Evidence map›Paper›PMID 36514121›Full record

ArticleJournal of translational medicine2022

An extensive bioinformatics study on the role of mitochondrial solute carrier family 25 in PC and its mechanism behind affecting immune infiltration and tumor energy metabolism.

Qiang Zhang, Yubao Tang, Shuai Sun, Qiuyi Xie, Jie Yao, Xiaodong Wang, Jianjun Qian, Zhennan Li

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. MUC13-Associated Molecular Interactome in Pancreatic Cancer.Computational and structural biotechnology journal · 2026
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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

8 authors at 3 institutions in 1 country.

Qiang ZhangMedical College of Yangzhou University, Yangzhou, Jiangsu, 225000, China.
Yubao TangMedical College of Yangzhou University, Yangzhou, Jiangsu, 225000, China.
Shuai SunDalian Medical University, Dalian, 111600, Liaoning, China.
Qiuyi XieMedical College of Yangzhou University, Yangzhou, Jiangsu, 225000, China.
Jie YaoDepartment of Hepatobiliary and Pancreatic Surgery, Northern Jiangsu People's Hospital, Yangzhou, 225001, Jiangsu, China.
Xiaodong WangDepartment of Hepatobiliary and Pancreatic Surgery, Northern Jiangsu People's Hospital, Yangzhou, 225001, Jiangsu, China.
Jianjun QianDepartment of Hepatobiliary and Pancreatic Surgery, Northern Jiangsu People's Hospital, Yangzhou, 225001, Jiangsu, China.
Zhennan LiDepartment of Hepatobiliary and Pancreatic Surgery, Northern Jiangsu People's Hospital, Yangzhou, 225001, Jiangsu, China. doclizn@outlook.com.
Northern Jiangsu People's Hospital · CNYangzhou University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral metabolic disorders and malignancies are directly related to abnormal mitochondrial solute carrier family 25 (SLC25A) members activity. However, its biological role in pancreatic cancer (PC) is not entirely understood.

methodsThe lasso method was used to create a novel prognostic risk model for PC based on SLC25A members, and its roles in tumor immunology and energy metabolism were explored. Furthermore, co-expression networks were constructed for SLC25A11, SLC25A29, and SLC25A44. Single-cell RNA sequencing (ScRNA-seq) revealed the distribution of gene expression in PC. Tumor immune infiltration was examined with the TIMER database. Lastly, drug sensitivity was investigated, and co-transcriptional factors were predicted.

resultsIn the present study, a novel prognostic risk model was established and validated for PC based on SLC25A members. The high-risk group had a lower activation of oxidative phosphorylation and a more abundant immune infiltration phenotype than the low-risk group. According to co-expression network studies, SLC25A11, SLC25A29, and SLC25A44 were involved in the energy metabolism of PC and prevented tumor growth, invasion, and metastasis. ScRNA-seq research also pointed to their contribution to the tumor microenvironment. Moreover, the recruitment of numerous immune cells was positively correlated with SLC25A11 and SLC25A44 but negatively correlated with SLC25A29. Additionally, the sensitivity to 20 Food and Drug Administration-approved antineoplastic medicines was strongly linked to the aforementioned genes, where cisplatin sensitivity increased with the up-regulation of SLC25A29. Finally, the Scleraxis BHLH Transcription Factor (SCX) and other proteins were hypothesized to co-regulate the mRNA transcription of the genes.

conclusionSLC25A members are crucial for tumor immune and energy metabolism in PC, and SLC25A11, SLC25A29, and SLC25A44 can be used as favorable prognostic markers. The use of these markers will provide new directions to unravel their action mechanisms in PC.

Indexed as

Pancreatic NeoplasmsBiomarkers, TumorCarnitine AcyltransferasesComputational BiologyEnergy MetabolismHumansMitochondriaMitochondrial ProteinsPrognosisTumor MicroenvironmentBiomarkers, TumorCarnitine AcyltransferasesMitochondrial ProteinsSLC25A29 protein, human

Identifiers

PMID36514121
PMCPMC9746138
OpenAlexW4311316803

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LicenceCC BY
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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.