Related Experiment Video

Updated: Jan 14, 2026

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.3K

The Novel ROCK Inhibitor Fasudil Derivative Fasudil-D-6h Prevents Tumour Progression by Regulating the Adherens

Jinghui Liang1, Mu Tang2, Lieliang Wang2

  • 1Department of Comprehensive Radiotherapy, Jiangxi Cancer Hospital & Institute, Nanchang City, Jiangxi Province, People's Republic of China.

Breast Cancer (Dove Medical Press)
|January 13, 2026
PubMed
Abstract

Insights

A new ROCK inhibitor, fasudil-D-6h, effectively reduces triple-negative breast cancer (TNBC) growth by restoring cell junction integrity. This drug shows promise as a novel therapeutic for TNBC, offering a new treatment avenue.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Triple-negative breast cancer (TNBC) is aggressive with limited treatment options.
  • Rho-associated coiled-coil containing protein kinase (ROCK) signaling drives TNBC progression via cytoskeletal remodeling and epithelial-mesenchymal transition (EMT).
  • The role of ROCK in disrupting epithelial integrity via adherens and tight junctions in TNBC is underexplored.

Purpose of the Study:

  • To investigate the anti-tumor efficacy of fasudil-D-6h, a novel ROCK inhibitor derivative.
  • To elucidate the novel mechanism of action of fasudil-D-6h in TNBC, focusing on epithelial integrity.

Main Methods:

  • Assessed proliferation (CCK-8) and apoptosis (flow cytometry) of fasudil-D-6h in TNBC cell lines (MDA-MB-231, MCF-7).
  • Performed transcriptome sequencing on treated cells to identify differentially expressed genes (DEGs) and enriched pathways.
  • Evaluated in vivo efficacy in a mouse model and validated gene/protein expression (ROCK1/2, Cdc42, Rac3, Src, ZO-1, Occludin, Claudin-1) via qRT-PCR and Western blotting.

Main Results:

  • Fasudil-D-6h significantly inhibited proliferation and induced apoptosis in TNBC cells.
  • Transcriptomic analysis revealed significant enrichment in the adherens junction pathway.
  • Fasudil-D-6h treatment downregulated ROCK1/2 and upregulated CDC42, RAC3, SRC, ZO-1, OCCLUDIN, and CLAUDIN-1, reducing tumor growth in vivo.

Conclusions:

  • Fasudil-D-6h demonstrates potent anti-tumor effects in TNBC through a mechanism involving the restoration of adherens and tight junction integrity.
  • The drug's distinct mechanism and derivation from a clinically approved compound suggest strong translational potential for TNBC therapy.
Keywords:
ROCK inhibitoradherens junctionbreast cancer signalling pathwayfasudil-D-6htriple-negative breast cancer

More Related Videos

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

12.6K
Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

8.7K

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.5K
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
7.2K
Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
2.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.6K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.5K