FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4307998944> ?p ?o ?g. }

• W4307998944 abstract "Epithelial-mesenchymal transition (EMT) is a reversible cellular program that transiently places epithelial (E) cells into pseudo-mesenchymal (M) cell states. The malignant progression and resistance of many types of carcinomas depends on EMT activation, partial EMT and hybrid E/M status in neoplastic cells. EMT is activated by tumor microenvironmental TGF&beta; signal and EMT-inducing transcription factors, such as ZEB1/2 in tumor cells. However, reverse EMT factors are less studied. We demonstrate that transcription factor SCAND1 can revert mesenchymal and hybrid E/M phenotype of cancer cells to a more epithelial, less invasive status and inhibit their proliferation and migration. SCAND1 is a SCAN domain-containing protein and hetero-oligomerizes with SCAN-zinc finger transcription factors, such as MZF1, for accessing DNA and transcriptional co-repression of target genes. We found that SCAND1-MZF1 co-expression and interaction correlated with maintaining epithelial features, whereas the simultaneous loss of SCAND1 and MZF1 correlated with mesenchymal features of tumor cells. Overexpression of SCAND1 over endogenous MZF1 in DU-145 prostate cancer cells reverted their hybrid E/M status into cobblestone morphology with increased epithelial adhesion by E-cadherin and &beta;-catenin relocation. Consistently, co-expression analysis in TCGA PanCancer Atlas revealed that both SCAND1 and MZF1 co-express and are negatively correlated with EMT driver genes, including CTNNB1, ZEB1, ZEB2 and TGFBR, in prostate tumor specimens. In addition, SCAND1 overexpression suppressed tumor cell proliferation by reducing the MAP3K-MEK-ERK signaling pathway. Of note, SCAND1-overexpressing DU-145 cells migrated slower than control cells with decreased lymph node metastasis of prostate cancer in a mouse tumor xenograft model. Kaplan-Meyer analysis showed high expression of MZF1 and SCAND1 to correlate with better prognoses in pancreatic cancer and head and neck cancers, although with poorer prognosis in kidney cancer. Overall, these data suggest that the combination of SCAND1-MZF1 complexes may revert the EMT mechanism in cancer to establish an epithelial phenotype. These effects seem to include co-repression of EMT-driver genes and suppression of tumor cell proliferation via inhibition of the MAP3K-MEK-ERK signaling pathway." @default.
• W4307998944 created "2022-11-07" @default.
• W4307998944 creator A5018799755 @default.
• W4307998944 creator A5023855553 @default.
• W4307998944 creator A5067098965 @default.
• W4307998944 creator A5075568199 @default.
• W4307998944 creator A5085873910 @default.
• W4307998944 date "2022-10-31" @default.
• W4307998944 modified "2023-10-01" @default.
• W4307998944 title "SCAND1 Reverts EMT and Suppresses Tumor Growth and Collective Migration" @default.
• W4307998944 doi "https://doi.org/10.20944/preprints202210.0475.v1" @default.
• W4307998944 hasPublicationYear "2022" @default.
• W4307998944 type Work @default.
• W4307998944 citedByCount "0" @default.
• W4307998944 crossrefType "posted-content" @default.
• W4307998944 hasAuthorship W4307998944A5018799755 @default.
• W4307998944 hasAuthorship W4307998944A5023855553 @default.
• W4307998944 hasAuthorship W4307998944A5067098965 @default.
• W4307998944 hasAuthorship W4307998944A5075568199 @default.
• W4307998944 hasAuthorship W4307998944A5085873910 @default.
• W4307998944 hasBestOaLocation W43079989441 @default.
• W4307998944 hasConcept C104317684 @default.
• W4307998944 hasConcept C121608353 @default.
• W4307998944 hasConcept C137738243 @default.
• W4307998944 hasConcept C1491633281 @default.
• W4307998944 hasConcept C198826908 @default.
• W4307998944 hasConcept C2779013556 @default.
• W4307998944 hasConcept C2779256057 @default.
• W4307998944 hasConcept C502942594 @default.
• W4307998944 hasConcept C54355233 @default.
• W4307998944 hasConcept C62112901 @default.
• W4307998944 hasConcept C76419328 @default.
• W4307998944 hasConcept C86339819 @default.
• W4307998944 hasConcept C86803240 @default.
• W4307998944 hasConcept C95444343 @default.
• W4307998944 hasConceptScore W4307998944C104317684 @default.
• W4307998944 hasConceptScore W4307998944C121608353 @default.
• W4307998944 hasConceptScore W4307998944C137738243 @default.
• W4307998944 hasConceptScore W4307998944C1491633281 @default.
• W4307998944 hasConceptScore W4307998944C198826908 @default.
• W4307998944 hasConceptScore W4307998944C2779013556 @default.
• W4307998944 hasConceptScore W4307998944C2779256057 @default.
• W4307998944 hasConceptScore W4307998944C502942594 @default.
• W4307998944 hasConceptScore W4307998944C54355233 @default.
• W4307998944 hasConceptScore W4307998944C62112901 @default.
• W4307998944 hasConceptScore W4307998944C76419328 @default.
• W4307998944 hasConceptScore W4307998944C86339819 @default.
• W4307998944 hasConceptScore W4307998944C86803240 @default.
• W4307998944 hasConceptScore W4307998944C95444343 @default.
• W4307998944 hasLocation W43079989441 @default.
• W4307998944 hasOpenAccess W4307998944 @default.
• W4307998944 hasPrimaryLocation W43079989441 @default.
• W4307998944 hasRelatedWork W2072529897 @default.
• W4307998944 hasRelatedWork W2235698069 @default.
• W4307998944 hasRelatedWork W2766649156 @default.
• W4307998944 hasRelatedWork W2936134572 @default.
• W4307998944 hasRelatedWork W2937327588 @default.
• W4307998944 hasRelatedWork W2953462016 @default.
• W4307998944 hasRelatedWork W2999831276 @default.
• W4307998944 hasRelatedWork W3125309376 @default.
• W4307998944 hasRelatedWork W4288859386 @default.
• W4307998944 hasRelatedWork W2461652051 @default.
• W4307998944 isParatext "false" @default.
• W4307998944 isRetracted "false" @default.
• W4307998944 workType "article" @default.