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1.
Article in English | WPRIM | ID: wpr-881069

ABSTRACT

Polyphyllin I (PPI) purified from Polyphyllarhizomes displays puissant cytotoxicity in many kinds of cancers. Several researches investigated its anti-cancer activity. But novel mechanisms are still worth investigation. This study aimed to explore PPI-induced endoplasmic reticulum (ER) stress as well as the underlying mechanism in non-small cell lung cancer (NSCLC). Cell viability or colony-forming was detected by MTT or crystal violet respectively. Cell cycle, apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential were assessed by flow cytometry. Gene and protein levels were evaluated by qRT-PCR and immunoblotting respectively. Protein interaction was determined by immunoprecipitation or immunofluorescence assay. Gene overexpression or silencing was carried out by transient transfection with plasmids or small interfering RNAs. The Cancer Genome Atlas (TCGA) database was used for Gene Set Enrichment Analysis (GSEA), survival analysis, gene expression statistics or pathway enrichment assay. PPI inhibited the propagation of NSCLC cells, increased non-viable apoptotic cells, arrested cell cycle at G2/M phase, induced ROS levels but failed to decrease mitochondrial membrane potential. High levels of GRP78 indicates poor prognosis in NSCLC patients. PPI selectively suppressed unfolded protein response (UPR)-induced GRP78 expression, subsequently protected CHOP from GRP78-mediated ubiquitination and degradation. We demonstrated that the natural product PPI, obtained from traditional herbal medicine, deserves for further study as a valuable candidate for lead compound in the chemotherapy of NSCLC.

2.
Article in English | WPRIM | ID: wpr-773642

ABSTRACT

Multidrug resistance (MDR) is one of the major obstacles in cancer chemotherapy. Our previous study has shown that icariin could reverse MDR in MG-63 doxorubicin-resistant (MG-63/DOX) cells. It is reported that icariin is usually metabolized to icariside II and icaritin. Herein, we investigated the effects of icariin, icariside II, and icaritin (ICT) on reversing MDR in MG-63/DOX cells. Among these compounds, ICT exhibited strongest effect and showed no obvious cytotoxicity effect on both MG-63 and MG-63/DOX cells ranging from 1 to 10 μmol·L. Furthermore, ICT increased accumulation of rhodamine 123 and 6-carboxyfluorescein diacetate and enhanced DOX-induced apoptosis in MG-63/DOX cells in a dose-dependent manner. Further studies demonstrated that ICT decreased the mRNA and protein levels of multidrug resistance protein 1 (MDR1) and multidrug resistance-associated protein 1 (MRP1). We also verified that blockade of STAT3 phosphorylation was involved in the reversal effect of multidrug resistance in MG-63/DOX cells. Taken together, these results indicated that ICT may be a potential candidate in chemotherapy for osteosarcoma.


Subject(s)
ATP Binding Cassette Transporter, Subfamily B , Genetics , Metabolism , Antineoplastic Agents , Pharmacology , Apoptosis , Cell Line, Tumor , Cell Survival , Dose-Response Relationship, Drug , Doxorubicin , Metabolism , Pharmacology , Toxicity , Drug Resistance, Multiple , Drug Resistance, Neoplasm , Flavonoids , Pharmacology , Gene Expression Regulation, Neoplastic , Humans , Multidrug Resistance-Associated Proteins , Genetics , Metabolism , Osteosarcoma , Drug Therapy , Metabolism , Pathology , Phosphorylation , Rhodamine 123 , Metabolism , STAT3 Transcription Factor , Metabolism , Triterpenes , Pharmacology
3.
Article in English | WPRIM | ID: wpr-812432

ABSTRACT

Multidrug resistance (MDR) is one of the major obstacles in cancer chemotherapy. Our previous study has shown that icariin could reverse MDR in MG-63 doxorubicin-resistant (MG-63/DOX) cells. It is reported that icariin is usually metabolized to icariside II and icaritin. Herein, we investigated the effects of icariin, icariside II, and icaritin (ICT) on reversing MDR in MG-63/DOX cells. Among these compounds, ICT exhibited strongest effect and showed no obvious cytotoxicity effect on both MG-63 and MG-63/DOX cells ranging from 1 to 10 μmol·L. Furthermore, ICT increased accumulation of rhodamine 123 and 6-carboxyfluorescein diacetate and enhanced DOX-induced apoptosis in MG-63/DOX cells in a dose-dependent manner. Further studies demonstrated that ICT decreased the mRNA and protein levels of multidrug resistance protein 1 (MDR1) and multidrug resistance-associated protein 1 (MRP1). We also verified that blockade of STAT3 phosphorylation was involved in the reversal effect of multidrug resistance in MG-63/DOX cells. Taken together, these results indicated that ICT may be a potential candidate in chemotherapy for osteosarcoma.


Subject(s)
ATP Binding Cassette Transporter, Subfamily B , Genetics , Metabolism , Antineoplastic Agents , Pharmacology , Apoptosis , Cell Line, Tumor , Cell Survival , Dose-Response Relationship, Drug , Doxorubicin , Metabolism , Pharmacology , Toxicity , Drug Resistance, Multiple , Drug Resistance, Neoplasm , Flavonoids , Pharmacology , Gene Expression Regulation, Neoplastic , Humans , Multidrug Resistance-Associated Proteins , Genetics , Metabolism , Osteosarcoma , Drug Therapy , Metabolism , Pathology , Phosphorylation , Rhodamine 123 , Metabolism , STAT3 Transcription Factor , Metabolism , Triterpenes , Pharmacology
4.
Article in Chinese | WPRIM | ID: wpr-329958

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of cis-combretastatin-A1 phosphate (cis-CA1P) on tumor cell proliferation, and its effects on the blood vessel formations.</p><p><b>METHODS</b>MTT and IC50 values were used to assess the inhibitory effects of cis-CA1P on tumor cell proliferation. Chicken embryo chorioallantoic membrane and thoracic aorta annulations isolated from rats were used to investigate the effects of cis-CAIP on the blood vessel formation.</p><p><b>RESULTS</b>Cis-CA1P concentration-dependently inhibited the proliferations of several cancer cell lines, including human gastric carcinoma cell line MGC-803, human leukemic monocyte lymphoma cell line U937, human melanoma cell line A375, human colon cancer cell line HCT116, human breast carcinoma cell line MDA-MB-231, and human leukemia cell line K562. Cis-CAIP significantly decreased the formation of blood vessels in chicken embryo chorioallantoic membrane and in thoracic aorta annulations.</p><p><b>CONCLUSION</b>Cis-CA1P inhibits cancer cell proliferation and prevents blood vessel formation.</p>


Subject(s)
Animals , Aorta , Cell Line, Tumor , Cell Proliferation , Chick Embryo , Chorioallantoic Membrane , Humans , In Vitro Techniques , Neovascularization, Pathologic , Phosphates , Pharmacology , Rats , Stilbenes , Chemistry , Pharmacology
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