Ontogenetic changes in the expression of estrogen receptor β in mouse duodenal epithelium

Choijookhuu, Narantsog; Hino, Shinjiro; Oo, Phyu Synn; Batmunkh, Baatarsuren; Mohmand, Noor Ali; Kyaw, Myat Tin Htwe; Hishikawa, Yoshitaka

doi:10.1016/j.clinre.2015.01.004

Cited by 9 publications

(4 citation statements)

References 40 publications

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“…Total cell lysates were prepared using hot sodium dodecyl sulfate (SDS) buffer containing 0.9% SDS, 15 mM EDTA, 8 mM unlabeled methionine, and a protease inhibitor cocktail. Lysates were boiled for 10 min, cooled, diluted in 0.3% SDS, adjusted to contain 33 mM Tris/acetate, pH 8.5, and 1.7% Triton X-100, and sonicated using a Bioruptor (Cosmo Bio Inc., Tokyo, Japan) [8]. Lysates were centrifuged at 15,000 rpm for 20 min at 4°C.…”

Section: Methodsmentioning

confidence: 99%

The HDAC Inhibitor, SAHA, Combined with Cisplatin Synergistically Induces Apoptosis in Alpha-fetoprotein-producing Hepatoid Adenocarcinoma Cells

Kyaw

Yamaguchi

Choijookhuu

et al. 2019

Acta Histochem. Cytochem

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Hepatoid adenocarcinoma (HAC) is a rare and aggressive gastrointestinal tract cancer that is characterized by hepatic differentiation and production of alpha-fetoprotein (AFP). Cisplatin is mainly used to treat HAC, but the efficacy is poor. Recently, the histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), was approved as an anticancer agent. In this study, we investigated the anticancer effect of SAHA in combination with cisplatin in VAT-39 cells, a newly established HAC cell line. Cell viability and apoptosis were examined by MTT assay, flow cytometry and TUNEL assay. Expression of H3S10, cleaved caspase-3, Bax, and Bcl-2 were evaluated by immunohistochemistry and western blotting. AFP levels were examined in VAT-39 cells and culture medium. Combined treatment with cisplatin and SAHA efficiently inhibited cell proliferation and decreased cell viability. Apoptotic cells, but not necrotic cells, were significantly increased following the combined treatment, and an increase in the Bax/Bcl-2 ratio indicated that the combination of cisplatin and SAHA induced apoptosis through the mitochondrial pathway. VAT-39 cells treated with cisplatin and SAHA also partially lost their main characteristic of AFP production. We conclude that cisplatin and SAHA have a synergistic anticancer effect of inducing apoptosis, and that this combination treatment may be effective for HAC.

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Section: Methodsmentioning

confidence: 99%

The HDAC Inhibitor, SAHA, Combined with Cisplatin Synergistically Induces Apoptosis in Alpha-fetoprotein-producing Hepatoid Adenocarcinoma Cells

Kyaw

Yamaguchi

Choijookhuu

et al. 2019

Acta Histochem. Cytochem

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“…Liver tissues were homogenized in hot SDS lysis buffer with a glass-teflon homogenizer, as described previously. 27 After centrifugation of the homogenate at 15,000 rpm for 30 min at 4C, the supernatant was collected and stored at −80C. The protein concentration in each preparation was determined using a bicinchoninic acid (BCA) assay kit.…”

Section: Methodsmentioning

confidence: 99%

HMGB2 Promotes De Novo Lipogenesis to Accelerate Hepatocyte Proliferation During Liver Regeneration

Choijookhuu,

Yano,

Lkham-Erdene

et al. 2024

J Histochem Cytochem.

