Evidence map›Paper›PMID 35509067›Full record

ArticleJournal of translational medicine2022

TPI1 activates the PI3K/AKT/mTOR signaling pathway to induce breast cancer progression by stabilizing CDCA5.

Xiaoying Jin, Dandan Wang, Mengxia Lei, Yan Guo, Yuqing Cui, Fengzhi Chen, Weiling Sun, Xuesong Chen

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 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 86 citations in OpenAlex.

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  11. The moonlighting functions of glycolytic enzymes in tumorigenesis.Cellular oncology (Dordrecht, Netherlands) · 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 1 institution in 1 country.

Xiaoying Jin *The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, China.
Dandan Wang *The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, China.
Mengxia Lei *The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, China.
Yan GuoThe Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, China.
Yuqing CuiThe Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, China.
Fengzhi ChenThe Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, China.
Weiling SunDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, China. sunweiling@hrbmu.edu.cn.
Xuesong ChenThe Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, China. cxs1978@ems.hrbmu.edu.cn.ORCID 0000-0003-4332-7559
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTriosephosphate isomerase 1 (TPI1), as a key glycolytic enzyme, is upregulated in multiple cancers. However, expression profile and regulatory mechanism of TPI1 in breast cancer (BRCA) remain mysterious.

methodsWestern blotting and immunohistochemistry (IHC) assays were used to investigate the expression of TPI1 in BRCA specimens and cell lines. TPI1 correlation with the clinicopathological characteristics and prognosis of 362 BRCA patients was analyzed using a tissue microarray. Overexpression and knockdown function experiments in cells and mice models were performed to elucidate the function and mechanisms of TPI1-induced BRCA progression. Related molecular mechanisms were clarified using co-IP, IF, mass spectrometric analysis, and ubiquitination assay.

resultsWe have found TPI1 is highly expressed in BRCA tissue and cell lines, acting as an independent indicator for prognosis in BRCA patients. TPI1 promotes BRCA cell glycolysis, proliferation and metastasis in vitro and in vivo. Mechanistically, TPI1 activates phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway to regulate epithelial-mesenchymal transformation (EMT) and aerobic glycolysis, which is positively mediated by cell division cycle associated 5 (CDCA5). Moreover, TPI1 interacts with sequestosome-1 (SQSTM1)/P62, and P62 decreases the protein expression of TPI1 by promoting its ubiquitination in MDA-MB-231 cells.

conclusionsTPI1 promotes BRCA progression by stabilizing CDCA5, which then activates the PI3K/AKT/mTOR pathway. P62 promotes ubiquitin-dependent proteasome degradation of TPI1. Collectively, TPI1 promotes tumor development and progression, which may serve as a therapeutic target for BRCA.

Indexed as

Breast NeoplasmsPhosphatidylinositol 3-KinasesAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMammalsMicePhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktSignal TransductionAdaptor Proteins, Signal TransducingCDCA5 protein, humanCell Cycle ProteinsMTOR protein, humanPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCDCA5Epithelial–mesenchymal transformation (EMT)GlycolysisPI3K/AKT/mTORTPI1

Identifiers

PMID35509067
PMCPMC9066866
OpenAlexW4229017444

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.