Evidence map›Paper›PMID 28482903›Full record

ArticleJournal of experimental & clinical cancer research : CR2017

Heat shock factor 1 inhibits the mitochondrial apoptosis pathway by regulating second mitochondria-derived activator of caspase to promote pancreatic tumorigenesis.

Wenjin Liang, Yong Liao, Jing Zhang, Qi Huang, Wei Luo, Jidong Yu, Jianhua Gong, Yi Zhou, Xuan Li, Bo Tang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. An HSF1-JMJD6-HSP feedback circuit promotes cell adaptation to proteotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. The EGFR-HSF1 axis accelerates the tumorigenesis of pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2021
    Article
  15. Review
  16. The Multifaceted Role of HSF1 in Tumorigenesis.Advances in experimental medicine and biology · 2020
    Review
  17. HSF1 as a Cancer Biomarker and Therapeutic Target.Current cancer drug targets · 2019
    Review
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Wenjin LiangDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Yong LiaoDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Jing ZhangDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Qi HuangDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Wei LuoDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Jidong YuDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Jianhua GongDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Yi ZhouDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Xuan LiDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China.
Bo TangDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China. dytangbo@163.com.
Songqing HeDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China. gl190679136@163.com.
Jinghong YangDepartment of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, 541004, Guangxi, People's Republic of China. yangjinghong64@163.com.
Guilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAs a relatively conservative transcriptional regulator in biological evolution, heat shock factor 1 (HSF1) is activated by, and regulates the expression of heat shock proteins (HSPs) in response to a variety of stress conditions. HSF1 also plays a key role in regulating the development of various tumors; however, its role in pancreatic cancer and the specific underlying mechanism are not clear.

methodsWe first examined HSF1 expression in pancreatic cancer tissues by immunohistochemistry, and then studied its clinical significance. We then constructed HSF1-siRNA to investigate the potential of HSF1 to regulate apoptosis, proliferation and the cell cycle of pancreatic cancer cells and the underlying mechanism both in vitro and in vivo. Protein chip analysis was used subsequently to explore the molecular regulation pathway. Finally, second mitochondria-derived activator of caspase (SMAC)-siRNA was used to validate the signaling pathway.

resultsHSF1 was highly expressed in pancreatic cancer tissues and the level of upregulation was found to be closely related to the degree of pancreatic cancer differentiation and poor prognosis. After HSF1-silencing, we found that pancreatic cancer cell proliferation decreased both in vitro and in vivo and the apoptotic cell ratio increased, while the mitochondrial membrane potential decreased, and the cells were arrested at the G0/G1 phase. In terms of the molecular mechanism, we confirmed that HSF1 regulated SMAC to inhibit mitochondrial apoptosis in pancreatic cancer cells, and to promote the occurrence of pancreatic tumors. SMAC silencing reversed the effects of HSF1 silencing.

conclusionOur study provides evidence that HSF1 functions as a novel oncogene in pancreatic tumors and is implicated as a target for the diagnosis and treatment of pancreatic cancer.

Indexed as

ApoptosisSignal TransductionAdultAgedAnimalsApoptosis Regulatory ProteinsCell CycleCell Line, TumorCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalFemaleGene ExpressionHeat Shock Transcription FactorsHeterograftsHumansApoptosis Regulatory ProteinsDIABLO protein, humanHeat Shock Transcription FactorsHSF1 protein, humanIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsApoptosisHeat shock factor 1Heat shock proteinsOncogenePancreatic cancerProliferationSMAC

Identifiers

PMID28482903
PMCPMC5422968
OpenAlexW2612492181

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.