Crosstalk from Adipocytokine signaling pathway to Estrogen signaling pathway

List of curated literature with evidence for crosstalk from Adipocytokine signaling pathway to Estrogen signaling pathway

  • Cellular and molecular crosstalk between leptin receptor and estrogen receptor-{alpha} in breast cancer: molecular basis for a novel therapeutic setting.

    • PubMed ID : 20410173
    • Molecule in Adipocytokine signaling pathway: LEPR
    • Species : Homo sapiens
    • Transcription : no
    • Sentence from paper : These observations support the notion that there is a general crosstalk between leptin and estrgoens that show widely overlapping effects in terms of metabolic and molecular actions.

  • Cellular and molecular crosstalk between leptin receptor and estrogen receptor-{alpha} in breast cancer: molecular basis for a novel therapeutic setting.

    • PubMed ID : 20410173
    • Molecule in Adipocytokine signaling pathway: LEP
    • Species : Homo sapiens
    • Transcription : no

    • Molecule in Estrogen signaling pathway: ESR1
    • Tissue : MCF-7 cell
    • Regulation type : Activating
    • Sentence from paper : on MCF 7 cells, rleptin induced a strong phosphorylation of the signal transducer and activator of transcription (STAT) 3 and of the extracellular related kinase 1/2 pathways with an increased cell viability and proliferation associated with an increased expression of ERalpha receptor

  • Leptin regulates estrogen receptor gene expression in ATDC5 cells through the extracellular signal regulated kinase signaling pathway.

    • PubMed ID : 22135239
    • Molecule in Adipocytokine signaling pathway: LEP
    • Species : Homo sapiens
    • Transcription : unknown

    • Molecule in Estrogen signaling pathway: ESR1
    • Tissue : chondrocyte
    • Regulation type : Activating
    • Sentence from paper : Binai et al. [2009] demonstrated that ERalpha stimulated the leptin-mediated STAT3 in the cytoplasm in breast cancer cells indpepndent of ERalpha ligands, underlying a srosstalk between leptin stimulation and ERalpha expression

  • Chronic leptin treatment sensitizes MCF-7 breast cancer cells to estrogen.

    • PubMed ID : 22178935
    • Molecule in Adipocytokine signaling pathway: LEP
    • Species : Homo sapiens
    • Transcription : unknown
    • Sentence from paper : The study supports the existence of a crosstalk between leptin and estrogen, in which leptin might play an important role potentiating ht mitogenic action o festrogen, probably by alteration of ERalpha to ERbeta ratio

  • Stage specific effect of leptin on the expressions of estrogen receptor and extracellular matrix in a model of chondrocyte differentiation.

    • PubMed ID : 23357303
    • Molecule in Adipocytokine signaling pathway: LEP
    • Species : Homo sapiens
    • Transcription : unknown
    • Sentence from paper : The crosstalk between leptin and estrogen resceptor was differentiation stage specific

Molecules mediating the crosstalk
Molecule in Adipocytokine signaling pathwayMolecule in Estrogen signaling pathwayTissueSpeciesPubMed Identifier
LEPRESR1breast cancer cellHomo sapiens20410173
LEPESR1MCF-7 cellHomo sapiens20410173
LEPESR1chondrocyteHomo sapiens22135239
LEPESR1/ESR2breast cancer cellHomo sapiens22178935
LEPESR1/ESR2chondrocyteHomo sapiens23357303

Note: "Unknown" indicates that the molecule has not been identified.

Note: We direct each interaction from the molecule in the first pathway to the molecule in the second pathway. The direction of the interaction does not imply that the first molecule regulates the second molecule or that they directly interact. Hence, the interactions in this network may be indirect and may not indicate any mechanism.

Attribute NameDescription
Pathway A

The name of the upstream (first) pathway in a pair of crosstalking pathways.

Pathway B

The name of the downstream (second) pathway in a pair of crosstalking pathways.

Pubmed Query

The string used as a structured query in PubMed that returned the recorded PMID as a result.

PMID

The PubMed identifier for the reported publication.
We recorded "NO_RESULTS_FOR_PUBMED_QUERY" as a dummy PMID when the PubMed query returned no results.

Crosstalk

yes, if Pathway A elicits a downstream transcriptional response in Pathway B.
no, otherwise.

Transcriptional

yes, if the crosstalk is transcriptional.
no, otherwise.

Regulation type

The downstream effect on Pathway B. This attribute can take one of the following two values:

  • Activating: Stimulation of Pathway A up-regulates a gene or activates a protein that is representative of Pathway B.
  • Inhibiting: Stimulation of Pathway A down-regulates a gene or inhibits a protein that is representative of Pathway B.
Molecule A*

The molecule in Pathway A responsible for mediating crosstalk to Pathway B.

Molecule A Identifier

Unique identifier for Molecule A in the namespace recorded in "Molecule A Source", e.g., the UniProt ID of a protein.

Molecule A Source

The name of database that the value in "Molecule A Identifier" comes from, e.g., "UniProt" if the molecule is a protein.

Molecule B*

The molecule in Pathway B responsible for mediating crosstalk from Pathway A.

Molecule B Identifier

Unique identifier for Molecule B in the namespace recorded in "Molecule B Source", e.g., the UniProt ID of a protein.

Molecule B Source

The name of database that the value in "Molecule B Identifier" comes from, e.g., "UniProt" if the molecule is a protein.

Species

The name of the species in which the crosstalk was observed.

Tissue

The name of the tissue or cell line in which the crosstalk was observed.

BTO ID

The BRENDA Tissue Ontology (BTO) Identifier of the tissue or cell line in which the crosstalk was observed.

Condition

Notes on the experimental condition in the publication.

Sentence from paper

The sentence in the publication supporting the crosstalk. We record a sentence only if it states that Pathway A increases or decreases Pathway B signaling. The sentence may also include information about the proteins or genes responsible for mediating the crosstalk.

Misleading evidence for crosstalk

A sentence in the paper that appears to support evidence for crosstalk when the study does not conclude there is crosstalk.

Additional notes

A curator's notes that may provide rationale for the values recorded for the attributes.

*This attribute may represent either an individual molecule or several molecules. We use the following syntax for this attribute.

  • colon (:): The molecules participate in the complex, e.g., SMAD3:SMAD4 in the case of crosstalk from the TGF-beta signaling pathway to the Hippo signaling pathway (the complex consisting of SMAD3 and SMAD4 mediates this crosstalk).
  • slash (/): Either of the molecules can mediate the crosstalk, e.g., YAP1/WWTR1 for the same pair of pathways (YAP1 or WWTR1 can mediate the crosstalk).
  • comma (,): All the molecules are required for the crosstalk but they do not form a complex, e.g., TSC2,RPTOR for the crosstalk from the MAPK signaling pathway to the mTOR signaling pathway (both TSC2 and RPTOR act as mediators).
  • brackets ([]): If we cannot identify the specific molecule, we record all molecules in the family, e.g., [TEAD1/TEAD2/TEAD3/TEAD4]. In this case, the publication only listed the protein TEAD as mediating the crosstalk (from the Hippo signaling pathway to the Wnt signaling pathway).