Crosstalk from Estrogen signaling pathway to Hedgehog signaling pathway
Oestrogen receptor-alpha contributes to the regulation of the hedgehog signalling pathway in ERalpha-positive gastric cancer.
- Sentence from paper : One finding is that the ERα pathway affects the Hh pathway, because E2 induces both ERα pathway activation and Shh induction, followed by Hh pathway activation, and all of these phenomena were almost completely suppressed by blockade of the ERα pathway
Estrogen receptor α and hedgehog signal pathway developmental biology of gastric adenocarcinoma.
- PubMed ID : 22281977
- Molecule in Estrogen signaling pathway: unknown
- Species : Homo sapiens
- Transcription : no
- Molecule in Hedgehog signaling pathway: unknown
- Tissue : stomach
- Regulation type : Unknown
- Sentence from paper : During development and oncogenesis, Hh and ERalpha pathways can directly regulate key components of each other
Oestrogen receptor-alpha regulates non-canonical Hedgehog-signalling in the mammary gland.
- Sentence from paper : Our data also showed that stimulation by N-Shh of primary mammary epithelial cells activated Erk1/2 in both an ERα and c-src-dependent manner
Estrogen promotes stemness and invasiveness of ER-positive breast cancer cells through Gli1 activation.
- PubMed ID : 24889938
- Molecule in Estrogen signaling pathway: estrogen
- Species : Homo sapiens
- Transcription : yes
- Sentence from paper : We found that estrogen induced transcriptional activation of Gli1 through enriching ER occupancy at the Gli1 gene promoter and gene body
Combination of cyclopamine and tamoxifen promotes survival and migration of mcf-7 breast cancer cells--interaction of hedgehog-gli and estrogen receptor signaling pathways.
- Sentence from paper : It was shown that upregulation of ERα by E2 also upregulated Shh which canonically activated Hh-Gli signaling and Gli1 expression in human breast cancer cells
|Molecule in Estrogen signaling pathway||Molecule in Hedgehog signaling pathway||Tissue||Species||PubMed Identifier|
|Esr1||Shh||mesenchymal cell||Mus musculus||24769368|
|estrogen||GLI1||breast cancer cell, cancer stem cell||Homo sapiens||24889938|
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.
XTalkDB does not contain any molecules mediating the crosstalk.
The name of the upstream (first) pathway in a pair of crosstalking pathways.
The name of the downstream (second) pathway in a pair of crosstalking pathways.
The string used as a structured query in PubMed that returned the recorded PMID as a result.
The PubMed identifier for the reported publication.
yes, if Pathway A elicits a downstream transcriptional response in Pathway B.
yes, if the crosstalk is transcriptional.
The downstream effect on Pathway B. This attribute can take one of the following two values:
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.
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.
The name of the species in which the crosstalk was observed.
The name of the tissue or cell line in which the crosstalk was observed.
The BRENDA Tissue Ontology (BTO) Identifier of the tissue or cell line in which the crosstalk was observed.
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.
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).