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Hypoxia-Inducible Factor-1-Dependent Repression of <i>E-cadherin</i> in von Hippel-Lindau Tumor Suppressor–Null Renal Cell Carcinoma Mediated by TCF3, ZFHX1A, and ZFHX1B

2006· article· en· 408 citations· W2045181115 on OpenAlex· 10.1158/0008-5472.can-05-3719

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.

Machine scores (provisional)

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Opus teacher head0.024
GPT teacher head0.305
Teacher spread
0.280 · how far apart the two teachers sit on this one work
Validation status
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Abstract

A critical event in the pathogenesis of invasive and metastatic cancer is E-cadherin loss of function. Renal clear cell carcinoma (RCC) is characterized by loss of function of the von Hippel-Lindau tumor suppressor (VHL), which negatively regulates hypoxia-inducible factor-1 (HIF-1). Loss of E-cadherin expression and decreased cell-cell adhesion in VHL-null RCC4 cells were corrected by enforced expression of VHL, a dominant-negative HIF-1alpha mutant, or a short hairpin RNA directed against HIF-1alpha. In human RCC biopsies, expression of E-cadherin and HIF-1alpha was mutually exclusive. The expression of mRNAs encoding TCF3, ZFHX1A, and ZFHX1B, which repress E-cadherin gene transcription, was increased in VHL-null RCC4 cells in a HIF-1-dependent manner. Thus, HIF-1 contributes to the epithelial-mesenchymal transition in VHL-null RCC by indirect repression of E-cadherin.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

The record

Venue
Cancer Research
Topic
Cancer, Hypoxia, and Metabolism
Field
Biochemistry, Genetics and Molecular Biology
Canadian institutions
Funders
U.S. Public Health ServiceNational Cancer InstituteNational Institutes of HealthUniversity of PennsylvaniaYork UniversityJohns Hopkins University
Keywords
CadherinBiologyCancer researchNull cellSuppressorHypoxia-inducible factorsTumor suppressor geneSmall hairpin RNAPsychological repressionRenal cell carcinomaTranscription factorCellCancerGene expressionGenePathologyCarcinogenesisMedicineRNAGenetics
Has abstract in OpenAlex
yes