Evidence map›Paper›PMID 27326259›Full record

ArticleJournal of Cancer2016

Downregulation of Ubiquitin-conjugating Enzyme UBE2D3 Promotes Telomere Maintenance and Radioresistance of Eca-109 Human Esophageal Carcinoma Cells.

Hui Yang, Lin Wu, Shaobo Ke, Wenbo Wang, Lei Yang, Xiaojia Gao, Hongyan Fang, Haijun Yu, Yahua Zhong, Conghua Xie and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Systematic analysis ofTranslational andrology and urology · 2026
    Article
  2. Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Identification of HPV16-p16Epigenetics · 2021
    Article
  7. Review
  8. Article
  9. Article
  10. Role of TMPRSS4 Modulation in Breast Cancer Cell Proliferation.Asian Pacific journal of cancer prevention : APJCP · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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

12 authors at 3 institutions in 1 country.

Hui Yang1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;
Lin Wu1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;; 3. Department of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Shaobo Ke1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;
Wenbo Wang1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;; 2. Department of Radiation Oncology & Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan, China;
Lei Yang1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;; 2. Department of Radiation Oncology & Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan, China;
Xiaojia Gao1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;
Hongyan Fang1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;
Haijun Yu1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;; 2. Department of Radiation Oncology & Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan, China;
Yahua Zhong1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;; 2. Department of Radiation Oncology & Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan, China;
Conghua Xie1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;; 2. Department of Radiation Oncology & Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan, China;
Fuxiang Zhou1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;; 2. Department of Radiation Oncology & Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan, China;
Yunfeng Zhou1. Hubei Key Laboratory of Tumor Biological Behavior, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, China;; 2. Department of Radiation Oncology & Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan, China;
Zhongnan Hospital of Wuhan University · CNWuhan University · CNHubei Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitin-conjugating enzyme UBE2D3 is an important member of the ubiquitin-proteasome pathways. Our previous study showed that the expression of UBE2D3 was negatively related to human telomerase reverse transcriptase (hTERT) and radioresistance in human breast cancer cells. However, in esophageal carcinoma, the exact effects and mechanisms of UBE2D3 in radioresistance remain unclear. This study shows that UBE2D3 knockdown was associated with significant increases in radioresistance to X-rays, telomerase activity, telomere length, and telomere shelterins. UBE2D3 knockdown-mediated radioresistance was related to a decrease in the spontaneous and ionizing radiation-induced apoptosis, resulting from a decrease in the Bax/Bcl-2 ratio. Furthermore, UBE2D3 downregulation was associated with increased G1-S phase transition and prolonged IR-induced G2/M arrest through over expression of cyclin D1, decrease of CDC25A expression and promotion of the ATM/ATR-Chk1-CDC25C pathway. Moreover, UBE2D3 downregulation reduced spontaneous DNA double-strand breaks and accelerated the repair of DNA damage induced by IR. The current data thus demonstrate that UBE2D3 downregulation enhances radioresistance by increased telomere homeostasis and prolonged IR-induced G2/M arrest, but decreases the IR-induced apoptosis and the number of DNA damage foci. These results suggest that UBE2D3 might be a potential molecular target to improve radiotherapy effects in esophageal carcinoma.

Indexed as

DNA damage repair.esophageal carcinomaradioresistancetelomere maintenanceUBE2D3

Identifiers

PMID27326259
PMCPMC4911883
OpenAlexW2420408268

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.