Evidence map›Paper›PMID 29633065›Full record

ArticleMolecular and cellular biochemistry2018

KDM4B promotes DNA damage response via STAT3 signaling and is a target of CREB in colorectal cancer cells.

Wei-Wu Deng, Qian Hu, Zheng-Ren Liu, Qiu-Hong Chen, Wen-Xiang Wang, Huai-Gen Zhang, Qin Zhang, Yuan-Lu Huang, Xue-Kang Zhang

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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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

9 authors.

Wei-Wu DengDepartment of Anesthesiology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Qian HuDepartment of Anesthesiology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Zheng-Ren LiuGeneral Surgery, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Qiu-Hong ChenDepartment of Anesthesiology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Wen-Xiang WangDepartment of Anesthesiology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Huai-Gen ZhangDepartment of Anesthesiology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Qin ZhangDepartment of Anesthesiology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Yuan-Lu HuangDepartment of Anesthesiology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Xue-Kang ZhangDepartment of Anesthesiology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China. xuekangzhang71@gmail.com.

Funding

Natural Science Foundation of China (NSFC) 81660096
6 · The paper itself

Abstract

Resistance to radiotherapy is a major limitation for the successful treatment of colorectal cancer (CRC). Recently, accumulating evidence supports a critical role of epigenetic regulation in tumor cell survival upon irradiation. Lysine Demethylase 4B (KDM4B) is a histone demethylase involved in the oncogenesis of multiple human cancers but the underlying mechanisms have not been fully elucidated. Here we show that KDM4B is overexpressed in human colorectal cancer (CRC) tumors and cell lines. In CRC cells, KDM4B silencing induces spontaneous double-strand breaks (DSBs) formation and potently sensitizes tumor cells to irradiation. A putative mechanism involved suppression of Signal Transducer and Activator of Transcription 3 (STAT3) signaling pathway, which is essential for efficient repair of damaged DNA. Overexpression of STAT3 in KMD4B knockdown cells largely attenuates DNA damage triggered by KDM4B silencing and increases cell survival upon irradiation. Moreover, we find evidence that transcription factor CAMP Responsive Element Binding Protein (CREB) is a key regulator of KMD4B expression by directly binding to a conserved region in KMD4B promoter. Together, our findings illustrate the significance of CREB-KDM4B-STAT3 signaling cascade in DNA damage response, and highlight that KDM4B may potentially be a novel oncotarget for CRC radiotherapy.

Indexed as

DNA Breaks, Double-StrandedSignal TransductionCell Line, TumorColorectal NeoplasmsCyclic AMP Response Element-Binding ProteinGamma RaysHumansJumonji Domain-Containing Histone DemethylasesNeoplasm ProteinsRadiation ToleranceSTAT3 Transcription FactorCREB1 protein, humanCyclic AMP Response Element-Binding ProteinJumonji Domain-Containing Histone DemethylasesKDM4B protein, humanNeoplasm ProteinsSTAT3 protein, humanSTAT3 Transcription FactorColorectal cancerCREBDNA damage repairKDM4BSTAT3

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Registered trials

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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.