inhibits Osteosarcoma Progression by Regulating miR-338-3p/RAB14 Axis</p>

Zhang

Wang

Ren

et al. 2020

OTT

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Background: Currently, plenty of studies have demonstrated that lncRNAs can act as crucial roles during the progression of various tumors, including osteosarcoma (OS), and emerging evidences indicated that lncRNAs are abundant and stable in exosomes. The objective of this study is to reveal the dysregulated lncRNAs in OS plasma exosomes and explore their functions in OS. Materials and Methods: Microarray was performed to analyze dysregulated exosomal lncRNAs. Western blot, qRT-PCR assays, and Dual-luciferase reporter assay were used to verify the interaction among cancer susceptibility 15 (CASC15), miR-338-3p, and RAB14. Cck-8, colony formation assay, and transwell assay were performed to explore and characterize the effects of CASC15 on OS cells. Animal experiments were used to verify the effects of CASC15 in vivo. Results: Upregulated CASC15 was observed in OS plasma exosomes compared with control, and the same expression was observed in the OS tissues and cell lines. Further assays indicated that CASC15 knockdown could restrain the proliferation, migration, and invasion of OS cells, and inhibit the growth of OS in xenograft models. Furthermore, our results demonstrated CASC15 regulated OS progression via acting as miR-338-3p sponge, and RAB14 was a direct downstream target of miR-338-3p. Rescue experiments verified CASC15 promotes OS cell growth and metastasis by upregulating RAB14 expression. Conclusion: Overall, our findings indicate that CASC15 plays a key role in OS progression by targeting the miR-338-3p/RAB14 axis and can serve as a possible therapeutic target for OS patients.

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Section: Dovepresssupporting

confidence: 62%

<p>LncRNA CASC15 is Upregulated in Osteosarcoma Plasma Exosomes and CASC15 Knockdown Inhibits Osteosarcoma Progression by Regulating miR-338-3p/RAB14 Axis</p>

Zhang

Wang

Ren

et al. 2020

OTT

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“…Various long non-coding RNAs and miRNAs have been shown to regulate the EMT and, thus, affect the metastatic behavior of tumor cells [ 74 ]. Especially, these RNAs modulate the expression of transcription factors, such as zinc finger E-box binding homeobox 1 (ZEB1) [ 77 , 78 , 79 ], Twist1 [ 80 ], or signal transducer and activator of transcription 3 (STAT3) [ 81 ] and signaling pathways, including the Wnt/β-catenin and NOTCH pathways [ 82 , 83 ].…”

Section: Mechanisms Of Metastasis Formationmentioning

confidence: 99%

Metastatic Progression of Osteosarcomas: A Review of Current Knowledge of Environmental versus Oncogenic Drivers

Odri

Tchicaya-Bouanga

Yoon

et al. 2022

Cancers

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Metastases of osteosarcomas are heterogeneous. They may grow simultaneously with the primary tumor, during treatment or shortly after, or a long time after the end of the treatment. They occur mainly in lungs but also in bone and various soft tissues. They can have the same histology as the primary tumor or show a shift towards a different differentiation path. However, the metastatic capacities of osteosarcoma cells can be predicted by gene and microRNA signatures. Despite the identification of numerous metastasis-promoting/predicting factors, there is no efficient therapeutic strategy to reduce the number of patients developing a metastatic disease or to cure these metastatic patients, except surgery. Indeed, these patients are generally resistant to the classical chemo- and to immuno-therapy. Hence, the knowledge of specific mechanisms should be extended to reveal novel therapeutic approaches. Recent studies that used DNA and RNA sequencing technologies highlighted complex relations between primary and secondary tumors. The reported results also supported a hierarchical organization of the tumor cell clones, suggesting that cancer stem cells are involved. Because of their chemoresistance, their plasticity, and their ability to modulate the immune environment, the osteosarcoma stem cells could be important players in the metastatic process.

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“…Plasma levels of miR-22 were also found to be an independent diagnostic and prognostic biomarker in osteosarcoma (Diao et al, 2020). Moreover, at the cellular level, miR-22 overexpression impaired proliferation and EMT in osteosarcoma by targeting Twist1 (Zhu et al, 2020). These studies suggest that EMT and distant metastasis are tightly regulated in osteosarcoma.…”

Section: Discussionmentioning

confidence: 79%

A Novel Six Metastasis-Related Prognostic Gene Signature for Patients With Osteosarcoma

Zheng

Xia

et al. 2021

Front. Cell Dev. Biol.

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Osteosarcoma is the most common malignant bone tumor, and although there has been significant progress in its management, metastases often herald incurable disease. Here we defined genes differentially expressed between primary and metastatic osteosarcoma as metastasis-related genes (MRGs) and used them to construct a novel six-MRG prognostic signature for overall survival of patients with osteosarcoma. Validation in internal and external datasets confirmed satisfactory accuracy and generalizability of the prognostic model, and a nomogram based on the signature and clinical variables was constructed to aid clinical decision-making. Of the six MRGs, FHIT is a well-documented tumor suppressor gene that is poorly defined in osteosarcoma. Consistent with tumor suppressor function, FHIT was downregulated in osteosarcoma cells and human osteosarcoma samples. FHIT overexpression inhibited osteosarcoma proliferation, migration, and invasion both in vitro and in vivo. Mechanistically, FHIT overexpression upregulate the epithelial marker E-cadherin while repressing the mesenchymal markers N-cadherin and vimentin. Our six-MRG signature represents a novel and clinically useful prognostic biomarker for patients with osteosarcoma, and FHIT might represent a therapeutic target by reversing epithelial to mesenchymal transition.

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Downregulation of miR-22 Contributes to Epithelial-Mesenchymal Transition in Osteosarcoma by Targeting Twist1

Cited by 13 publications

References 39 publications

<p>LncRNA CASC15 is Upregulated in Osteosarcoma Plasma Exosomes and CASC15 Knockdown Inhibits Osteosarcoma Progression by Regulating miR-338-3p/RAB14 Axis</p>

<p>LncRNA CASC15 is Upregulated in Osteosarcoma Plasma Exosomes and CASC15 Knockdown Inhibits Osteosarcoma Progression by Regulating miR-338-3p/RAB14 Axis</p>

Metastatic Progression of Osteosarcomas: A Review of Current Knowledge of Environmental versus Oncogenic Drivers

A Novel Six Metastasis-Related Prognostic Gene Signature for Patients With Osteosarcoma

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