Evidence map›Paper›PMID 35713314›Full record

ArticleActa biochimica et biophysica Sinica2022

TMEM106A transcriptionally regulated by promoter methylation is involved in invasion and metastasis of hepatocellular carcinoma.

Shiming Shi, Biao Wang, Jinglei Wan, Lina Song, Guiqi Zhu, Junxian Du, Luxi Ye, Qianqian Zhao, Jialiang Cai, Qing Chen and 4 more

Erratum issuedOpen access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Mechanistic Insights into Tumorigenesis from Serum Proteins.medRxiv : the preprint server for health sciences · 2025
    Article
  6. Article
  7. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Shiming ShiLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Biao WangLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Jinglei WanLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Lina SongLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Guiqi ZhuLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Junxian DuLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Luxi YeDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Qianqian ZhaoDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Jialiang CaiLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Qing ChenDepartment of General Surgery, Zhongshan Hospital (South), Fudan University, Shanghai Public Health Clinical Center, Fudan University, Shanghai 200083, China.
Kun XiaoLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Jian HeDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Lei YuLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Zhi DaiLiver Cancer Institute, Zhongshan Hospital, Fudan University & State Key Laboratory of Genetic Engineering, Fudan University, Shanghai 200032, China.
Fudan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression of transmembrane protein 106A (TMEM106A) has been reported to be dysregulated in several types of cancers. However, the role of TMEM106A in hepatocellular carcinoma (HCC) is still unknown. In the present study, we demonstrate that TMEM106A is markedly downregulated in HCC compared with normal liver tissue. In particular, tumor-specific DNA methylation of TMEM106A is frequently observed in tumor tissues from HCC patients. Immunohistochemistry and pyrosequencing reveal a significant relationship between TMEM106A methylation and downregulation of protein expression. Receiver operating characteristic (ROC) curve analysis reveals that methylation of TMEM106A in tumor samples is different from that in non-malignant adjacent tissues of HCC patients. Moreover, HCC patients with TMEM106A hypermethylation have a poor clinical prognosis. 5-Aza-2'-deoxycytidin treatment of hypermethylated TMEM106A in highly metastatic HCC cells increases the expression of TMEM106A. Functional assays reveal that overexpression of TMEM106A significantly suppresses the malignant behavior of HCC cells

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorCell MovementDNA MethylationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplasm Metastasisepithelial mesenchymal transitionhepatocellular carcinomametastasismethylationtransmembrane protein 106A

Identifiers

PMID35713314
PMCPMC9827947
OpenAlexW4281919051

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.