ROCK1 (Rho Associated Coiled-Coil Containing Protein Kinase 1)

Its mechanism of action is distinctively linked to the restoration of genes critical to adherens and tight junction integrity. Given its derivation from the clinically viable fasudil, fasudil-D-6h presents a strong translational potential as a novel therapeutic agent for TNBC.

GDM rats were randomly divided into a model group, a fasudil (FA) (RhoA/RocK inhibitor) group (10 mg/kg), low-dose (100 mg/kg) and high-dose (200 mg/kg) baicalin groups, and a high-dose baicalin combined with LPA (RhoA/RocK activator) group (200 mg/kg baicalin+1 mg/kg LPA ), with 12 rats in each group...LPA could obviously weaken the improvement effects of baicalin on blood lipid metabolism and immune function in GDM rats. Conclusion Baicalin may improve blood lipid metabolism and immune function in GDM rats by inhibiting the RhoA/ROCK pathway.

This discovery enables the first cancer therapy that simultaneously enhances normal tissue function while eliminating tumors. "Over-WNTing" effectively treats adenomas and both mouse and patient-derived CRC, establishing a therapeutic paradigm that exploits fundamental differences in cellular WNT biology to achieve the dual benefit of eliminating cancer while promoting healthy tissue regeneration.

These findings indicate that ROCK2 promotes EMT process and tumor progression in PC-3 cells. Targeting ROCK2 may represent a promising therapeutic strategy for androgen-independent prostate cancer.

Suppressing CREB with pAAV-A-CREB reduced neuronal survival, underscoring its role in autophagy and neuroprotection. These findings provide mechanistic insight into stroke-induced molecular alterations and identify autophagy and cAMP pathways within the penumbra as promising therapeutic targets.

CREB1 binding to the PRKCH promoter was validated using luciferase reporter assays. Collectively, these findings reveal a novel ROCK1-ERK2-CREB1-PRKCH signaling pathway that coordinates EMT and metabolic reprogramming to drive CRC liver metastasis, highlighting PRKCH as a promising therapeutic target in advanced CRC.

This study elucidates acrylamide's potential oncogenic role in EC, identifying ROCK1, CLK1, SIRT1, and PSENEN as key mediators. These findings underscore the interplay between dietary exposures and EC pathogenesis, suggesting novel therapeutic targets. Further validation is needed to translate these insights into preventive and therapeutic strategies.

Our findings reveal that CTB-31O20.2 contributes to HCC progression by modulating miR-139-5p and ROCK1 expression. These results highlight CTB-31O20.2 as a potential therapeutic target in HCC, providing a new perspective on the mechanisms driving HCC pathogenesis and progression.

Collectively, our results suggest that a low expression pattern of ATOX1/ROCK1 can predict better clinical outcomes in LUAD. Combining the inhibition of these two targets can reach a significantly better therapeutic effect than targeting either alone.

Vitro experiments revealed that reducing the expression of ROCK1 and TFPI tended to decrease the formation of vascular-like tubes on Matrix-Gel™ compared to the control siRNA groups. Our findings suggest that ROCK1 and TFPI contribute to GBM metastasis through vasculogenic mimicry.

In hormone-resistant EC cells, ROCK1 inhibition restored sensitivity to progesterone therapy...By elucidating the relationship between ECM stiffness, ROCK1/YAP1 signaling, and treatment sensitivity, this study highlights the potential of targeting the ROCK1/YAP1 axis as a therapeutic strategy. ROCK1 serves as both a biomarker for prognosis and a target for improving personalized treatment approaches, offering new avenues to enhance clinical outcomes for EC patients.

P2, N=40, Not yet recruiting, The Methodist Hospital Research Institute