CDH3 (Cadherin 3)

Mechanistically, ARHGAP36, through the arginine-rich domain at the N-terminal, binds to β-catenin to stabilize P-cadherin expression in a way accompanying with, and mutually exclusive from, its interaction with PKAc to activate RhoA signaling. Thus, this study unveiled a heretofore unrecognized coordination mechanism for entosis, where ARHGAP36 engages both adherens junction and actomyosin to drive cell-in-cell formation, providing a promising cancer therapeutic target.

Results demonstrated that CDH3 was highly and specifically expressed in TNBC (HCC1806), with [89Zr]Zr-DFO-11E10C11 clearly delineating tumor lesions (72 h SUVmax, 2.11 ± 0.31) and [177Lu]Lu-DOTA-11E10C11 significantly inhibiting tumor growth (TGI, 74.94%) without inducing hematologic toxicity or damage to normal organs, indicating favorable safety. In conclusion, CDH3 is a promising theranostic target for TNBC, and the 89Zr/177Lu-11E10C11 dual-functional probe successfully achieved an integrated "diagnosis-therapy" strategy, offering a novel approach with translational potential for precision management of TNBC.

JAK1 and JAK2 inhibition worsens cochlear damage in mice exposed to aminoglycosides.

P1, N=37, Active, not recruiting, Amgen | N=220 --> 37 | Trial completion date: Feb 2028 --> Apr 2026 | Trial primary completion date: Jun 2027 --> Apr 2026 | Recruiting --> Active, not recruiting

Genes such as SYP show significant differential expression in both T2DM and RC and may play significant roles in the progression of T2DM and RC. Transcription factor analysis suggested that SP1 could regulate multiple hub genes. Molecular docking indicated that SP1 is a potential target for active components like stearic acid and EGCG in Ginkgo biloba, highlighting its potential as a therapeutic agent for T2DM and RC.

1.This study investigated the synergistic effect of L-arginine (iNOS substrate) combined with 5-fluorouracil (5-FU, iNOS inducer) on epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC).2.In vitro, the combination significantly inhibited HCC cell proliferation, invasion, migration, and upregulated iNOS. It also decreased mesenchymal markers (N-cadherin, vimentin, Snail, Slug) and increased epithelial E-cadherin.3.In vivo, using DEN-induced HCC rats, the combination group showed extensive tumor necrosis, reduced mitoses, enhanced iNOS, reduced mesenchymal markers, elevated E-cadherin, fewer pseudopodia, and increased cytoplasmic vacuolation compared to the model group.4.Thus, L-arginine + 5-FU synergistically inhibits HCC metastasis by suppressing EMT via iNOS upregulation.

Cdh11, but not Cdh2, in CAFs is important for collective migration. These findings highlight how differential cadherin-mediated communication between cells maintains organization during collective migration.

CDH3 is a key marker and functional driver of basal-like prostate cancer. Therapeutic strategies leveraging CDH3, including ADCs and CAR T cells, demonstrate strong preclinical efficacy, supporting the development of CDH3-targeted treatments to overcome resistance in aggressive prostate cancer.

Transcriptome analysis revealed that combination treatment decreased the expression of pro-proliferative and migratory genes (e.g., PDPN, CDH3), while increasing the expression of anti-migratory (RND3) and pro-apoptotic genes (e.g., XAF1, SEMA3A). Thus, combination treatment significantly reduces tumor cell proliferation and migration; however, further studies on surviving cells are needed.

The selective HTR2A receptor antagonist ketanserin has the potential to alleviate this toxicological impact. Our study presents an efficient, cost-effective toxicological analysis using network toxicology, offering new insights into dioxin-associated liposarcoma.

In conclusion, m6A RNA modification may contribute to SKCM metastasis by regulating the expression of CDH3, KRT17, PKP1 and CRABP2, as well as modulating the tumor immune microenvironment. These findings offer novel insights into the metastatic mechanisms of SKCM and identify potential biomarkers for its diagnosis, prognosis and targeted immunotherapy.

TN demonstrates potential as a therapeutic agent for NPC, primarily through activation of the MAPK signaling pathway and autophagy. Key targets, including RELA, CASP8, PPARG, MAPK14, MAPK8, HDAC1, ERBB2, and CASP1, have been identified as critical mediators of TN's effects, highlighting its role in promoting autophagy and enhancing NPC treatment.