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Cited by 175

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

microRNA-143, down-regulated in osteosarcoma, promotes apoptosis and suppresses tumorigenicity by targeting Bcl-2

Open access
Ji·2010·Oncology Reports

Abstract

Deregulated microRNAs and their roles in tumorigenesis are still largely unknown. Here, we focused on the roles of miR-143 in osteosarcoma, as previous reports have suggested its importance in some other types of cancer. We found that miR-143 was down-regulated in osteosarcoma cell lines and primary tumor samples, and the restoration of miR-143 reduced cell viability, promoted cell apoptosis and suppressed tumorigenicity. Additionally, Bcl-2, an important antiapoptotic molecule, was identified to be a novel direct target of miR-143, and the proapoptotic function of miR-143 is further suggested to be mainly through the targeting of Bcl-2 expression. Collectively, our data identify the important roles of miR-143 in osteosarcoma pathogenesis and indicate its potential application in cancer therapy.

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Crossref · 10.3892/or_00000994

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Metadata

Authors
Ji
Venue
Oncology Reports
Published
2010-09-27
Volume
24
Issue
5
Pages
1363-9
ISSN
  • 1021-335X (ISSN-L)
  • 1791-2431
OpenAlex
W2134167837
Cited by
175
References
1
FWCI
4.52
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: microRNA-143, down-regulated in osteosarcoma, promotes apoptosis and suppresses tumorigenicity by targeting Bcl-2. https://app.cochat.ai/papers/10.3892/or_00000994
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Ji. (2010). microRNA-143, down-regulated in osteosarcoma, promotes apoptosis and suppresses tumorigenicity by targeting Bcl-2. Oncology Reports. https://doi.org/10.3892/or_00000994

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.