Evidence map›Paper›PMID 28677721›Full record

ArticleInternational journal of oncology2017

Zinc-finger protein 545 is inactivated due to promoter methylation and functions as a tumor suppressor through the Wnt/β-catenin, PI3K/AKT and MAPK/ERK signaling pathways in colorectal cancer.

Shili Xiang, Tingxiu Xiang, Qian Xiao, Yunhai Li, Bianfei Shao, Tao Luo

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

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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

6 authors at 3 institutions in 1 country.

Shili XiangDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Tingxiu XiangMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Qian XiaoDepartment of Breast and Thyroid, The Hospital of Chongqing Traditional Chinese Medicine, Chongqing 400011, P.R. China.
Yunhai LiMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Bianfei ShaoMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Tao LuoDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNFirst People's Hospital of Chongqing · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor, zinc-finger protein 545 (ZNF545), that belongs to the Kruppel-associated box zinc-finger protein (KRAB-ZFP) family, acts as a tumor suppressor and is inactivated by promoter methylation in cancers such as nasopharyngeal carcinoma, breast cancer, and gastric cancer, but its role in colorectal cancer (CRC) is unknown. The purpose of this study was to characterize the ZNF545 expression, methylation status, biological function, and related molecular mechanisms in CRC. The results showed that ZNF545 was expressed in adult normal colorectal tissues, but downregulated or silenced in CRC cell lines, and this mechanism was reversed by demethylation treatment with 5-aza-2'-deoxycytidine and trichostatin A. The results also showed that the expression of ZNF545 in primary CRC tissues was significantly downregulated compared to adjacent tissues (p<0.05). Overexpression of ZNF545 caused CRC cell cycle arrest and apoptosis, suppressed cell proliferation, and suppressed colony formation and migration in vitro, showing that ZNF545 can function as a tumor suppressor. This function was also shown in nude mice. Furthermore, Wnt/β‑catenin, phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT), and mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) signaling pathways participated in the regulation of ZNF545 in CRC cells. Together, the results suggested that ZNF545 functions as a tumor suppressor in CRC and is frequently inactivated by promoter methylation.

Indexed as

AnimalsApoptosisCell Cycle CheckpointsCell ProliferationColorectal NeoplasmsDNA MethylationFemaleGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMiceNuclear ProteinsPromoter Regions, GeneticWnt Signaling PathwayXenograft Model Antitumor AssaysNuclear ProteinsZFP82 protein, human

Identifiers

PMID28677721
PMCPMC5564408
OpenAlexW2731865309

What OpenQuestion 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 OpenQuestion graph.