P-coumaric acid regulates exon 12 splicing of the ATP7B gene by modulating hnRNP A1 protein expressions

Lin, Ying; Ho, Tsung Jung; Lin, Ting Hsu; Hsu, Wei Yi; Huang, Shao Mei; Liao, Chien-Chang; Lai, Chih Ho; Liu, Xiang; Tsang, Hsinyi; Lai, Chien Chen; Tsai, Fuu Jen

doi:10.7603/s40681-015-0010-0

Cited by 35 publications

(30 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Whole cell lysates (50 µg) with equal protein concentrations were obtained using the Protein Assay kit from Bio-Rad Laboratories, Inc. (Hercules, CA, USA) according to the manufacturer's protocol and further separated by SDS-PAGE (8–12%) and transferred onto a polyvinylidene fluoride membrane (EMD Millipore) as previously described (23–25). After blocking the membrane with blocking buffer [Tris-buffered saline with Tween-20 (TBST) containing 5% non-fat milk and 0.1% NaN 3 ], they were hybridized separately with primary antibodies.…”

Section: Methodsmentioning

confidence: 99%

Synergistic inhibition of leukemia WEHI-3 cell growth by arsenic trioxide and Hedyotis diffusa Willd extract in vitro and in vivo

Kuo

Liu

Way

et al. 2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Arsenic trioxide (ATO) is clinically used to treat acute promyelocytic leukemia (APL); however, the therapeutic dose of ATO may prompt critical cardiac side effects. Combination therapy may be used to improve the therapeutic efficiency. To evaluate this possibility, the present study determined the combined effects of Hedyotis diffusa Willd (HDW) extract and ATO in leukemic WEHI-3 cells. The results demonstrated that co-treatment of HDW with ATO resulted in a synergistic augmentation of cytotoxicity in cells at the concentration tested. In order to investigate the potential therapeutic application for leukemia, the combined effects of HDW and ATO were analyzed on the WEHI-3 cell-induced orthotopic leukemia animal model in vivo. The WEHI-3 cells in mice with leukemia were established by injecting murine WEHI-3 cells into BALB/c mice, and treating them with HDW and/or combined with ATO. The results indicated that HDW alone or HDW combined with ATO promoted the total survival rate of mice with leukemia, and these effects are dose-dependent. HDW alone or HDW combined with ATO did not affect the body weight, decreased the spleen weight and did not affect the liver weight. Furthermore, the results demonstrated that HDW alone or HDW combined with ATO resulted in a synergistic augmentation of apoptosis in WEHI-3 cells at the concentration tested. In order to further reveal the detailed mechanism of this synergistic effect on apoptosis, apoptosis-related proteins were also evaluated. The data revealed that HDW alone or HDW combined with ATO induced the expression of death receptor 4 (DR4) and DR5 and the activation of poly adenosine diphosphate ribose polymerase, caspase-3, −8 and −9. Furthermore, HDW alone or HDW combined with ATO decreased the expression levels of B-cell lymphoma 2, B-cell lymphoma-extra large and survivin, and increased the expression levels of Bak and t-Bid. Altogether, the results indicate that the combination of HDW with ATO may be a promising strategy used to increase the clinical efficacy of ATO in the treatment of APL.

show abstract

Section: Methodsmentioning

confidence: 99%

Synergistic inhibition of leukemia WEHI-3 cell growth by arsenic trioxide and Hedyotis diffusa Willd extract in vitro and in vivo

Kuo

Liu

Way

et al. 2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

show abstract

“…After transfer, the membranes were incubated with blocking buffer of 5% non‐fat dry milk in Tris‐buffered saline containing Tween‐20 at room temperature for 1 h, added first antibodies overnight. After washing, HRP‐conjugated secondary antibodies were added at room temperature for 1 h. The bound antibodies were visualized using the enhanced chemiluminescence kit (NEN Life Science Products, Inc, Boston, MA, USA) as described previously …”

Section: Methodsmentioning

confidence: 99%

“…After washing, HRP-conjugated secondary antibodies were added at room temperature for 1 h. The bound antibodies were visualized using the enhanced chemiluminescence kit (NEN Life Science Products, Inc, Boston, MA, USA) as described previously. [22][23][24]…”

