Evidence map›Paper›PMID 28350098›Full record

ArticleOncology reports2017

SLC3A2 is upregulated in human osteosarcoma and promotes tumor growth through the PI3K/Akt signaling pathway.

Bin Zhu, Dongdong Cheng, Lei Hou, Shumin Zhou, Tao Ying, Qingcheng Yang

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Article
  5. Review
  6. Article
  7. [Glutamine metabolic reprogramming in regulating the occurrence and development of osteosarcoma].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
  8. Article
  9. The role of CD98 heavy chain in cancer development.Histology and histopathology · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Role of ferroptosis in esophageal cancer and corresponding immunotherapy.World journal of gastrointestinal oncology · 2023
    Review
  15. Review
  16. Review
  17. Article
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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

6 authors at 3 institutions in 1 country.

Bin ZhuDepartment of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Dongdong ChengDepartment of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Lei HouDepartment of Breast and Thyroid Surgery, The General Hospital of Jinan Military Command, Jinan, Shandong 116000, P.R. China.
Shumin ZhouDepartment of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Tao YingDepartment of Ultrasound, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Qingcheng YangDepartment of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Shanghai Sixth People's Hospital · CNShanghai Jiao Tong University · CNGeneral Hospital of Jinan Military Command · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence indicates that SLC3A2 (solute carrier family 3 member 2) is upregulated and correlates with tumor growth in multiple types of cancers, while the role of SLC3A2 in human osteosarcoma (OS) is rarely discussed. Thus, the aim of the present study was to demonstrate the expression of SLC3A2 in human osteosarcoma and reveal its biological function and the underlying mechanisms. RT-PCR, western blot analysis and immunohistochemistry (IHC) were used to assess the expression of SLC3A2 in OS samples and cell lines. Cell cycle, Cell Counting Kit-8 (CCK-8) and colony formation assays were used to test the cell survival capacity. To investigate the potential mechanism by which SLC3A2 regulates OS growth, we used a slide-based antibody array. We demonstrated that SLC3A2 was upregulated in OS cell lines as well as OS tissues. High expression of SLC3A2 was correlated with clinical stage and tumor size in OS. Reduced expression of SLC3A2 inhibited OS cell proliferation through G2/M phase arrest. Most importantly, we found that SLC3A2 may regulate OS growth through the PI3K/Akt signaling pathway. In conclusion, SLC3A2 is upregulated in OS and plays a crucial role in tumor growth. Targeting SLC3A2 may provide a new therapeutic strategy for OS.

Indexed as

AdolescentAdultBone NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationFemaleFusion Regulatory Protein 1, Heavy ChainGene Knockdown TechniquesHumansMaleOsteosarcomaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionUp-RegulationFusion Regulatory Protein 1, Heavy ChainPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSLC3A2 protein, human

Identifiers

PMID28350098
PMCPMC5428444
OpenAlexW2599846384

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.