Abstract:
:Galectin-9 (Gal-9) enhances tumor immunity mediated by T cells, macrophages, and dendritic cells. Its expression level in various cancers correlates with prognosis. Furthermore, Gal-9 directly induces apoptosis in various cancers; however, its mechanism of action and bioactivity has not been clarified. We evaluated Gal-9 antitumor effect against esophageal squamous cell carcinoma (ESCC) to analyze the dynamics of apoptosis-related molecules, elucidate its mechanism of action, and identify relevant changes in miRNA expressions. KYSE-150 and KYSE-180 cells were treated with Gal-9 and their proliferation was evaluated. Gal-9 inhibited cell proliferation in a concentration-dependent manner. The xenograft mouse model established with KYSE-150 cells was administered with Gal-9 and significant suppression in the tumor growth observed. Gal-9 treatment of KYSE-150 cells increased the number of Annexin V-positive cells, activation of caspase-3, and collapse of mitochondrial potential, indicating apoptosis induction. c-Jun NH2-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) phosphorylation were activated and could be involved in apoptosis. Therefore, Gal-9 induces mitochondria-mediated apoptosis of ESCC and inhibits cell proliferation in vitro and in vivo with JNK and p38 activation.
journal_name
Int J Mol Scijournal_title
International journal of molecular sciencesauthors
Chiyo T,Fujita K,Iwama H,Fujihara S,Tadokoro T,Ohura K,Matsui T,Goda Y,Kobayashi N,Nishiyama N,Yachida T,Morishita A,Kobara H,Mori H,Niki T,Hirashima M,Himoto T,Masaki Tdoi
10.3390/ijms20112634subject
Has Abstractpub_date
2019-05-29 00:00:00issue
11issn
1422-0067pii
ijms20112634journal_volume
20pub_type
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