Evidence map›Paper›PMID 35907137›Full record

ArticleHuman cell2022

TMEM97 is transcriptionally activated by YY1 and promotes colorectal cancer progression via the GSK-3β/β-catenin signaling pathway.

Dong Mao, Xiaowei Zhang, Zhaoping Wang, Guannan Xu, Yun Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
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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

5 authors at 2 institutions in 1 country.

Dong MaoDepartment of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, No. 2, The Fifth Section of Renmin Street, Jinzhou, Liaoning Province, China.
Xiaowei ZhangDepartment of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, No. 2, The Fifth Section of Renmin Street, Jinzhou, Liaoning Province, China.
Zhaoping WangDepartment of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, No. 2, The Fifth Section of Renmin Street, Jinzhou, Liaoning Province, China.
Guannan XuDepartment of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, No. 2, The Fifth Section of Renmin Street, Jinzhou, Liaoning Province, China.
Yun ZhangDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Jinzhou Medical University, No. 2, The Fifth Section of Renmin Street, Jinzhou, Liaoning Province, China. zysz2020@yeah.net.ORCID http://orcid.org/0000-0001-7740-4423
Jinzhou Medical University · CNFirst Affiliated Hospital of Liaoning Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transmembrane protein 97 (TMEM97) is a conserved integral membrane protein highly expressed in various human cancers, including colorectal cancer (CRC), and it exhibits pro-tumor roles in breast cancer, gastric cancer, and glioma. However, whether TMEM97 participates in CRC progression is not fully understood. The expression of mRNA and protein was evaluated by real-time qPCR, western blotting, immunofluorescent, and immunohistochemical staining. TMEM97 functions in cell proliferation, apoptosis, migration, and invasion were assessed by CCK-8, flow cytometry, and transwell assays. The roles of TMEM97 in CRC cells in vivo was investigated using a subcutaneous xenograft model. The transcriptional regulation of TMEM97 was explored by luciferase reporter and ChIP assays. The silencing of TMEM97 inhibited migration and invasion of CRC cells in vitro and led to suppressed growth and enhanced apoptosis in CRC cells and xenografts, whereas overexpression of TMEM97 displayed opposite effects. Mechanistically, TMEM97 knockdown caused a reduction of the proliferating marker PCNA and an increase of pro-apoptotic proteins (cleaved caspase 8/3/7 and cleaved PARP) in CRC cells. TMEM97 also positively regulated the β-catenin signaling pathway in CRC cells and xenografts by modulating the phosphorylated-GSK-3β and active (non-phospho) β-catenin levels. Interestingly, YY1, a well-recognized oncogenic transcription factor, was identified to bind to the TMEM97 promoter and enhance its transcriptional activity, and silencing of TMEM97 abolished YY1-mediated pro-tumor effects on CRC cells. Our results suggest that TMEM97 is transcriptionally activated by YY1 and promotes CRC progression via the GSK-3β/β-catenin signaling pathway, providing that TMEM97 might be a novel therapeutic target for preventing CRC development.

Indexed as

beta CateninColorectal NeoplasmsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansMembrane ProteinsWnt Signaling PathwayYY1 Transcription Factorbeta CateninGlycogen Synthase Kinase 3 betaMembrane ProteinsTMEM97 protein, humanYY1 protein, humanYY1 Transcription FactorColorectal cancerTranscriptional regulationTransmembrane protein 97YY1 transcription factorβ-catenin signaling pathway

Identifiers

PMID35907137
OpenAlexW4288684483

What OpenQuestion holds

Textmetadata
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.