Evidence map›Paper›PMID 34730281›Full record

ArticleThoracic cancer2021

The promoter hypermethylation of SULT2B1 accelerates esophagus tumorigenesis via downregulated PER1.

Zhuo Li, Meng-Yan Li, Ling-Ling Wang, Lei Li, Qing-Yun Chen, Ying-Hui Zhu, Yan Li, Yan-Ru Qin, Xin-Yuan Guan

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2021. 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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Period 1 (Histology and histopathology · 2025
    Article
  2. Article
  3. Review
  4. Article
  5. Human sulfotransferaseFrontiers in genetics · 2024
    Review
  6. Review
  7. Corrigendum.Thoracic cancer · 2022
    Article
  8. The Advances in Epigenetics for Cancer Radiotherapy.International journal of molecular sciences · 2022
    Review
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Zhuo LiState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China.ORCID 0000-0001-6589-877X
Meng-Yan LiDepartment of Radiation Oncology, Guangzhou Concord Cancer Center, Guangzhou, China.
Ling-Ling WangDepartment of Oncology, Zhengzhou People's Hospital, Zhengzhou, China.
Lei LiState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Qing-Yun ChenDepartment of Medical Research, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Ying-Hui ZhuState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Yan LiState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Yan-Ru QinDepartment of Clinical Oncology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
Xin-Yuan GuanState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Sun Yat-sen University · CNFirst Affiliated Hospital of Zhengzhou University · CNGuangdong Academy of Medical Sciences · CNZhengzhou People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal cancer is currently the eighth most common tumor in the world and a leading cause of cancer death. SULT2B1 plays crucial roles in tumorigenesis. The purpose of this study is to explore the role of SULT2B1 in esophageal squamous cell carcinoma (ESCC).

methodsThe expression of SULT2B1 and its clinicopathological characteristics were evaluated in ESCC cohorts. Bisulfite genomic sequencing and methylation specific PCR were used to detect the promoter hypermethylation of the SULT2B1 gene. The effects of SULT2B1 on the biological characters of ESCC cells were identified on functional assays. Subcutaneous xenograft models revealed the role of SULT2B1 in vivo with tumor growth. RNA-Seq analysis and qRT-PCR were performed to recognize the targeted effect of SULT2B1 on PER1.

resultsSULT2B1 was not expressed or at a low level in most patients with ESCC or in ESCC cell lines, and this was accompanied by poor clinical prognosis. Furthermore, the downregulation of SULT2B1 occurred in promoter hypermethylation. According to the functional results, overexpression of SULT2B1 could inhibit tumoral proliferation in vitro and retard tumor growth in vivo, whereas SULT2B1 knockdown could accelerate ESCC progression. Mechanistically, SULT2B1 targeted PER1 at the mRNA level during post-transcriptional regulation. Finally, PER1 was verified as a suppressor and poor-prognosis factor in ESCC.

conclusionsSULT2B1 loss is a consequence owing to its ability to promote hypermethylation. In addition, it serves as a suppressor and poor-prognosis factor because of the post-transcriptional regulation of PER1 in ESCC.

Indexed as

AgedAnimalsCarcinogenesisCell Line, TumorCell ProliferationDNA MethylationDown-RegulationEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleHumansMaleMiceMice, Inbred BALB CMiddle AgedPeriod Circadian ProteinsPER1 protein, humanPer1 protein, mousePeriod Circadian ProteinsSulfotransferasesSULT2B1b protein, mouseSULT2B1 protein, humancircadian rhythmESCChypermethylationproliferationSULT2B1

Identifiers

PMID34730281
PMCPMC8671905
OpenAlexW3209991418

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.