Evidence map›Paper›PMID 38713155›Full record

ArticleAging2024

AURKB promotes colorectal cancer progression by triggering the phosphorylation of histone H3 at serine 10 to activate CCNE1 expression.

Ling Li, Ke Xie, Honghu Xie, Lei Wang, Zhong Li, Qicheng Lu, Jin Feng

Abstract read
In one paragraph

Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
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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

7 authors.

Ling LiDepartment of Gastrointestinal Surgery, The First People’s Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Ke XieDepartment of Gastrointestinal Surgery, The First People’s Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Honghu XieDepartment of Gastrointestinal Surgery, The First People’s Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Lei WangDepartment of Gastrointestinal Surgery, The First People’s Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Zhong LiDepartment of Gastrointestinal Surgery, The First People’s Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Qicheng LuDepartment of Gastrointestinal Surgery, The First People’s Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Jin FengDepartment of Gastrointestinal Surgery, The First People’s Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aurora kinase B (AURKB) initiates the phosphorylation of serine 10 on histone H3 (pH3S10), a crucial process for chromosome condensation and cytokinesis in mammalian mitosis. Nonetheless, the precise mechanisms through which AURKB regulates the cell cycle and contributes to tumorigenesis as an oncogenic factor in colorectal cancer (CRC) remain unclear. Here, we report that AURKB was highly expressed and positively correlated with Ki-67 expression in CRC. The abundant expression of AURKB promotes the growth of CRC cells and xenograft tumors in animal model. AURKB knockdown substantially suppressed CRC proliferation and triggered cell cycle arrest in G2/M phase. Interestingly, cyclin E1 (CCNE1) was discovered as a direct downstream target of AURKB and functioned synergistically with AURKB to promote CRC cell proliferation. Mechanically, AURKB activated CCNE1 expression by triggering pH3S10 in the promoter region of CCNE1. Furthermore, it was showed that the inhibitor specific for AURKB (AZD1152) can suppress CCNE1 expression in CRC cells and inhibit tumor cell growth. To conclude, this research demonstrates that AURKB accelerated the tumorigenesis of CRC through its potential to epigenetically activate CCNE1 expression, suggesting AURKB as a promising therapeutic target in CRC.

Indexed as

Aurora Kinase BCell ProliferationColorectal NeoplasmsCyclin EHistonesOncogene ProteinsAnimalsCell Line, TumorDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudePhosphorylationAURKB protein, humanAurora Kinase BCCNE1 protein, humanCyclin EHistonesOncogene ProteinsSerineAURKBCCNE1cell cyclecolorectal cancerpolyploidy

Identifiers

PMID38713155
PMCPMC11132018

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.