Evidence map›Paper›PMID 34975151›Full record

ArticleOncogene2022

FGD3 binds with HSF4 to suppress p65 expression and inhibit pancreatic cancer progression.

Feng Guo, Xiang Cheng, Boping Jing, Heshui Wu, Xin Jin

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
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  4. RELA Ablation Contributes to Progression of Hepatocellular Carcinoma with TP53Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Article
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  7. Extracellular matrix stiffness regulates colorectal cancer progression via HSF4.Journal of experimental & clinical cancer research : CR · 2025
    Article
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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 3 institutions in 1 country.

Feng GuoDepartment of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.ORCID http://orcid.org/0000-0003-0882-5296
Xiang ChengCancer center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Boping JingDepartment of Ultrasound, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430022, P.R. China.
Heshui WuDepartment of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Heshuiwu@hust.edu.cn.ORCID http://orcid.org/0000-0002-2268-7275
Xin JinDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. jinxinxy2@csu.edu.cn.ORCID http://orcid.org/0000-0001-6461-6005
Union Hospital · CNCentral South University · CNWuhan Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is regarded as the most lethal solid tumor worldwide. Deregulated and constitutively activated NF-κB signaling is one of the major characteristics of pancreatic cancer. The total expression level and subcellular localization of RelA/p65 have been shown to determine the activation of canonical NF-κB signaling in pancreatic cancer. FGD3, which is involved in regulating the actin cytoskeleton and cell shape, has been reported to inhibit cancer cell migration and predict a favorable prognosis in multiple types of cancer. However, the specific role of FGD3 in pancreatic cancer is still unknown. In this study, we conducted a systematic investigation of the cancer-related role of FGD3 in pancreatic cancer. We demonstrated that FGD3 was abnormally downregulated in pancreatic cancer tissues and that low expression of FGD3 was associated with unfavorable prognosis in patients with pancreatic cancer. Then, we showed that FGD3 inhibited pancreatic cancer cell proliferation, invasion and metastasis in vivo and in vitro. Moreover, we revealed that FGD3 silencing activated the NF-κB signaling pathway by promoting HSF4 nuclear translocation and increasing p65 expression in pancreatic cancer cells. Therefore, our results identified a novel and targetable FGD3/HSF4/p65 signaling axis in pancreatic cancer cells.

Indexed as

Cell ProliferationPancreatic NeoplasmsTranscription Factor RelAAnimalsCell Line, TumorCell MovementDisease ProgressionFemaleGene Expression Regulation, NeoplasticHeat Shock Transcription FactorsHumansMaleMiceMice, NudePrognosisSignal TransductionHeat Shock Transcription FactorsRELA protein, humanTranscription Factor RelATranscription Factors

Identifiers

PMID34975151
OpenAlexW4206020093

What Socratic 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 Socratic graph.