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RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE216382 | GEO | 2025/10/21

REPOSITORIES: GEO

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RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [shRNA]

Project description:Constitutive activation of Wnt/β-catenin signaling drives tumor initiation, maintenance, and metastasis in numerous preclinical models. Within the nucleus, β-catenin interacts with transcription factors of the TCF/LEF (T cell factor/lymphoid enhancer factor, TCFs) family. The transcriptional program mediated by these β-catenin/TCF interactions promotes cell proliferation, epithelial-mesenchymal transition (EMT), and a cancer stem-cell phenotype. COLO320DM is a human colorectal cancer line with an activated Wnt/ β-catenin pathway driven by an APC mutation. Here, we apply a doxycycline-inducible shRNA to knockdown (KD) CTNNB1 (encoding β-catenin) and study the impact on the global transcriptome of COLO320DM. We also design and express an shRNA-resistant rescue cDNA to rule out any potential off-target effect. The results reveal a global gene expression change upon CTNNB1-KD that is consistent with β-catenin’s role in serving as a signal hub downstream of the canonical Wnt pathway.

2025-10-21 | GSE216381 | GEO

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [PDX]

2025-10-21 | GSE228260 | GEO

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [in vivo]

2025-10-21 | GSE216380 | GEO

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [in vitro]

Project description:Genetic and epigenetic alterations in the Wnt signaling pathway leading to constitutive activation of the driver oncogene β-catenin occur in at least 20% of all human cancers. Pharmacologic suppression of aberrant β-catenin transcriptional activity through direct targeting of its downstream effectors has proven elusive despite decades of effort. We developed conformationally hyperstabilized α-helical peptides – which we refer to as Helicons – that directly bind β-catenin with sub-nanomolar affinity and exhibit good cytosolic exposure. COLO320DM is a human colorectal cancer line with an activated Wnt/ β-catenin pathway driven by an APC mutation. Here, we characterize the global effects of Helicon treatment on COLO320DM cells in vitro by whole-transcriptome RNA sequencing. As expected, Helicon 4 treatment had both time- and dose-dependent effects on the COLO320DM transcriptional profile. In particular, the Hallmark Wnt/β-catenin gene set was significantly down-regulated as early as six-hour at 10uM. The result validates the on-target inhibition of β-catenin signaling through disruption of its interaction with TCF/LEF transcription factors by active Helicons. COLO320DM is a human colorectal cancer line with an activated Wnt/ β-catenin pathway driven by an APC mutation. Here, we characterized the global effects of Helicon treatment on COLO320DM cells in vitro by whole-transcriptome RNA sequencing. As expected, Helicon 4 treatment had both time- and dose-dependent effects on the COLO320DM transcriptional profile. In particular, the Hallmark Wnt/β-catenin gene set was significantly down-regulated in as early as six -hours at 10 μuM. The result validates the on-target inhibition of β-catenin signaling through disruption of its interaction with TCF/LEF transcription factors by active Helicons.

2025-10-21 | GSE216379 | GEO

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor

Project description:RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor

| PRJNA893369 | ENA

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [PDX]

Project description:RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [PDX]

| PRJNA949163 | ENA

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [shRNA]

Project description:RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [shRNA]

| PRJNA893372 | ENA

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [in vivo]

Project description:RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [in vivo]

| PRJNA893371 | ENA

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [in vitro]

Project description:RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [in vitro]

| PRJNA893370 | ENA

The intestine-specific transcription factor Cdx2 inhibits beta-catenin/TCF transcriptional activity by disrupting the beta-catenin-TCF protein complex.

Project description:Cdx2 is an intestine-specific transcription factor known to regulate proliferation and differentiation. We have reported previously that Cdx2 limits the proliferation of human colon cancer cells by inhibiting the transcriptional activity of the beta-catenin-T-cell factor (TCF) bipartite complex. Herein we further elucidate this mechanism. Studies with a classic Cdx2 target gene and a canonical Wnt/beta-catenin/TCF reporter suggest that Cdx2 regulates these promoters by distinctly different processes. Specifically, inhibition of beta-catenin/TCF activity by Cdx2 does not require Cdx2 transcriptional activity. Instead, Cdx2 binds beta-catenin and disrupts its interaction with the DNA-binding TCF factors, thereby silencing beta-catenin/TCF target gene expression. Using Cdx2 mutants, we map the Cdx2 domains required for the inhibition of beta-catenin/TCF activity. We identify a subdomain in the N-terminus that is highly conserved and when mutated significantly reduces Cdx2 inhibition of beta-catenin/TCF transcriptional activity. Mutation of this subdomain also abrogates Cdx2's anti-proliferative effects in colon cancer cells. In summary, we conclude that Cdx2 binds beta-catenin and disrupts the beta-catenin-TCF complex. Considering the pivotal role of beta-catenin/TCF activity in driving proliferation of normal intestinal epithelial and colon cancer cells, our findings suggest a novel mechanism for Cdx2-mediated regulation of Wnt/beta-catenin signaling and cell proliferation.

| S-EPMC2812568 | biostudies-literature

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