DCN (Decorin)

The results showed that the combination of the two further enhanced tumor-killing effects. In vivo experiments further confirmed that OAV-Decorin can promote IFN-γ expression, suppress TGF-β expression, improve the tumor-suppressive microenvironment, and ultimately achieve an antitumor effect.

In conclusion, promoting DCN-mediated ferroptosis might be a potential strategy for enhancing the sensitivity of enzalutamide in PCa cells. This study delineates a novel mechanism by which DCN downregulation suppresses ferroptosis and drives enzalutamide resistance in CRPC.

Our study reveals that DCN functions as a tumor-suppressive factor by enhancing T cell response, and proposes the potential of exogenous DCN as a supplement to cancer immunotherapy.

In summary, this study is the first to demonstrate the potential clinical utility of on-treatment monitoring of systemic DCN in patients with pancreatic cancer. The findings also provide interesting leads for further research into how DCN may interact with the immune microenvironment to promote tumour development and the emergence of chemoresistance.

Overexpression of wild type Decorin, but not its glycosaminoglycan (GAG)-removed mutant in cancer cells decreased mean spheroid size, invasion through Collagen I matrix, and migration on fibronectin matrix scaffolds. Our results suggest that downregulation of an extracellular inhibitor of colonization occurs both in the seed and soil components of the metastatic toolkit; in addition, the GAG chains of Decorin may be crucial to its carcinomatosis-inhibiting functions.

These findings have deepened our current understanding of CAF-mediated mechanisms in GC, contributing to the development of precision diagnostics and therapeutics in GC.

A program of RT or HIIT can increase levels of myokines (an effect considered beneficial given their potential cancer-suppressive effects) and inhibit growth of MDA-MB-231 cells in survivors of breast cancer. In addition, development of the anti-tumor environment may be mediated by exercise-related changes in muscle strength and body composition.

Two stroma subtypes were identified: subtype 1 with higher bone content, lower vessel density, MetA-enrichment and better prognosis compared to subtype 2 that exhibited higher tumor proliferation and lower PSA expression. Most metastases contained regions of both stroma subtypes.

Moreover, cinobufagin effectively reduced the levels of EGFR and active EGFR, and inhibited Erk phosphorylation, which may contribute to its anti-gastric cancer effects. Cinobufagin is capable of suppressing gastric tumor growth in mice likely through the DCN/EGFR pathway and may serve as a potential treatment option for gastric cancer.

Mechanistically, EGR3 was identified as a transcriptional activator of DCN, and EGR3 knockdown reversed the tumor-suppressive effects of DCN. Our findings demonstrated that DCN exerted antitumor effects in liver cancer via transcriptional activation by EGR3, providing a novel therapeutic target for liver cancer treatment.

The two key regulatory axes, hsa_circ_0072088/hsa-miR-532-3p/MMP14 and hsa_circ_0049271/hsa-miR-224-5p/DCN, might be involved in carcinogenesis, prognosis and immune infiltration of LUAD.

A single bout of RT or HIIT can increase levels of anti-cancer myokines and reduce the growth of MDA-MB-231 cells in vitro in survivors of breast cancer, potentially contributing to a lower risk of recurrence. This highlights the importance of exercise as a treatment with promising anti-cancer effects.