Evidence map›Paper›PMID 36817861›Full record

ArticleBioMed research international2023

Identification of RALA as a Therapeutic Target and Prognostic Predictor of Osteosarcoma.

Gentao Fan, Yan Zhu, Hao Zhu, Lingfeng Yu, Zhen Wang, Chenjun Zhai, Guangxin Zhou, Jianning Zhao, Yicun Wang

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. 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

9 authors at 3 institutions in 1 country.

Gentao FanJinling Hospital Department of Orthopaedics Nanjing Medical University, Nanjing, Jiangsu 210002, China.ORCID https://orcid.org/0000-0002-8483-4883
Yan ZhuJinling Hospital Department of Orthopaedics Nanjing Medical University, Nanjing, Jiangsu 210002, China.ORCID https://orcid.org/0000-0002-9726-2546
Hao ZhuDepartment of Orthopedics, Affiliated Jianhu Hospital of Nantong University, No. 666 Nanhuan Road, Jianhu, Yancheng, 224700 Jiangsu, China.ORCID https://orcid.org/0000-0002-3147-8678
Lingfeng YuDepartment of Orthopaedics, Affiliated Jinling Hospital Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.
Zhen WangJinling Hospital Department of Orthopaedics Nanjing Medical University, Nanjing, Jiangsu 210002, China.
Chenjun ZhaiDepartment of Orthopedics, Yixing People's Hospital, 75, Tongzhenguan Road, Yixing 214200, China.
Guangxin ZhouDepartment of Orthopaedics, Affiliated Jinling Hospital Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.ORCID https://orcid.org/0000-0002-0252-2473
Jianning ZhaoJinling Hospital Department of Orthopaedics Nanjing Medical University, Nanjing, Jiangsu 210002, China.ORCID https://orcid.org/0000-0003-4741-3825
Yicun WangDepartment of Orthopaedics, Affiliated Jinling Hospital Medical School of Nanjing University, Nanjing, Jiangsu 210002, China.ORCID https://orcid.org/0000-0003-4067-1637
Nanjing General Hospital of Nanjing Military Command · CNJiangsu University · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Osteosarcoma (OS) is the most common primary aggressive sarcoma of bone, with massive aberrant expression of oncogenes related to the development of OS. RALA, a kind of small Ras-like guanosine triphosphatases, has been identified as a potential therapeutic target in several types of tumor, but its role in OS remains largely unknown. Methods: Abnormal expression of RALA was proven in the Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), Therapeutically Applicable Research to Generate Effective Treatments (TARGET), and RNA-sequence of samples and cell lines. The role of RALA in OS was analyzed in terms of DNA methylation, immune cell infiltration, and patient survival. The cancer-promoting effect of RALA was demonstrated in cell lines and xenograft osteosarcoma models. A prognostic scoring model incorporating RALA as an indicator was established with the clinical samples that we collected. Results: The results showed that RALA was highly expressed in human OS tissues and cell lines. Survival analysis demonstrated that RALA was the sole independent risk factor for poor overall survival and disease-free survival in OS patients and impacted the proportion of infiltrating immune cells and DNA methylation in the OS tumor microenvironment. By gene-gene interaction analysis, we found that the expression of RALA was highly correlated to the expression of ABCE1. Similar to RALA, upregulated ABCE1 is correlated with poor survival outcome of OS patients. In addition, the functional experiment demonstrated that higher expression of RALA promoted the proliferation, migration, and invasion of OS cells. In vivo results were similar with the in vitro results. We examined m6a methylation-related genes and found that m6A methylation is responsible for the abnormal expression of RALA. Finally, the prognostic prediction model of RALA could be used to predict the long-term outcome of OS patients. Conclusions: We identified RALA as an oncogene in OS, and RALA upregulation in a concerted manner with ABCE1 was significantly associated with worse outcomes of OS patients. Targeting RALA may prove to be a novel target for OS immunotherapy in future clinical practice.

Indexed as

Bone NeoplasmsOsteosarcomaBone and BonesCell MovementHumansPrognosisral GTP-Binding ProteinsTumor MicroenvironmentRALA protein, humanral GTP-Binding Proteins

Identifiers

PMID36817861
PMCPMC9936457
OpenAlexW4319345158

What OpenQuestion holds

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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.