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Your search keyword '"Wen, Wen"' showing total 4 results
4 results on '"Wen, Wen"'

1. Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway

Author

Ming Jen Fan, Fu Shin Chueh, Rick Sai-Chuen Wu, Han‑Yu Chou, Wen Wen Huang, Yi Shih Ma, Jing Gung Chung, Ching Lung Liao, and Yung Lin Chu

Subjects
0301 basic medicine, Cancer Research, Cell, Apoptosis, Biochemistry, chemistry.chemical_compound, 0302 clinical medicine, Cytotoxic T cell, bcl-2-Associated X Protein, Membrane Potential, Mitochondrial, medicine.diagnostic_test, DNA ladder, Articles, Cell cycle, Chromatin, Mitochondria, Tongue Neoplasms, Cell biology, G2 Phase Cell Cycle Checkpoints, Gene Expression Regulation, Neoplastic, medicine.anatomical_structure, Proto-Oncogene Proteins c-bcl-2, Oncology, 030220 oncology & carcinogenesis, SCC-4 cells, Molecular Medicine, Signal Transduction, Cell Survival, Antineoplastic Agents, DNA Fragmentation, Biology, Nitric Oxide, Flow cytometry, 03 medical and health sciences, Cell Line, Tumor, Genetics, medicine, Humans, DAPI, Molecular Biology, Bufalin, Bufanolides, 030104 developmental biology, chemistry, Cancer cell, Apoptosis Regulatory Proteins, Reactive Oxygen Species, bufalin, DNA Damage
Abstract

The aim of the present study was to investigate the cytotoxic effects of bufalin on SCC-4 human tongue cancer cells. Cell morphological changes and viability were examined using phase contrast microscopy and flow cytometry, respectively. The results indicated that bufalin induced morphological changes and reduced total viable cells. Apoptotic cell death was analyzed by DAPI staining and DNA gel electrophoresis; the results revealed that bufalin induced cell apoptosis. Levels of reactive oxygen species (ROS), Ca2+, nitric oxide (NO) and mitochondrial membrane potential (ΔΨm) were measured by flow cytometry, and bufalin was observed to increase Ca2+ and NO production, decrease the ΔΨm and reduce ROS production in SCC-4 cells. In addition, western blotting was performed to detect apoptosis-associated protein expression. The results demonstrated that bufalin reduced the expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and increased the expression of the pro-apoptotic protein, Bcl-2-associated X protein. However, bufalin treatment also increased the expression of other apoptosis-associated proteins such as apoptosis-inducing factor and endonuclease G in SCC-4 cells. Based on these findings, bufalin may induce apoptotic cell death via mitochondria-dependent pathways in human tongue cancer SCC-4 cells.

Published
2017

2. Bufalin Induces Apoptotic Cell Death in Human Nasopharyngeal Carcinoma Cells through Mitochondrial ROS and TRAIL Pathways.

Author

Su, En-Yun, Chu, Yung-Lin, Chueh, Fu-Shin, Ma, Yi-Shih, Peng, Shu-Fen, Huang, Wen-Wen, Liao, Ching-Lung, Huang, An-Cheng, and Chung, Jing-Gung

Subjects
REACTIVE oxygen species, ANALYSIS of variance, ANTINEOPLASTIC agents, APOPTOSIS, BIOLOGICAL assay, CELL culture, CELLULAR signal transduction, DIMETHYL sulfoxide, FLOW cytometry, GLUTAMINE, HETEROCYCLIC compounds, PENICILLIN, CHINESE medicine, NASOPHARYNX cancer, PROTEINS, SERUM, STREPTOMYCIN, WESTERN immunoblotting, DATA analysis software, CELL survival, DESCRIPTIVE statistics, PHARMACODYNAMICS
Abstract

The aim of this study was to investigate the effects of bufalin on human nasopharyngeal carcinoma NPC-TW 076 cells in vitro. Bufalin is a cardiotonic steroid and a key active ingredient of the Chinese medicine ChanSu. The extracts of Chansu are used for various cancer treatments in China. In the present study, bufalin induced cell morphological changes, decreased total cell viability and induced G2/M phase arrest of cell cycle in NPC-TW 076 cells. Results also indicated that bufalin induced chromatin condensation (cell apoptosis) and DNA damage by DAPI staining and comet assay, respectively. The induced apoptotic cell death was further confirmed by annexin-V/PI staining assay. In addition, bufalin also increased ROS and Ca 2 + production and decreased the levels of Δ Ψ m . Furthermore, the alterations of ROS, ER stress and apoptosis associated protein expressions were investigated by Western blotting. Results demonstrated that bufalin increased the expressions of ROS associated proteins, including SOD (Cu/Zn), SOD2 (Mn) and GST but decreased that of catalase. Bufalin increased ER stress associated proteins (GRP78, IRE-1 α , IRE-1 β , caspase-4, ATF-6 α , Calpain 1, and GADD153). Bufalin increased the pro-apoptotic proteins Bax, and apoptotic associated proteins (cytochrome c, caspase-3, -8 and -9, AIF and Endo G) but reduced anti-apoptotic protein Bcl-2 in NPC-TW 076 cells. Furthermore, bufalin elevated the expressions of TRAIL-pathway associated proteins (TRAIL, DR4, DR5, and FADD). Based on these findings, we suggest bufalin induced apoptotic cell death via caspase-dependent, mitochondria-dependent and TRAIL pathways in human nasopharyngeal carcinoma NPC-TW 076 cells. [ABSTRACT FROM AUTHOR]

