Evidence mapPaperPMID 40514657Full record

ArticleJournal of translational medicine2025

TTI1 contributes to radioresistance by activating ATM pathway in rectal cancer.

Jingying Wang, Lili Li, Yuan Qin, Wenyi Zhang

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Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Jingying WangDepartment of Dermatology and Venereology, The First Affiliated Hospital of Wenzhou Medical University, WenZhou, China.
Lili LiDepartment of Oncologic Radiochemotherapy, The First Affiliated Hospital of Wenzhou Medical University, WenZhou, China.
Yuan QinSchool of Basic Medical Science, Wenzhou Medical University, WenZhou, China.
Wenyi ZhangDepartment of Oncologic Radiochemotherapy, The First Affiliated Hospital of Wenzhou Medical University, WenZhou, China. mikezhang10@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTTI1 has been reported as a critical protein in oncogenesis, migration and invasion of various cancers. And its expression level was increased in rectal cancer (RC). However, the biological role of TTI1 in RC is unclear. In the course of exploratory study, we found that TTI1 expression was elevated in radioresistant RC. Therefore, the study was designed to investigate the role of TTI1 in the radiotherapy of RC.

methodsThe proliferative activity of RC cells treated by irradiation was performed using MTT assay and colony formation assay in vitro as well as nude mouse tumour xenograft assay in vivo. Various methods including western blot, qRT-PCR, flow cytometry, and comet assay were used to exploring the molecular mechanism of TTI1 in radiotherapy of RC. The organoid and PDX models were used to analyse the radiotherapy sensitization effect of suppressing ATM signaling pathway.

resultsTTI1 expression was significantly increased in radioresistant RC. The clinical study demonstrated that significantly elevated TTI1 expression resulted in a poor tumour response in RC patients treated with irradiation. TTI1 knockdown could enhance sensitivity of RC cells to irradiation while TTI1 overexpression had the opposite effect. TTI1 could enhance irradiation-induced DNA damage repair through activating ATM signaling pathway. Blocking ATM signaling pathway could enhance the sensitivity of RC tissue to irradiation.

conclusionsTTI1 was identified as a critical factor in regulating resistance of RC to irradiation. TTI1 could be regarded as a credible biomarker for predicting radiotherapeutic effect and prognosis. Inhibition of ATM signaling pathway may be a novel method to overcome radioresistance.

Indexed as

Ataxia Telangiectasia Mutated ProteinsDNA-Binding ProteinsRadiation ToleranceRectal NeoplasmsSignal TransductionAnimalsCell Line, TumorCell ProliferationDNA DamageDNA RepairFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CAtaxia Telangiectasia Mutated ProteinsATM protein, humanDNA-Binding ProteinsATMDNA damage repairRAD51RadioresistanceRadiosensitivityRadiotherapyRectal cancerTTI1

Identifiers

PMID40514657
PMCPMC12166592

What Socratic holds

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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 Socratic graph.