Biological and Pharmaceutical Bulletin
The Pharmaceutical Society of Japan, established in 1880, is one of Japan’s oldest and most distinguished academic societies. The Society currently has around 18,000 members. It publishes three monthly scientific journals. Chemical and Pharmaceutical Bulletin (Chem. Pharm. Bull.) began publication in 1953 as Pharmaceutical Bulletin. It covers chemistry fields in the pharmaceutical and health sciences. Biological and Pharmaceutical Bulletin (Biol. Pharm. Bull.) began publication in 1978 as the Journal of Pharmacobio-Dynamics. It covers various biological topics in the pharmaceutical and health sciences. A fourth Society journal, the Journal of Health Science, was merged with Biol. Pharm. Bull. in 2012. Yakugaku Zasshi (Japanese for “Pharmaceutical Science Journal”) has the longest history, with publication beginning in 1881. Yakugaku Zasshi is published mostly in Japanese, except for some articles related to clinical pharmacy and pharmaceutical education, which are published in English.
The main aim of the Society’s journals is to advance the pharmaceutical sciences with research reports, information exchange, and high-quality discussion. The average review time for articles submitted to the journals is around one month for first decision. The complete texts of all of the Society’s journals can be freely accessed through J-STAGE. The Society’s editorial committee hopes that the content of its journals will be useful to your research, and also invites you to submit your own work to the journals.

Chairman of Committee
Ken-ichi Hosoya
Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama



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9,046 registered articles
(updated on April 23, 2017)
Online ISSN : 1347-5215
Print ISSN : 0918-6158
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Volume 40 (2017) Issue 4 Pages 495-503
Growth Inhibition of Refractory Human Gallbladder Cancer Cells by Retinol, and Its Mechanism of Action

Among the constituents of the essential nutrient vitamin A, retinol is a potent suppressor of refractory cancer cell growth linked to tumor progression, showing greater efficacy than retinoic acid (RA). However, the mechanisms of retinol action on human refractory cancer are not known well. In the current study, we examined the actions of retinol on proliferation of human gallbladder cancer NOZ C-1 cells. Retinol and RA inhibited the proliferation of human NOZ C-1 cells in dose-dependent manner, while RA was less potent than retinol. Cell incorporation of RA was approximately two-fold higher than retinol and was not correlated with anti-proliferative activity. Retinol did not affect caspase-3 activity or mRNA expression of Bax and Bcl-2, which are associated with apoptosis. In addition, protein expression of phosphorylated extracellular signal-regulated kinase (p-ERK)/ERK and p-Akt/Akt were not significantly changed by retinol treatment. In contrast, retinol treatment significantly increased the mRNA expression of endoplasmic reticulum (ER) stress factors (heme oxygenase 1 (HMOX1), CCAAT/enhancer-binding protein homologous protein (CHOP), 78 kDa glucose-regulated protein (GRP78), and DnaJ (Hsp40) homolog, subfamily B, member 9 (DNAJB9)). Furthermore, the number of cells in the G0/G1 phase was increased, while the number of cells in the S phase were decreased by retinol treatment. Retinol increased expression of the autophagy-associated protein, LC3-II. These results indicate that retinol is a potent suppressor of gallbladder cancer cell growth by mechanisms that involve ER stress, which results in autophagy and cell cycle delay. This suggests that retinol might be useful for anticancer prevention and therapy in the clinic.

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In their report, Li et al. described that vitamin A (retinol) inhibits cancer cell growth via endoplasmic reticulum (ER) stress. Retinal is a more potent suppressor of refractory human gallbladder cancer cell growth linked to tumor progression than retinoic acid (RA). Although cellular incorporation of RA is higher than retinol, it was not correlated with anti-proliferative activity. Retinol did not induce apoptosis or suppress MEK/ERK and PI3K/Akt pathways. However, it significantly increased the expression of ER stress related genes and autophagy-associated protein (LC3-II) and the number of cells in the G0/G1 phase. This result indicates that retinol suppresses gallbladder cancer cell growth by mechanisms involving ER stress, autophagy, and cell cycle delay. Retinol might be useful for the prevention and treatment of cancer.



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