Evidence map›Paper›PMID 34839347›Full record

ArticleCell death & disease2021

SLC25A1 promotes tumor growth and survival by reprogramming energy metabolism in colorectal cancer.

Ying Yang, Jiaxing He, Bo Zhang, Zhansheng Zhang, Guozhan Jia, Shiqi Liu, Tao Wu, Xianli He, Nan Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.5field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Metabolic reprogramming signature predicts immunotherapy efficacy in lung adenocarcinoma: TargetingChinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025
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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

9 authors at 1 institution in 1 country.

Ying Yang *Department of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China.
Jiaxing He *Department of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China.
Bo ZhangDepartment of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China.
Zhansheng ZhangDepartment of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China.
Guozhan JiaDepartment of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China.
Shiqi LiuDepartment of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China.
Tao WuDepartment of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China. 504435076@qq.com.ORCID 0000-0002-3645-0914
Xianli HeDepartment of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China. wanghe@fmmu.edu.cn.ORCID 0000-0001-6869-9418
Nan WangDepartment of General Surgery, Tangdu Hospital, the Air Force Medical University, Xi'an, 710038, China. wangnandoc@163.com.ORCID 0000-0003-1389-9900
Tang Du Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal lipid metabolism has been commonly observed in various human cancers, including colorectal cancer (CRC). The mitochondrial citrate carrier SLC25A1 (also known as mitochondrial citrate/isocitrate carrier, CIC), has been shown to play an important role in lipid metabolism regulation. Our bioinformatics analysis indicated that SLC25A1 was markedly upregulated in CRC. However, the role of SLC25A1 in the pathogenesis and aberrant lipid metabolism in CRC remain unexplored. Here, we found that SLC25A1 expression was significantly increased in tumor samples of CRC as compared with paired normal samples, which is associated with poor survival in patients with CRC. Knockdown of SLC25A1 significantly inhibited the growth of CRC cells by suppressing the progression of the G1/S cell cycle and inducing cell apoptosis both in vitro and in vivo, whereas SLC25A1 overexpression suppressed the malignant phenotype. Additionally, we demonstrated that SLC25A1 reprogrammed energy metabolism to promote CRC progression through two mechanisms. Under normal conditions, SLC25A1 increased de novo lipid synthesis to promote CRC growth. During metabolic stress, SLC25A1 increased oxidative phosphorylation (OXPHOS) to protect protects CRC cells from energy stress-induced cell apoptosis. Collectively, SLC25A1 plays a pivotal role in the promotion of CRC growth and survival by reprogramming energy metabolism. It could be exploited as a novel diagnostic marker and therapeutic target in CRC.

Indexed as

AnimalsColorectal NeoplasmsEnergy MetabolismHumansLipid MetabolismMaleMiceMice, NudeMitochondrial ProteinsOrganic Anion TransportersSurvival AnalysisTransfectionMitochondrial ProteinsOrganic Anion TransportersSlc25a1 protein, mouse

Identifiers

PMID34839347
PMCPMC8627508
OpenAlexW3215455563

What OpenQuestion holds

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LicenceCC BY
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.