Evidence map›Paper›PMID 38480537›Full record

ArticleArchives of toxicology2024

Cellular senescence gene TACC3 associated with colorectal cancer risk via genetic and DNA methylated alteration.

Hengyang Shen, Yang Chen, Menghuan Xu, Jieyu Zhou, Changzhi Huang, Zhenling Wang, Yu Shao, Hongqiang Zhang, Yunfei Lu, Shuwei Li and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Archives of toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. 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 at 3 institutions in 2 countries.

Hengyang Shen *Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Yang Chen *Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Menghuan Xu *Department of Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Jieyu ZhouDepartment of Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Changzhi HuangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Zhenling WangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Yu ShaoDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Hongqiang ZhangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Yunfei LuDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Shuwei LiDepartment of Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China. shuweili@njmu.edu.cn.
Zan FuDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China. fuzan1971@njmu.edu.cn.ORCID 0000-0002-3397-0770
Jiangsu Province Hospital · CNNanjing Medical University · CNMinistry of Education · KR

Funding

National Natural Science Foundation of China 82103915National Natural Science Foundation of China 82172956Natural Science Foundation of Jiangsu Province BK20210535
6 · The paper itself

Abstract

Cell senescence genes play a vital role in the pathogenesis of colorectal cancer, a process that may involve the triggering of genetic variations and reversible phenotypes caused by epigenetic modifications. However, the specific regulatory mechanisms remain unclear. Using CellAge and The Cancer Genome Atlas databases and in-house RNA-seq data, DNA methylation-modified cellular senescence genes (DMCSGs) were validated by Support Vector Machine and correlation analyses. In 1150 cases and 1342 controls, we identified colorectal cancer risk variants in DMCSGs. The regulatory effects of gene, variant, and DNA methylation were explored through dual-luciferase and 5-azacytidine treatment experiments, complemented by multiple database analyses. Biological functions of key gene were evaluated via cell proliferation assays, SA-β-gal staining, senescence marker detection, and immune infiltration analyses. The genetic variant rs4558926 in the downstream of TACC3 was significantly associated with colorectal cancer risk (OR = 1.35, P = 3.22 × 10

Indexed as

Colorectal NeoplasmsDNA MethylationEpigenesis, GeneticMicrotubule-Associated ProteinsCell Cycle ProteinsCellular SenescenceCpG IslandsDNAGene Expression Regulation, NeoplasticHumansTumor MicroenvironmentCell Cycle ProteinsDNAMicrotubule-Associated ProteinsTACC3 protein, humanColorectal cancerDNA methylationSenescenceSusceptibilityTACC3

Identifiers

PMID38480537
OpenAlexW4392817355

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.