Evidence map›Paper›PMID 19211554›Full record

ArticleThe Journal of biological chemistry2009

BCL-xL is a target gene regulated by hypoxia-inducible factor-1{alpha}.

Ni Chen, Xueqin Chen, Rui Huang, Hao Zeng, Jing Gong, Wentong Meng, Yiping Lu, Fang Zhao, Lin Wang, Qiao Zhou

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.

  1. Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
  2. Article
  3. Article
  4. Article
  5. BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. circEZH2Cancer science · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Review

35 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 3 countries.

Ni ChenLaboratory of Pathology, Departments of Pathology and Urology, and Laboratory of Stem Cell Research, State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, Chengdu, China 610041.
Xueqin Chen
Rui Huang
Hao Zeng
Jing Gong
Wentong Meng
Yiping Lu
Fang Zhao
Lin Wang
Qiao Zhou
State Key Laboratory of BiotherapySichuan University · CNThe University of Texas MD Anderson Cancer Center · USUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha) plays pivotal roles in physiology and pathophysiology. Constitutive or hypoxia-induced HIF-1alpha overexpression is observed in many types of cancers including prostate adenocarcinoma, in which it is associated with resistance to apoptosis and therapeutic agents. BCL-xL, a hypoxia-responsive, anti-apoptotic protein of the Bcl-2 family, is also overexpressed in prostate carcinoma and many other cancers. Despite this connection, whether BCL-xL expression is directly regulated by HIF-1alpha is not known. We used prostate cancer PC-3 cell with constitutive high HIF-1alpha level as a model to address this important question. We first generated prostate cancer PC-3 cells in which HIF-1alpha was stably knocked-down (HIF-KD) by using small interference RNA. BCL-xL was dramatically decreased in HIF-KD PC-3 cells, in parallel with sensitization to apoptosis with caspase-3 activation as well as decreased cell proliferation. We then demonstrated that HIF-1alpha directly regulated BCL-xL transcription by binding to a hypoxia-responsive element in the BCL-xL promoter (-865 to -847) by reporter gene assay, chromatin immunoprecipitation, and electrophoretic mobility shift and supershift assays. HIF-1alpha-dependent BCL-xL overexpression may be an important mechanism by which HIF-1alpha protects prostate cancer cells from apoptosis and leads to treatment resistance.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBase Sequencebcl-X ProteinCaspase 3Cell Line, TumorCell ProliferationEnzyme ActivationHumansHypoxia-Inducible Factor 1MaleMolecular Sequence DataProstatic NeoplasmsRNA, Small InterferingSequence Homology, Nucleic Acidbcl-X ProteinCaspase 3Hypoxia-Inducible Factor 1RNA, Small Interfering

Identifiers

PMID19211554
PMCPMC2665055
OpenAlexW1976066269

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.