scholarly journals Clinical significance of micrometastasis in bone marrow of patients with gastric cancer and its relation to angiogenesis

1999 ◽  
Vol 2 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Yoshihiro Kakeji ◽  
Yoshihiko Maehara ◽  
Kotaro Shibahara ◽  
Shota Hasuda ◽  
Eriko Tokunaga ◽  
...  
2010 ◽  
Vol 17 (9) ◽  
pp. 2526-2533 ◽  
Author(s):  
Masaaki Iwatsuki ◽  
Koshi Mimori ◽  
Takeo Fukagawa ◽  
Hideshi Ishii ◽  
Takehiko Yokobori ◽  
...  

2007 ◽  
Vol 133 (12) ◽  
pp. 995-1000 ◽  
Author(s):  
Eiji Oki ◽  
Yoshihiro Kakeji ◽  
Hideo Baba ◽  
Kojiro Nishida ◽  
Tadashi Koga ◽  
...  

2012 ◽  
Vol 107 (8) ◽  
pp. 1345-1353 ◽  
Author(s):  
S Akiyoshi ◽  
T Fukagawa ◽  
H Ueo ◽  
M Ishibashi ◽  
Y Takahashi ◽  
...  

Oncogene ◽  
2021 ◽  
Vol 40 (12) ◽  
pp. 2296-2308
Author(s):  
Mei Wang ◽  
Xinxin Zhao ◽  
Rong Qiu ◽  
Zheng Gong ◽  
Feng Huang ◽  
...  

AbstractLymph node metastasis (LNM), a common metastatic gastric-cancer (GC) route, is closely related to poor prognosis in GC patients. Bone marrow-derived mesenchymal stem cells (BM-MSCs) preferentially engraft at metastatic lesions. Whether BM-MSCs are specifically reprogrammed by LNM-derived GC cells (LNM-GCs) and incorporated into metastatic LN microenvironment to prompt GC malignant progression remains unknown. Herein, we found that LNM-GCs specifically educated BM-MSCs via secretory exosomes. Exosomal Wnt5a was identified as key protein mediating LNM-GCs education of BM-MSCs, which was verified by analysis of serum exosomes collected from GC patients with LNM. Wnt5a-enriched exosomes induced YAP dephosphorylation in BM-MSCs, whereas Wnt5a-deficient exosomes exerted the opposite effect. Inhibition of YAP signaling by verteporfin blocked LNM-GC exosome- and serum exosome-mediated reprogramming in BM-MSCs. Analysis of MSC-like cells obtained from metastatic LN tissues of GC patients (GLN-MSCs) confirmed that BM-MSCs incorporated into metastatic LN microenvironment, and that YAP activation participated in maintaining their tumor-promoting phenotype and function. Collectively, our results show that LNM-GCs specifically educated BM-MSCs via exosomal Wnt5a-elicited activation of YAP signaling. This study provides new insights into the mechanisms of LNM in GC and BM-MSC reprogramming, and will provide potential therapeutic targets and detection indicators for GC patients with LNM.


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