Evidence map›Paper›PMID 37935810›Full record

ArticleMedical oncology (Northwood, London, England)2023

TCOF1 promotes the colorectal cancer progression by stabilizing β-catenin.

Hyeseon Yun, Ji-Eun You, Jun Ki Hong, Do Yeon Kim, Ji-U Lee, Dong-Hee Kang, Yea Seong Ryu, Dong-In Koh, Dong-Hoon Jin

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Article
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4 · The record

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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.

Hyeseon Yun *Asan Institute for Life Science, Asan Medical Center, Seoul, 05505, Republic of Korea.
Ji-Eun You *Asan Institute for Life Science, Asan Medical Center, Seoul, 05505, Republic of Korea.
Jun Ki Hong *Asan Institute for Life Science, Asan Medical Center, Seoul, 05505, Republic of Korea.
Do Yeon KimAsan Institute for Life Science, Asan Medical Center, Seoul, 05505, Republic of Korea.
Ji-U LeeAsan Institute for Life Science, Asan Medical Center, Seoul, 05505, Republic of Korea.
Dong-Hee KangAsan Institute for Life Science, Asan Medical Center, Seoul, 05505, Republic of Korea.
Yea Seong RyuAsan Institute for Life Science, Asan Medical Center, Seoul, 05505, Republic of Korea.
Dong-In KohAsan Institute for Life Science, Asan Medical Center, Seoul, 05505, Republic of Korea.
Dong-Hoon JinDepartment of Pharmacology, AMIST, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. inno183@amc.seoul.kr.ORCID http://orcid.org/0000-0002-1124-1518

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the highest mortality rates worldwide, and various studies reported to the occurrence of CRC. In particular, the Wnt/β-catenin pathway is known to be a major factor in the progression of CRC and β-catenin involved in the expression of its downstream target genes. We searched for TCOF1 through sliver staining to identify a new binding partner for β-catenin and to investigate the role of the gene involved in CRC. Treacle Ribosome Biogenesis Factor 1 (TCOF1) is a nucleolar protein that regulates the transcription of ribosomal DNA (rDNA). There are many reports of genetic studies on TCOF1 mutations and defects, but its function in CRC remains unknown. We demonstrated that TCOF1 and β-catenin expression in tissue microarray (TMA) containing 101 individual CRC and 17 adjacent normal samples. Additionally, the effects of TCOF1 knockdown or overexpression were examined proliferation, colony formation assay, western blot, and quantitative real-time PCR (qRT-PCR). TCOF1 knockdown or overexpression regulates cell proliferation about three-fold and the phosphorylation of β-catenin, cyclin D1 expression levels. Besides, we discovered the mechanism through which TCOF1 regulates the stability of β-catenin was involved in degradation through proteasome using ubiquitination assay. Finally, we confirmed the interaction of TCOF1 with the tankyrase inhibitor NVP-TNKS656, which destabilizes β-catenin through in vitro and in vivo. Collectively, this study shows that significantly correlation was observed that TCOF1 and β-catenin were risk factor for tumor progression. The stability of β-catenin via regulating TCOF1 expression could be a potential strategy for therapeutic with CRC.

Indexed as

beta CateninColorectal NeoplasmsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansNuclear ProteinsPhosphoproteinsWnt Signaling Pathwaybeta CateninNuclear ProteinsPhosphoproteinsTCOF1 protein, humanCell proliferationColorectal cancerTankyrase inhibitorTCOF1β-catenin

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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.