Evidence map›Paper›PMID 36371387›Full record

ArticleCell death & disease2022

ADCK1 is a potential therapeutic target of osteosarcoma.

Bao-Biao Zhuo, Lun-Qing Zhu, Chen Yao, Xi-Hua Wang, Shi-Xian Li, Rong Wang, Yuan Li, Zhuo-Yan Ling

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Therapeutic impacts of GNE‑477‑loaded HInternational journal of molecular medicine · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Bao-Biao Zhuo *Department of Pediatric Surgery, Affiliated Hospital of Xuzhou Medical University, Department of orthopedics, Xuzhou Children's Hospital, Xuzhou, China.
Lun-Qing Zhu *Department of Orthopaedics, Children's Hospital of Soochow University, Suzhou, China.
Chen Yao *Department of Orthopedics, Affiliated Hospital of Nanjing University of TCM, Jiangsu Province Hospital of TCM, Nanjing, China.
Xi-Hua WangXuzhou Medical University, Xuzhou, China.
Shi-Xian LiDepartment of Pediatric Surgery, Affiliated Hospital of Xuzhou Medical University, Department of orthopedics, Xuzhou Children's Hospital, Xuzhou, China.
Rong WangDepartment of Ultrasound, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China. drwangr81@163.com.ORCID 0000-0002-3563-9301
Yuan LiDepartment of Pediatric Surgery, Affiliated Hospital of Xuzhou Medical University, Department of orthopedics, Xuzhou Children's Hospital, Xuzhou, China. 872052383@qq.com.ORCID 0000-0001-6818-596X
Zhuo-Yan LingDepartment of Orthopedics, the Second Affiliated Hospital of Soochow University, Suzhou, China. lingzhuoyan@suda.edu.cn.ORCID 0000-0002-2709-1833
Xuzhou Medical College · CNSoochow University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We here showed that ADCK1 (AarF domain-containing kinase 1), a mitochondrial protein, is upregulated in human osteosarcoma (OS) tissues and OS cells. In primary and established OS cells, ADCK1 shRNA or CRISPR/Cas9-induced ADCK1 knockout (KO) remarkably inhibited cell viability, proliferation and migration, and provoked apoptosis activation. Conversely, ectopic ADCK1 overexpression exerted pro-cancerous activity by promoting OS cell proliferation and migration. ADCK1 depletion disrupted mitochondrial functions in OS cells and induced mitochondrial membrane potential reduction, ATP depletion, reactive oxygen species production. Significantly, ADCK1 silencing augmented doxorubicin-induced apoptosis in primary OS cells. mTOR activation is important for ADCK1 expression in OS cells. The mTOR inhibitors, rapamycin and AZD2014, as well as mTOR shRNA, potently decreased ADCK1 expression in primary OS cells. In nude mice, the growth of subcutaneous pOS-1 xenografts was largely inhibited when bearing ADCK1 shRNA or ADCK1 KO construct. Moreover, ADCK1 KO largely inhibited pOS-1 xenograft in situ growth in proximal tibia of nude mice. ADCK1 depletion, apoptosis activation and ATP reduction were detected in pOS-1 xenografts bearing ADCK1 shRNA or ADCK1 KO construct. Together, the mitochondrial protein ADCK1 is required for OS cell growth and is a novel therapeutic target of OS.

Indexed as

Bone NeoplasmsOsteosarcomaAdenosine TriphosphateAnimalsApoptosisCell Line, TumorCell ProliferationHumansMiceMice, NudeMitochondrial ProteinsRNA, Small InterferingTOR Serine-Threonine KinasesAdenosine TriphosphateMitochondrial ProteinsRNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID36371387
PMCPMC9653483
OpenAlexW4309046914

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.