Galectin-9 Induces Mitochondria-Mediated Apoptosis of Esophageal Cancer In Vitro and In Vivo in a Xenograft Mouse Model

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 clarifi...

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Published in:International journal of molecular sciences 2019-05, Vol.20 (11), p.2634
Main Authors: Chiyo, Taiga, Fujita, Koji, Iwama, Hisakazu, Fujihara, Shintaro, Tadokoro, Tomoko, Ohura, Kyoko, Matsui, Takanori, Goda, Yasuhiro, Kobayashi, Nobuya, Nishiyama, Noriko, Yachida, Tatsuo, Morishita, Asahiro, Kobara, Hideki, Mori, Hirohito, Niki, Toshiro, Hirashima, Mitsuomi, Himoto, Takashi, Masaki, Tsutomu
Format: Article
Language:English
Subjects:
Activation
Annexin V
Antitumor activity
Apoptosis
Autophagy
Biological activity
Cancer therapies
Caspase
Caspase-3
Cell cycle
Cell growth
Cell proliferation
Chemotherapy
Cytochrome
Dendritic cells
Esophageal cancer
Esophagus
Galectin-9
Kinases
Liver cancer
Lymphocytes
Lymphocytes T
Macrophages
MAP kinase
miRNA
Mitochondria
Phosphorylation
Protein kinase
Proteins
Squamous cell carcinoma
Transcription factors
Tumors
Xenografts
Xenotransplantation
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Summary: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 NH -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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms20112634