Evidence map›Paper›PMID 34913077›Full record

ArticleMolecular medicine reports2022

AIM2 inhibits the proliferation, invasion and migration, and promotes the apoptosis of osteosarcoma cells by inactivating the PI3K/AKT/mTOR signaling pathway.

Jianping Zheng, Changhao Liu, Jiandang Shi, Kun Wen, Xiangxin Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-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

27 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Endometriosis and the Hallmarks of Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2026
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  14. Article
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  17. The role of AIM2 in inflammation and tumors.Frontiers in immunology · 2024
    Review
  18. Article
  19. Review
  20. Review
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

5 authors at 4 institutions in 1 country.

Jianping Zheng *Department of Orthopedic Traumatology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region 750004, P.R. China.
Changhao Liu *Department of Orthopedics, Zhangye People's Hospital Affiliated to Hexi University, Zhangye, Gansu 734000, P.R. China.
Jiandang ShiDepartment of Spine Surgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region 750004, P.R. China.
Kun WenDepartment of Orthopedics, Ningxia Gemflower Hospital, Yinchuan, Ningxia Hui Autonomous Region 750006, P.R. China.
Xiangxin WangNingxia Medical University, Yinchuan, Ningxia Hui Autonomous Region 750001, P.R. China.
Ningxia Medical University General Hospital · CNHexi University · CNNingxia Hui Autonomous Region Peoples Hospital · CNNingxia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma is a primary bone tumor that mainly occurs in children and adolescents. Absent in melanoma 2 (AIM2) has been demonstrated to be involved in regulating the occurrence and development of cancer, exerting oncogenic and pro‑cancer effects; however, its role in osteosarcoma is poorly understood. The present study aimed to explore the function and molecular mechanism of AIM2 in the progression of osteosarcoma. In the present study, AIM2 expression was predicted using the Cancer Cell Line Encyclopedia database and examined in several osteosarcoma cell lines using reverse transcription‑quantitative PCR and western blotting. Following AIM2 overexpression, cell proliferation and apoptosis were examined using Cell Counting Kit‑8, colony formation and TUNEL staining assays. The expression levels of proteins related to apoptosis, epithelial‑mesenchymal transition (EMT) and the PI3K/AKT/mTOR signaling pathway were determined by western blotting. Additionally, cell invasion and migration were assessed using Transwell and wound healing assays. After addition of the PI3K/AKT/mTOR signaling pathway inhibitor LY294002 or activator 740Y‑P, cell function analysis was performed. The results demonstrated that AIM2 was expressed at low levels in osteosarcoma cell lines. AIM2 overexpression inhibited proliferation, invasion, migration and EMT, and promoted apoptosis in osteosarcoma cells. Furthermore, the levels of phosphorylated (p)‑PI3K, p‑AKT and p‑mTOR were markedly downregulated following AIM2 overexpression. Furthermore, LY294002 treatment had the same effects as AIM2 upregulation on osteosarcoma cell proliferation, apoptosis, invasion, migration and EMT. By contrast, 740Y‑P reversed the effects of AIM2 overexpression on the behavior of osteosarcoma cells. Overall, the findings of the present study demonstrated that AIM2 may inhibit the progression of osteosarcoma by inactivating the PI3K/AKT/mTOR signaling pathway, and suggested that AIM2 may be a promising marker for the treatment of osteosarcoma.

Indexed as

Gene Expression Regulation, NeoplasticBone NeoplasmsCell Line, TumorCell MovementCell ProliferationChromonesComputational BiologyDNA-Binding ProteinsDown-RegulationEpithelial-Mesenchymal TransitionHumansMorpholinesNeoplasm InvasivenessOsteosarcomaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAIM2 protein, humanAKT1 protein, humanChromonesDNA-Binding ProteinsMorpholinesMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases740Y‑Pabsent in melanoma 2epithelial‑mesenchymal transitionosteosarcomaPI3K/AKT/mTOR

Identifiers

PMID34913077
PMCPMC8711022
OpenAlexW4200247377

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.