FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2076665002> ?p ?o ?g. }

• W2076665002 endingPage "S202" @default.
• W2076665002 startingPage "S202" @default.
• W2076665002 abstract "ObjectiveAromatase inhibitors (AIs) have become the mainstay of the endocrine treatment of postmenopausal breast cancer and we have identified SUSD3 to be down-regulated in AI non-responsive patients. We previously demonstrated a direct regulatory role of ERα in SUSD3 expression with localization of SUSD3 to the outer cellular membrane. We hypothesized a possible role of SUSD3 in breast cancer cell-to-cell adhesion and/or migration.DesignBasic science research.Materials and MethodsMCF7 breast cancer cells were transfected with siRNA targeting SUSD3 or a control siRNA. Morphological changes were documented by phase contrast microscopy 48 and 72 hours post-transfection. Western blot analyses for focal adhesion kinase (FAK), Src, and phosphorylated paxillin (p-Pax) were performed after 72 hr of siRNA transfection. Wound healing, dispase, and aggregation assays were performed after 72hr siRNA transfections and results were documented by phase contrast microscopy.ResultsMorphological changes, including decreased presence of lamellipodia and filopodia, were observed in SUSD3 knockdown cells as compared to control at 48 hours. FAK and p-Pax protein levels were increased in SUSD3 knockdown cells as compared to control. Wound healing experiments revealed decreased motility (measured as % wound open) in SUSD3 knockdown cells (95% ± 4%) as compared to control (56% ± 4%). Dispase and aggregation assays revealed decreased cell-to-cell adhesion strength in SUSD3 knockdown cells compared to control.ConclusionIn conclusion, SUSD3 protein appears to play a role in breast cancer cell function as loss leads to decreased motility and adhesion. SUSD3 may be a key functional protein in the metastatic pathway and may prove to be a possible therapeutic target in breast cancer. ObjectiveAromatase inhibitors (AIs) have become the mainstay of the endocrine treatment of postmenopausal breast cancer and we have identified SUSD3 to be down-regulated in AI non-responsive patients. We previously demonstrated a direct regulatory role of ERα in SUSD3 expression with localization of SUSD3 to the outer cellular membrane. We hypothesized a possible role of SUSD3 in breast cancer cell-to-cell adhesion and/or migration. Aromatase inhibitors (AIs) have become the mainstay of the endocrine treatment of postmenopausal breast cancer and we have identified SUSD3 to be down-regulated in AI non-responsive patients. We previously demonstrated a direct regulatory role of ERα in SUSD3 expression with localization of SUSD3 to the outer cellular membrane. We hypothesized a possible role of SUSD3 in breast cancer cell-to-cell adhesion and/or migration. DesignBasic science research. Basic science research. Materials and MethodsMCF7 breast cancer cells were transfected with siRNA targeting SUSD3 or a control siRNA. Morphological changes were documented by phase contrast microscopy 48 and 72 hours post-transfection. Western blot analyses for focal adhesion kinase (FAK), Src, and phosphorylated paxillin (p-Pax) were performed after 72 hr of siRNA transfection. Wound healing, dispase, and aggregation assays were performed after 72hr siRNA transfections and results were documented by phase contrast microscopy. MCF7 breast cancer cells were transfected with siRNA targeting SUSD3 or a control siRNA. Morphological changes were documented by phase contrast microscopy 48 and 72 hours post-transfection. Western blot analyses for focal adhesion kinase (FAK), Src, and phosphorylated paxillin (p-Pax) were performed after 72 hr of siRNA transfection. Wound healing, dispase, and aggregation assays were performed after 72hr siRNA transfections and results were documented by phase contrast microscopy. ResultsMorphological changes, including decreased presence of lamellipodia and filopodia, were observed in SUSD3 knockdown cells as compared to control at 48 hours. FAK and p-Pax protein levels were increased in SUSD3 knockdown cells as compared to control. Wound healing experiments revealed decreased motility (measured as % wound open) in SUSD3 knockdown cells (95% ± 4%) as compared to control (56% ± 4%). Dispase and aggregation assays revealed decreased cell-to-cell adhesion strength in SUSD3 knockdown cells compared to control. Morphological changes, including decreased presence of lamellipodia and filopodia, were observed in SUSD3 knockdown cells as compared to control at 48 hours. FAK and p-Pax protein levels were increased in SUSD3 knockdown cells as compared to control. Wound healing experiments revealed decreased motility (measured as % wound open) in SUSD3 knockdown cells (95% ± 4%) as compared to control (56% ± 4%). Dispase and aggregation assays revealed decreased cell-to-cell adhesion strength in SUSD3 knockdown cells compared to control. ConclusionIn conclusion, SUSD3 protein appears to play a role in breast cancer cell function as loss leads to decreased motility and adhesion. SUSD3 may be a key functional protein in the metastatic pathway and may prove to be a possible therapeutic target in breast cancer. In conclusion, SUSD3 protein appears to play a role in breast cancer cell function as loss leads to decreased motility and adhesion. SUSD3 may be a key functional protein in the metastatic pathway and may prove to be a possible therapeutic target in breast cancer." @default.