Published
2019
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3. Reactive Oxygen Species and Autophagy Associated Apoptosis and Limitation of Clonogenic Survival Induced by Zoledronic Acid in Salivary Adenoid Cystic Carcinoma Cell Line SACC-83

Author

Lin-Qian Yang, Xiyuan Ge, Yang Jiang, Jia Fu, Wen-Wen Yang, and Sheng-Lin Li

Subjects
Pathology, Cancer Treatment, Fluorescent Antibody Technique, lcsh:Medicine, Apoptosis, Biochemistry, Zoledronic Acid, Metastasis, Oxidative Damage, Mice, Spectrum Analysis Techniques, Molecular Cell Biology, Basic Cancer Research, Antineoplastic Combined Chemotherapy Protocols, Medicine and Health Sciences, Tumor Cells, Cultured, Drug Interactions, lcsh:Science, chemistry.chemical_classification, Mice, Inbred BALB C, Multidisciplinary, Bone Density Conservation Agents, Diphosphonates, Cell Cycle, Imidazoles, Flow Cytometry, Salivary Gland Neoplasms, Head and Neck Tumors, Carcinoma, Adenoid Cystic, Oncology, Spectrophotometry, Drug Therapy, Combination, Female, Cytophotometry, Research Article, medicine.drug, medicine.medical_specialty, Drug Research and Development, Paclitaxel, Adenoid cystic carcinoma, Blotting, Western, Mice, Nude, Biology, Research and Analysis Methods, Autophagy, medicine, Carcinoma, Animals, Humans, Salivary Gland Tumors, Clonogenic assay, Cell Proliferation, Pharmacology, Cisplatin, Reactive oxygen species, lcsh:R, Biology and Life Sciences, Cancers and Neoplasms, Cell Biology, medicine.disease, Xenograft Model Antitumor Assays, Zoledronic acid, chemistry, Cancer research, lcsh:Q, Clinical Medicine, Reactive Oxygen Species, Cytometry
Abstract

Salivary adenoid cystic carcinoma is an epithelial tumor in the head and neck region. Despite its slow growth, patients with salivary adenoid cystic carcinoma exhibit poor long term survival because of a high rate of distant metastasis. Lung and bone are common distant metastasis sites. Zoledronic acid, a third generation bisphosphonate, has been used for tumor-induced osteolysis due to bone metastasis and has direct antitumor activity in several human neoplasms. Here, we observed that zoledronic acid inhibited salivary adenoid cystic carcinoma cell line SACC-83 xenograft tumor growth in nude mice. In vitro, zoledronic acid induced apoptosis and reduced clonogenic survival in SACC-83. Flow cytometry and western blotting indicated that the cell cycle was arrested at G0/G1. Zoledronic acid treatment upregulated reactive oxygen species as well as the autophagy marker protein LC-3B. Reactive oxygen species scavenger N-acetylcysteine and autophagy antagonist 3-methyladenine decreased zoledronic acid-induced apoptosis and increased clonogenic survival. Silencing of the autophagy related gene Beclin-1 also decreased zoledronic acid-induced apoptosis and inhibition of clonogenic formation. In addition, isobolographic analysis revealed synergistic effects on apoptosis when zoledronic acid and paclitaxel/cisplatin were combined. Taken together, our results suggest that zoledronic acid induced apoptosis and reduced clonogenic survival via upregulation of reactive oxygen species and autophagy in the SACC-83 cell line. Thus, zoledronic acid should be considered a promising drug for the treatment of salivary adenoid cystic carcinoma.

Published
2014

4. Reactive Oxygen Species and Autophagy Associated Apoptosis and Limitation of Clonogenic Survival Induced by Zoledronic Acid in Salivary Adenoid Cystic Carcinoma Cell Line SACC-83.

Author

Ge, Xi-Yuan, Yang, Lin-Qian, Jiang, Yang, Yang, Wen-Wen, Fu, Jia, and Li, Sheng-Lin

Subjects
REACTIVE oxygen species, AUTOPHAGY, APOPTOSIS, ADENOID cystic carcinoma, CELL lines, METASTASIS
Abstract

Salivary adenoid cystic carcinoma is an epithelial tumor in the head and neck region. Despite its slow growth, patients with salivary adenoid cystic carcinoma exhibit poor long term survival because of a high rate of distant metastasis. Lung and bone are common distant metastasis sites. Zoledronic acid, a third generation bisphosphonate, has been used for tumor-induced osteolysis due to bone metastasis and has direct antitumor activity in several human neoplasms. Here, we observed that zoledronic acid inhibited salivary adenoid cystic carcinoma cell line SACC-83 xenograft tumor growth in nude mice. In vitro, zoledronic acid induced apoptosis and reduced clonogenic survival in SACC-83. Flow cytometry and western blotting indicated that the cell cycle was arrested at G0/G1. Zoledronic acid treatment upregulated reactive oxygen species as well as the autophagy marker protein LC-3B. Reactive oxygen species scavenger N-acetylcysteine and autophagy antagonist 3-methyladenine decreased zoledronic acid-induced apoptosis and increased clonogenic survival. Silencing of the autophagy related gene Beclin-1 also decreased zoledronic acid-induced apoptosis and inhibition of clonogenic formation. In addition, isobolographic analysis revealed synergistic effects on apoptosis when zoledronic acid and paclitaxel/cisplatin were combined. Taken together, our results suggest that zoledronic acid induced apoptosis and reduced clonogenic survival via upregulation of reactive oxygen species and autophagy in the SACC-83 cell line. Thus, zoledronic acid should be considered a promising drug for the treatment of salivary adenoid cystic carcinoma. [ABSTRACT FROM AUTHOR]

Published
2014
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