Section: Western Blotting For Examinations Of the Protein Levels Asmentioning

confidence: 99%

Casticin induced apoptotic cell death and altered associated gene expression in human colon cancer colo 205 cells

Shang

Liu

et al. 2016

Environmental Toxicology

View full text Add to dashboard Cite

Casticin, a polymethoxyflavone, derived from natural plant Fructus Viticis exhibits biological activities including anti-cancer characteristics. The anti-cancer and alter gene expression of casticin on human colon cancer cells and the underlying mechanisms were investigated. Flow cytometric assay was used to measure viable cell, cell cycle and sub-G1 phase, reactive oxygen species (ROS) and Ca productions, level of mitochondria membrane potential (ΔΨ ) and caspase activity. Western blotting assay was used to detect expression of protein level associated with cell death. Casticin induced cell morphological changes, decreased cell viability and induced G2/M phase arrest in colo 205 cells. Casticin increased ROS production but decreased the levels of ΔΨ , and Ca , increased caspase-3, -8, and -9 activities. The cDNA microarray indicated that some of the cell cycle associated genes were down-regulated such as cyclin-dependent kinase inhibitor 1A (CDKN1A) (p21, Cip1) and p21 protein (Cdc42/Rac)-activated kinase 3 (PAK3). TNF receptor-associated protein 1 (TRAP1), CREB1 (cAMP responsive element binding protein 1) and cyclin-dependent kinase inhibitor 1B (CDKN1B) (p27, Kip1) genes were increased but matrix metallopeptidase 2 (MMP-2), toll-like receptor 4 (TLR4), PRKAR2B (protein kinase, cAMP-dependent, regulatory, type II, bet), and CaMK4 (calcium/calmodulin-dependent protein kinase IV) genes were inhibited. Results suggest that casticin induced cell apoptosis via the activation of the caspase- and/or mitochondria-dependent signaling cascade, the accumulation of ROS and altered associated gene expressions in colo 205 human colon cancer cells.

show abstract

“…After washing with TBS-T buffer, membranes were incubated with primary antibodies against MMP-7, MMP-9, MMP-13, . The Biospectrum Imaging System (UVP, Inc., Upland, CA, USA) was used to detect the corresponding bands as previously described (28,32).…”

Section: Cell Migration and Invasion Analyzed With The Transwell Assaymentioning

confidence: 99%

Fisetin Suppresses Human Osteosarcoma U-2 OS Cell Migration and InvasionviaAffecting FAK, uPA and NF-ĸB Signaling PathwayIn Vitro

Chen

Peng

Lai

et al. 2019

In Vivo

View full text Add to dashboard Cite

Background/Aim: Evidence has indicated that fisetin induces cytotoxic effects in human cancer cell lines, including the inhibition of cell migration and invasion, however, the exact molecular mechanism of action of fisetin in human osteosarcoma cells remains unclear. Materials and Methods: The anti-metastatic mechanisms of fisetin in human osteosarcoma U-2 OS cells were investigated in vitro. Results: Fisetin reduced the viability of cells at different concentrations (2.5, 5 and 10 μM) as measured by flow cytometric assay. Fisetin suppressed cell mobility, migration and invasion of U-2 OS cells, as shown by wound healing assay and transwell filter chambers, respectively. The gelatin zymography assay showed that fisetin inhibited MMP-2 activity in U-2 OS cells. Results from western blotting indicated that fisetin reduced the levels

show abstract

P-coumaric acid regulates exon 12 splicing of the ATP7B gene by modulating hnRNP A1 protein expressions

Cited by 35 publications

References 30 publications

Synergistic inhibition of leukemia WEHI-3 cell growth by arsenic trioxide and Hedyotis diffusa Willd extract in vitro and in vivo

Synergistic inhibition of leukemia WEHI-3 cell growth by arsenic trioxide and Hedyotis diffusa Willd extract in vitro and in vivo

Casticin induced apoptotic cell death and altered associated gene expression in human colon cancer colo 205 cells

Fisetin Suppresses Human Osteosarcoma U-2 OS Cell Migration and InvasionviaAffecting FAK, uPA and NF-ĸB Signaling PathwayIn Vitro

Contact Info

Product

Resources

About