• W2076665002 created "2016-06-24" @default.
• W2076665002 creator A5002748459 @default.
• W2076665002 creator A5009298625 @default.
• W2076665002 creator A5040841777 @default.
• W2076665002 creator A5055584136 @default.
• W2076665002 date "2011-09-01" @default.
• W2076665002 modified "2023-09-25" @default.
• W2076665002 title "Sushi domain containing 3 (SUSD3) and its role in breast cancer cell morphology, migration, and adhesion" @default.
• W2076665002 doi "https://doi.org/10.1016/j.fertnstert.2011.07.783" @default.
• W2076665002 hasPublicationYear "2011" @default.
• W2076665002 type Work @default.
• W2076665002 sameAs 2076665002 @default.
• W2076665002 citedByCount "0" @default.
• W2076665002 crossrefType "journal-article" @default.
• W2076665002 hasAuthorship W2076665002A5002748459 @default.
• W2076665002 hasAuthorship W2076665002A5009298625 @default.
• W2076665002 hasAuthorship W2076665002A5040841777 @default.
• W2076665002 hasAuthorship W2076665002A5055584136 @default.
• W2076665002 hasBestOaLocation W20766650021 @default.
• W2076665002 hasConcept C109185818 @default.
• W2076665002 hasConcept C125705527 @default.
• W2076665002 hasConcept C137738243 @default.
• W2076665002 hasConcept C1491633281 @default.
• W2076665002 hasConcept C151166631 @default.
• W2076665002 hasConcept C153911025 @default.
• W2076665002 hasConcept C173396325 @default.
• W2076665002 hasConcept C185592680 @default.
• W2076665002 hasConcept C190283241 @default.
• W2076665002 hasConcept C502942594 @default.
• W2076665002 hasConcept C54009773 @default.
• W2076665002 hasConcept C54355233 @default.
• W2076665002 hasConcept C55493867 @default.
• W2076665002 hasConcept C58207958 @default.
• W2076665002 hasConcept C62478195 @default.
• W2076665002 hasConcept C81885089 @default.
• W2076665002 hasConcept C85789140 @default.
• W2076665002 hasConcept C86803240 @default.
• W2076665002 hasConcept C90301020 @default.
• W2076665002 hasConcept C95444343 @default.
• W2076665002 hasConceptScore W2076665002C109185818 @default.
• W2076665002 hasConceptScore W2076665002C125705527 @default.
• W2076665002 hasConceptScore W2076665002C137738243 @default.
• W2076665002 hasConceptScore W2076665002C1491633281 @default.
• W2076665002 hasConceptScore W2076665002C151166631 @default.
• W2076665002 hasConceptScore W2076665002C153911025 @default.
• W2076665002 hasConceptScore W2076665002C173396325 @default.
• W2076665002 hasConceptScore W2076665002C185592680 @default.
• W2076665002 hasConceptScore W2076665002C190283241 @default.
• W2076665002 hasConceptScore W2076665002C502942594 @default.
• W2076665002 hasConceptScore W2076665002C54009773 @default.
• W2076665002 hasConceptScore W2076665002C54355233 @default.
• W2076665002 hasConceptScore W2076665002C55493867 @default.
• W2076665002 hasConceptScore W2076665002C58207958 @default.
• W2076665002 hasConceptScore W2076665002C62478195 @default.
• W2076665002 hasConceptScore W2076665002C81885089 @default.
• W2076665002 hasConceptScore W2076665002C85789140 @default.
• W2076665002 hasConceptScore W2076665002C86803240 @default.
• W2076665002 hasConceptScore W2076665002C90301020 @default.
• W2076665002 hasConceptScore W2076665002C95444343 @default.
• W2076665002 hasIssue "3" @default.
• W2076665002 hasLocation W20766650021 @default.
• W2076665002 hasOpenAccess W2076665002 @default.
• W2076665002 hasPrimaryLocation W20766650021 @default.
• W2076665002 hasRelatedWork W2009671568 @default.
• W2076665002 hasRelatedWork W2069750158 @default.
• W2076665002 hasRelatedWork W2074251746 @default.
• W2076665002 hasRelatedWork W2084295528 @default.
• W2076665002 hasRelatedWork W2096180149 @default.
• W2076665002 hasRelatedWork W2165525793 @default.
• W2076665002 hasRelatedWork W2406152738 @default.
• W2076665002 hasRelatedWork W2415657002 @default.
• W2076665002 hasRelatedWork W3000225783 @default.
• W2076665002 hasRelatedWork W3012980842 @default.
• W2076665002 hasVolume "96" @default.
• W2076665002 isParatext "false" @default.
• W2076665002 isRetracted "false" @default.
• W2076665002 magId "2076665002" @default.
• W2076665002 workType "article" @default.