Evidence map›Paper›PMID 24618835›Full record

ArticlePloS one2014

Calycosin suppresses breast cancer cell growth via ERβ-dependent regulation of IGF-1R, p38 MAPK and PI3K/Akt pathways.

Jian Chen, Ruanling Hou, Xing Zhang, Yu Ye, Yong Wang, Jing Tian

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
9.6field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Biomolecules · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Pharmaceutical Values of Calycosin: One Type of Flavonoid Isolated fromEvidence-based complementary and alternative medicine : eCAM · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Induction of ApoptosisJournal of cancer prevention · 2019
    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

6 authors at 3 institutions in 1 country.

Jian ChenSchool of Basic Medical Sciences, Guilin Medical University, Guilin, China.
Ruanling HouDepartment of Physiology and Neurobiology, Xinxiang Medical University, Xinxiang, China.
Xing ZhangSchool of Basic Medical Sciences, Guilin Medical University, Guilin, China.
Yu YeDepartment of Emergency, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Yong WangDepartment of Physiology, School of Basic Medical Sciences, Guilin Medical University, Guilin, China.
Jing TianDepartment of Physiology, School of Basic Medical Sciences, Guilin Medical University, Guilin, China.
Guilin Medical University · CNFirst Affiliated Hospital of GuangXi Medical University · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that calycosin, a natural phytoestrogen structurally similar to estrogen, successfully triggered apoptosis of estrogen receptor (ER)-positive breast cancer cell line, MCF-7. To better understand the antitumor activities of calycosin against breast cancer, besides MCF-7 cells, another ER-positive cell line T-47D was analyzed here, with ER-negative cell lines (MDA-231, MDA-435) as control. Notably, calycosin led to inhibited cell proliferation and apoptosis only in ER-positive cells, particularly in MCF-7 cells, whereas no such effect was observed in ER-negative cells. Then we investigated whether regulation of ERβ, a subtype of ER, contributed to calycosin-induced apoptosis in breast cancer cells. The results showed that incubation of calycosin resulted in enhanced expression ERβ in MCF-7 and T-47D cells, rather than MDA-231 and MDA-435 cells. Moreover, with the upregulation of ERβ, successive changes in downstream signaling pathways were found, including inactivation of insulin-like growth factor 1 receptor (IGF-1R), then stimulation of p38 MAPK and suppression of the serine/threonine kinase (Akt), and finally poly(ADP-ribose) polymerase 1 (PARP-1) cleavage. However, the other two members of the mitogen-activated protein kinase (MAPK) family, extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK), were not consequently regulated by downregulated IGF-1R, indicating ERK 1/2 and JNK pathways were not necessary to allow proliferation inhibition by calycosin. Taken together, our results indicate that calycosin tends to inhibit growth and induce apoptosis in ER-positive breast cancer cells, which is mediated by ERβ-induced inhibition of IGF-1R, along with the selective regulation of MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt pathways.

Indexed as

Breast NeoplasmsCell DeathCell Line, TumorCell ProliferationDose-Response Relationship, DrugEstrogen Receptor betaFemaleGene Expression Regulation, NeoplasticHumansIsoflavonesMCF-7 Cellsp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-akt7,3'-dihydroxy-4'-methoxyisoflavoneEstrogen Receptor betaIsoflavonesp38 Mitogen-Activated Protein KinasesPARP1 protein, humanPhosphatidylinositol 3-KinasesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-aktReceptor, IGF Type 1

Identifiers

PMID24618835
PMCPMC3949755
OpenAlexW2039026538

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.