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Liver regeneration is a well-orchestrated compensatory process that is regulated by multiple factors. We recently reported the importance of the chromatin protein, a high-mobility group box 2 (HMGB2) in mouse liver regeneration. However, the molecular mechanism remains unclear. In this study, we aimed to study how HMGB2 regulates hepatocyte proliferation during liver regeneration. Seventy-percent partial hepatectomy (PHx) was performed in wild-type (WT) and HMGB2-knockout (KO) mice, and the liver tissues were used for microarray, immunohistochemistry, quantitative polymerase chain reaction (qPCR), and Western blotting analyses. In the WT mice, HMGB2-positive hepatocytes colocalized with cell proliferation markers. In the HMGB2-KO mice, hepatocyte proliferation was significantly decreased. Oil Red O staining revealed the transient accumulation of lipid droplets at 12–24 hr after PHx in the WT mouse livers. In contrast, decreased amount of lipid droplets were found in HMGB2-KO mouse livers, and it was preserved until 36 hr. The microarray, immunohistochemistry, and qPCR results demonstrated that the expression of lipid metabolism–related genes was significantly decreased in the HMGB2-KO mouse livers. The in vitro experiments demonstrated that a decrease in the amount of lipid droplets correlated with decreased cell proliferation activity in HMGB2-knockdown cells. HMGB2 promotes de novo lipogenesis to accelerate hepatocyte proliferation during liver regeneration:

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“…Total NOZ cell lysates were prepared using hot SDS buffer containing 0.9% SDS, 15 mM ethylenediaminetetraacetic acid (EDTA), 8 mM unlabeled methionine and a protease inhibitor cocktail. Lysates were boiled for 10 min, cooled and diluted in 0.3% SDS, then adjusted to contain 33 mM Tris/acetate, pH 8.5, and 1.7% Triton X-100 [ 13 ]. The protein concentration was determined using a Pierce BCA protein assay kit (Thermo Fisher Scientific).…”

Section: Methodsmentioning

confidence: 99%

Photodynamic Therapy Using a Novel Phosphorus Tetraphenylporphyrin Induces an Anticancer Effect via Bax/Bcl-xL-related Mitochondrial Apoptosis in Biliary Cancer Cells

Huynh

Yamaguchi

Choijookhuu

et al. 2020

Acta Histochem. Cytochem

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Photodynamic therapy (PDT) uses photosensitizer activation by light of a specific wavelength, and is a promising treatment for various cancers; however, the detailed mechanism of PDT remains unclear. Therefore, we investigated the anticancer effect of PDT using a novel phosphorus tetraphenylporphyrin (Ptpp) in combination with light emitting diodes (Ptpp-PDT) in the NOZ human biliary cancer cell line. Cell viability and apoptosis were examined by MTT assay, flow cytometry and TUNEL assay for 24 hr after Ptpp-PDT. MitoTracker and JC-1 were used as markers of mitochondrial localization and membrane potential. The levels of mitochondrial oxidative phosphorylation (OXPHOS) complexes, Bcl-2 family proteins, cytochrome c and cleaved caspase-3 were examined by western blotting and immunohistochemistry. The results revealed that Ptpp localized to mitochondria, and that Ptpp-PDT efficiently decreased cell viability in a dose- and time-dependent manner. JC-1 and OXPHOS complexes decreased, but apoptotic cells increased from 6 to 24 hr after Ptpp-PDT. A decrease in Bcl-xL and increases in Bax, cytochrome c and cleaved caspase-3 were also found from 6 to 24 hr after Ptpp-PDT. Based on these results, we conclude that Ptpp-PDT induces anticancer effects via the mitochondrial apoptotic pathway by altering the Bax/Bcl-xL ratio, and could be an effective treatment for human biliary cancer.

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Ontogenetic changes in the expression of estrogen receptor β in mouse duodenal epithelium

Cited by 9 publications

References 40 publications

The HDAC Inhibitor, SAHA, Combined with Cisplatin Synergistically Induces Apoptosis in Alpha-fetoprotein-producing Hepatoid Adenocarcinoma Cells

The HDAC Inhibitor, SAHA, Combined with Cisplatin Synergistically Induces Apoptosis in Alpha-fetoprotein-producing Hepatoid Adenocarcinoma Cells

HMGB2 Promotes De Novo Lipogenesis to Accelerate Hepatocyte Proliferation During Liver Regeneration

Photodynamic Therapy Using a Novel Phosphorus Tetraphenylporphyrin Induces an Anticancer Effect via Bax/Bcl-xL-related Mitochondrial Apoptosis in Biliary Cancer Cells

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