Evidence map›Paper›PMID 19154413›Full record

ArticleCancer science2009

Leptin induces functional activation of cyclooxygenase-2 through JAK2/STAT3, MAPK/ERK, and PI3K/AKT pathways in human endometrial cancer cells.

Jingchun Gao, Jianxin Tian, Yunyi Lv, Fangxin Shi, Fandou Kong, Hong Shi, Liyan Zhao

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.

  1. Pooled it
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  17. Review
  18. Review
  19. Role of Leptin and Adiponectin in Endometrial Cancer.International journal of molecular sciences · 2022
    Review
  20. Curcumol Attenuates Endometriosis by Inhibiting the JAK2/STAT3 Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Article

17 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

7 authors at 1 institution in 2 countries.

Jingchun GaoDepartment of Obstetrics and Gynecology, First Affiliated Hospital, Dalian Medical University, Dalian, Liaoning, China. jingchun_gao@yahoo.com
Jianxin Tian
Yunyi Lv
Fangxin Shi
Fandou Kong
Hong Shi
Liyan Zhao
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperleptinemia is a common feature of obese women who have a higher risk of endometrial cancer than women with normal weights, and epidemiologic studies have suggested a correlation between obesity and endometrial carcinoma. Therefore, understanding of the molecular mechanism involved in leptin signaling transduction is important in endometrial cancer prevention and treatment. In this study, both isoforms of the leptin receptor (Ob-R), the long form (Ob-Rb) and short form (Ob-Ra), were detected as being expressed in six endometrial cancer cell lines with various differentiation status by western blotting, and Ob-Ra was found to be more abundant than Ob-Rb in these cells. Moreover, the expressions of both isoforms were inversely correlated with histoprognostic grading. We also showed that leptin stimulated cell proliferation and induced activations of signal transducers and activators of transcription 3 (STAT3), extracellular signal-regulated kinase (ERK1/2), AKT, and cyclooxygenase (COX)-2 in endometrial cancer cells dose-dependently by [(3)H] thymidine incorporation assay and western blotting. Leptin-stimulation resulted in increased expression of COX-2 mRNA and prostaglandin E2 (PGE2) production of endometrial cancer cells by reverse transcription-polymerase chain reaction and enzyme immunoassay, respectively, which was effectively blocked by pharmacological inhibitors of Janus tyrosine kinase 2 (JAK2), AG490; of mitogen-activated protein kinase (MAPK) kinase, U0126; of phosphatidylinositol 3-kinase (PI3K), LY294002; and of COX-2, NS398. These results suggest that leptin promotes cell proliferation of endometrial cancer cells via the aforementioned multiple signal-transduction pathways. Leptin-induced functional activation of COX-2 is JAK2/STAT3-, MAPK/ERK-, and PI3K/AKT-dependent, indicating that COX-2 may be a critical factor of endometrial carcinogenesis in obesity.

Indexed as

Blotting, WesternCell Line, TumorCell ProliferationCyclooxygenase 2Endometrial NeoplasmsEnzyme ActivationFemaleHumansImmunoassayJanus Kinase 2LeptinMitogen-Activated Protein Kinase KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, LeptinReverse Transcriptase Polymerase Chain ReactionCyclooxygenase 2JAK2 protein, humanJanus Kinase 2LeptinMitogen-Activated Protein Kinase KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, LeptinSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID19154413
PMCPMC11158183
OpenAlexW2047140322

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.