Evidence map›Paper›PMID 37365560›Full record

ArticleBMC cancer2023

SLC25A32 promotes malignant progression of glioblastoma by activating PI3K-AKT signaling pathway.

Zhiwei Xue, Jiwei Wang, Zide Wang, Junzhi Liu, Jiangli Zhao, Xuchen Liu, Yan Zhang, Guowei Liu, Zhimin Zhao, Wenjie Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

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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

14 authors at 1 institution in 1 country.

Zhiwei Xue *Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Jiwei Wang *Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Zide WangDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Junzhi LiuDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Jiangli ZhaoDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Xuchen LiuDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Yan ZhangDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Guowei LiuDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Zhimin ZhaoDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Wenjie LiDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Qing ZhangDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Xingang LiDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Bin HuangDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
Xinyu WangDepartment of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China. wangxinyu@sdu.edu.cn.
Shandong University · CN

Funding

Clinical Research Center of Shandong University 2020SDUCRCB002National Natural Science Foundation of China 81702474National Natural Science Foundation of China 82203760Research Project of Jinan Microecological Biomedicine Shandong Laboratory JNL-2022003AResearch Project of Jinan Microecological Biomedicine Shandong Laboratory JNL-2022042CScience and Technology Development Plan of Shandong Province ZR2019ZD33Science and Technology Development Plan of Shandong Province ZR2020QH182Taishan Scholar Foundation of Shandong Province ts20110814
6 · The paper itself

Abstract

backgroundSolute carrier family 25 member 32 (SLC25A32) is an important member of SLC25A family and plays a role in folate transport metabolism. However, the mechanism and function of SLC25A32 in the progression of human glioblastoma (GBM) remain unclear.

methodsIn this study, folate related gene analysis was performed to explore gene expression profiles in low-grade glioma (LGG) and GBM. Western blotting, real-time quantitative PCR (qRT-PCR), and immunohistochemistry (IHC) were used to confirm the expression levels of SLC25A32 in GBM tissues and cell lines. CCK-8 assays, colony formation assays, and Edu assays were performed to assess the role of SLC25A32 on proliferation in GBM in vitro. A 3D sphere invasion assay and an ex vivo co-culture invasion model were performed to assess the effects of SLC25A32 on invasion in GBM.

resultsElevated expression of SLC25A32 was observed in GBM, and high SLC25A32 expression was associated with a high glioma grade and poorer prognosis. Immunohistochemistry performed with anti-SLC25A32 on samples from an independent cohort of patients confirmed these results. Knockdown of SLC25A32 inhibited the proliferation and invasion of GBM cells, but overexpression of SLC25A32 significantly promoted cell growth and invasion. These effects were mainly due to the activation of the PI3K-AKT-mTOR signaling pathway.

conclusionOur study demonstrated that SLC25A32 plays a significant role in promoting the malignant phenotype of GBM. Therefore, SLC25A32 can be used as an independent prognostic factor in patients with GBM, providing a new target for the comprehensive treatment of GBM.

Indexed as

Brain NeoplasmsGlioblastomaGliomaMembrane Transport ProteinsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionMembrane Transport ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSLC25A32 protein, humanFolateGlioblastomaMetabolismPI3K-AKTSLC25A32

Identifiers

PMID37365560
PMCPMC10294537
OpenAlexW4382022428

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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.