SHH (Sonic Hedgehog Signaling Molecule)

We concluded for the first time that the combination of SOR and ASH-AE generates antagonistic antitumor effect in HepG2 cells. Moreover, ASH-AE can inhibit proliferation of HepG2 cells and mitigate sorafenib-induced resistance-associated markers in HepG2 cells by targeting CD90+ cells via Hedgehog pathway modulation.

The findings highlight GD's potential as a promising therapeutic candidate for PDAC, with the ability to target both bulk tumor cells and PCSCs. By simultaneously suppressing tumor growth, stemness, and metastatic spread, GD may contribute to more effective treatment strategies and improved patient outcomes.

Consistently, GPC6 enhanced SHH pathway activity by upregulating GLI1 expression, supported ciliogenesis that is essential for signal transduction, and facilitated the secretion of SHH ligands via extracellular vesicles. These findings establish GPC6 as a critical regulator of SHH-MB progression and highlight its potential as a therapeutic target.

Mechanistically, SEL1L suppressed the expression of oncogenic Shh protein by promoting its ubiquitination-proteasomal degradation, thereby inhibiting EMT and improving cellular sensitivity to carboplatin in BRC cells via hedgehog signaling pathway. Our findings emphasize the tumor-suppressive function of endogenous SEL1L in BRC and demonstrate the crucial role of the SEL1L-Shh-Gli1 axis in controlling cancer cell progression, offering a promising foundation for the development of innovative therapeutics against BRC.

We have previously shown that the Sonic hedgehog (Shh) signaling pathway is targeted by cyclophosphamide (CYP) treatment, but the detailed mechanism by which this chemotherapy drug induces alopecia still remains largely unknown...Treatment with JAK inhibitors also rescued hair loss and upregulated Shh expression in mice with CIA, further supporting the role of the JAK/STAT1 signaling pathway in the regulation of Shh during CIA. Taken together, our results provide new insights into the molecular mechanisms of CIA.

Viewing remyelination as a dynamic balance between these two cellular systems helps explain why this repair process often fails. Ultimately, understanding these migratory programs as an interconnected system, rather than as isolated components, is essential for developing more effective interventions that promote functional myelin repair in demyelinating diseases.

Prognostic core genes (SHH: EMILIN3, CD163; GP3/GP4: SEMA3A, TULP1) predicted survival outcomes and demonstrated diagnostic specificity. This first comprehensive TME atlas of MB subtypes elucidate mechanisms of immunosuppressive niche formation and provides actionable core targets for precision immunotherapy.

When considering congenital disorders, disruptions in EGL development are associated with conditions such as medulloblastomas, DWM, and pilocytic astrocytoma. The review highlights major research gaps and underscores the need for further human-specific studies to enhance understanding and guide therapies for cerebellar disorders.

The PRKD1 E710D hotspot mutation and protein expression of PRKD1 and HH components (SHH, IHH, SMO, and GLI-1) were detected in PAC regardless of tissue invasion, although HH proteins contributed to the morphogenesis of this rare oral cancer. Additionally, the positive correlation between the expression of PRKD1 and HH pathway components (IHH, SMO, and GLI-1) suggests a possible interaction between these proteins, independent of the HH pathway ligand.

Endothelial NRP1 positivity combined with limited vascular-astrocytic interaction and aberrant GFAP expression in SHH-MB may contribute to dysregulated angiogenesis and tumor progression. These findings warrant further investigation to explore their prognostic and therapeutic implications.

Loss of Pten in normal or SmoM2-expressing GCPs increases proliferation and enhances their progenitor state initially but by 12 days Pten mutant SmoM2 tumors are highly differentiated due to increased survival of non-proliferating GCPs. Furthermore, macrophage infiltration and cytotoxicity is reduced in differentiated regions of tumors lacking Pten , indicating cell nonautonomous change contribute to accelerated tumor growth.