Evidence map›Paper›PMID 31752184›Full record

ArticleCancers2019

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

Ju Yeon Oh, Eun Ho Kim, Yeon-Joo Lee, Sei Sai, Sun Ha Lim, Jang Woo Park, Hye Kyung Chung, Joon Kim, Guillaume Vares, Akihisa Takahashi and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Zoledronic acid induces ferroptosis by upregulating POR in osteosarcoma.Medical oncology (Northwood, London, England) · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 2 countries.

Ju Yeon OhLaboratory of Biochemistry, School of Life Sciences and Biotechnology, Korea University, Seongbuk-gu, Seoul 136-701, Korea.
Eun Ho KimDepartment of Biochemistry, School of Medicine, Daegu Catholic University, Nam-gu, Daegu 42472, Korea.
Yeon-Joo LeeDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Korea.ORCID 0000-0002-6605-8761
Sei SaiDepartment of Basic Medical Sciences for Radiation Damages, National Institute of Radiological Sciences, Chiba 263-8555, Japan.
Sun Ha LimDepartment of Biochemistry, School of Medicine, Daegu Catholic University, Nam-gu, Daegu 42472, Korea.
Jang Woo ParkKorea Drug Development Platform using Radio-isotope, Korea Institute of Radiological & Medical Sciences, Seoul 139-706, Korea.
Hye Kyung ChungKorea Drug Development Platform using Radio-isotope, Korea Institute of Radiological & Medical Sciences, Seoul 139-706, Korea.
Joon KimLaboratory of Biochemistry, School of Life Sciences and Biotechnology, Korea University, Seongbuk-gu, Seoul 136-701, Korea.
Guillaume VaresCell Signal Unit, Okinawa Institute of Science and Technology Graduate University (OIST), Okinawa 1919-1, Japan.ORCID 0000-0002-6191-9032
Akihisa TakahashiGunma University Heavy Ion Medical Center, Maebashi 371-8511, Gunma, Japan.ORCID 0000-0002-9960-2153
Youn Kyoung JeongResearch Center for Radiotherapy, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea.
Mi-Sook KimDepartment of Radiation Oncology, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea.
Chang-Bae KongDepartment of Orthopaedic Surgery, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea.
Korea Institute of Radiological and Medical Sciences · KRDaegu Catholic University · KRKorea University · KRGunma University Hospital · JPOkinawa Institute of Science and Technology Graduate University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

autophagymiR-212osteosarcomazoledronic acid

Identifiers

PMID31752184
PMCPMC6895802
OpenAlexW2987117152

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.