Evidence map›Paper›PMID 37147883›Full record

ArticleThe journal of pathology. Clinical research2023

KLF2 inhibits colorectal cancer progression and metastasis by inducing ferroptosis via the PI3K/AKT signaling pathway.

Jia Li, Ji Ling Jiang, Yi Mei Chen, Wei Qi Lu

Open access · goldAbstract read
In one paragraph

Article in The journal of pathology. Clinical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.9field-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

36 citing papers in PubMed, 45 citations in OpenAlex.

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  8. The mechanism of Akkermansia muciniphila inhibiting the proliferation of colorectal cancer cells via ferroptosis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
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  13. Cells · 2025
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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

4 authors at 3 institutions in 1 country.

Jia LiDepartment of General Surgery, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, PR China.
Ji Ling JiangDepartment of General Surgery, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, PR China.
Yi Mei ChenDepartment of Breast Surgery, Shenzhen Women & Children's Health Care Hospital, Shenzhen, PR China.
Wei Qi LuDepartment of Gastrointestinal Surgery, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, PR China.
Shenzhen Pingle Orthopedic Hospital · CNFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CNShenzhen Maternity and Child Healthcare Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Krüppel-like factor 2 (KLF2) belongs to the zinc finger family and is thought to be a tumor suppressor gene due to its low expression in various cancer types. However, its functional role and molecular pathway involvement in colorectal cancer (CRC) are not well defined. Herein, we investigated the potential mechanism of KLF2 in CRC cell invasion, migration, and epithelial-mesenchymal transition (EMT). We utilized the TCGA and GEPIA databases to analyze the expression of KLF2 in CRC patients and its correlation with different CRC stages and CRC prognosis. RT-PCR, western blot, and immunohistochemistry assays were used to measure KLF2 expression. Gain-of-function assays were performed to evaluate the role of KLF2 in CRC progression. Moreover, mechanistic experiments were conducted to investigate the molecular mechanism and involved signaling pathways regulated by KLF2. Additionally, we also conducted a xenograft tumor assay to evaluate the role of KLF2 in tumorigenesis. KLF2 expression was low in CRC patient tissues and cell lines, and low expression of KLF2 was associated with poor CRC prognosis. Remarkably, overexpressing KLF2 significantly inhibited the invasion, migration, and EMT capabilities of CRC cells, and tumor growth in xenografts. Mechanistically, KLF2 overexpression induced ferroptosis in CRC cells by regulating glutathione peroxidase 4 expression. Moreover, this KLF2-dependent ferroptosis in CRC cells was mediated by inhibiting the PI3K/AKT signaling pathway that resulted in the suppression of invasion, migration, and EMT of CRC cells. We report for the first time that KLF2 acts as a tumor suppressor in CRC by inducing ferroptosis via inhibiting the PI3K/AKT signaling pathway, thus providing a new direction for CRC prognosis assessment and targeted therapy.

Indexed as

Colorectal NeoplasmsFerroptosisCell Line, TumorCell ProliferationHumansKruppel-Like Transcription FactorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTranscription FactorsKLF2 protein, humanKruppel-Like Transcription FactorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTranscription Factorscolorectal cancerferroptosisKLF2metastasispathway

Identifiers

PMID37147883
PMCPMC10397377
OpenAlexW4372332183

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.