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  1. 原著論文

Synergistic Autophagy Effect of miR-212-3p in Zoledronic Acid-Treated In Vitro and Orthotopic In Vivo Models and in Patient-Derived Osteosarcoma Cells

https://repo.qst.go.jp/records/78077
https://repo.qst.go.jp/records/78077
3680cc77-19c8-4fdc-8002-e6dc1ad89b31
Item type 学術雑誌論文 / Journal Article(1)
公開日 2019-12-19
タイトル
タイトル Synergistic Autophagy Effect of miR-212-3p in Zoledronic Acid-Treated In Vitro and Orthotopic In Vivo Models and in Patient-Derived Osteosarcoma Cells
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Yeon Oh, Ju

× Yeon Oh, Ju

WEKO 999199

Yeon Oh, Ju

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Ho Kim, Eun

× Ho Kim, Eun

WEKO 999200

Ho Kim, Eun

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Yeon-Joo, Lee

× Yeon-Joo, Lee

WEKO 999201

Yeon-Joo, Lee

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Sai, Sei

× Sai, Sei

WEKO 999202

Sai, Sei

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Ha Lim, Sun

× Ha Lim, Sun

WEKO 999203

Ha Lim, Sun

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Woo Park, Jang

× Woo Park, Jang

WEKO 999204

Woo Park, Jang

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Kyung Chung, Hye

× Kyung Chung, Hye

WEKO 999205

Kyung Chung, Hye

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Kim, Joon

× Kim, Joon

WEKO 999206

Kim, Joon

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Vares, Guillaume

× Vares, Guillaume

WEKO 999207

Vares, Guillaume

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Takahashi, Akihisa

× Takahashi, Akihisa

WEKO 999208

Takahashi, Akihisa

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Kyoung Jeong, Youn

× Kyoung Jeong, Youn

WEKO 999209

Kyoung Jeong, Youn

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Mi-Sook, Kim

× Mi-Sook, Kim

WEKO 999210

Mi-Sook, Kim

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Chang-Bae, Kong

× Chang-Bae, Kong

WEKO 999211

Chang-Bae, Kong

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Sei, Sai

× Sei, Sai

WEKO 999212

en Sei, Sai

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抄録
内容記述タイプ Abstract
内容記述 Osteosarcoma (OS) originates from osteoid bone tissues and is prone to metastasis, resulting in a high mortality rate. Although several treatments are available for OS, an effective cure does not exist for most patients with advanced OS. Zoledronic acid (ZOL) is a third-generation bisphosphonate that inhibits osteoclast-mediated bone resorption and has shown efficacy in treating bone metastases in patients with various types of solid tumors. Here, we sought to clarify the mechanisms through which ZOL inhibits OS cell proliferation. ZOL treatment inhibited OS cell proliferation, viability, and colony formation. Autophagy inhibition by RNA interference against Beclin-1 or ATG5 inhibited ZOL-induced OS cell death. ZOL induced autophagy by repressing the protein kinase B/mammalian target of rapamycin/p70S6 kinase pathway and extracellular signal-regulated kinase signaling-dependent autophagy in OS cell lines and patient-derived OS cells. Microarrays of miRNA showed that ZOL increased the levels of miR-212-3p, which is known to play an important role in autophagy, in OS in vitro and in vivo systems. Collectively, our data provided mechanistic insight into how increased miR-212-3p through ZOL treatment induces autophagy synergistically in OS cells, providing a preclinical rationale for conducting a broad-scale clinical evaluation of ZOL + miR-212-3p in treating OS.
書誌情報 Cancers

巻 11, 号 11, p. 1812, 発行日 2019-11
出版者
出版者 MDPI
ISSN
収録物識別子タイプ ISSN
収録物識別子 2072-6694
PubMed番号
識別子タイプ PMID
関連識別子 31752184
DOI
識別子タイプ DOI
関連識別子 10.3390/cancers11111812
関連サイト
識別子タイプ URI
関連識別子 https://www.mdpi.com/2072-6694/11/11/1812
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