Evidence map›Paper›PMID 40091780›Full record

ArticleCancer science2025

Lnc-TPT1-AS1/CBP/ATIC Axis Mediated Purine Metabolism Activation Promotes Breast Cancer Progression.

Yiyun Zhang, Hanyu Zhang, Mingcui Li, Yanling Li, Zhuo-Ran Wang, Weilun Cheng, Yansong Liu, Zhengbo Fang, Ang Zheng, Jingxuan Wang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

11 authors.

Yiyun ZhangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Hanyu ZhangDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Mingcui LiDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yanling LiDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhuo-Ran WangDepartment of Clinical Medicine, First Clinical Medical College of Anhui Medical University, Hefei, China.
Weilun ChengDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yansong LiuDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhengbo FangDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Ang ZhengThe First Hospital of China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0003-1078-6660
Jingxuan WangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Fei MaDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.ORCID https://orcid.org/0000-0002-7068-8846

Funding

National Natural Science Foundation of China 82002791National Natural Science Foundation of China 82203873Natural Science Foundation of Heilongjiang Province YQ2019H018Natural Science Foundation of Heilongjiang Province YQ2024H016
6 · The paper itself

Abstract

The purine biosynthetic pathway was recently identified to play a crucial role in breast cancer progression. However, little was known about the regulatory mechanisms of long non-coding RNA in breast cancer purine metabolism. In this study, we discovered that LncRNA TPT1-AS1 (TPT1-AS1) was downregulated in breast cancer tissues. Its introduction in breast cancer cells markedly suppressed tumor growth and metastasis in xenograft tumor models. Mass spectrometric analysis suggested that the purine biosynthetic pathway was activated in TPT1-AS1-knockdown MCF-7 cells. Inosine monophosphate (IMP), the product of de novo purine biosynthesis, was significantly upregulated. Mechanistically, we found that TPT1-AS1 could physically interact with CBP (CREB-binding protein), which consequently led to the loss of H3K27Ac in the promoter area of ATIC, the key enzyme of IMP synthesis. This process could block breast cancer purine metabolism and inhibit breast cancer progression. In conclusion, our findings illustrate the role of non-coding RNAs in breast cancer purine metabolism reprogramming and present a potential candidate for breast cancer therapy.

Indexed as

Breast NeoplasmsCREB-Binding ProteinPurinesRNA, Long NoncodingAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceMice, Inbred BALB CMice, NudeXenograft Model Antitumor AssaysCREB-Binding ProteinpurinePurinesRNA, Long NoncodingATICbreast cancerCBPLnc TPT1‐AS1purine metabolism

Identifiers

PMID40091780
PMCPMC12127116

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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.