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1.
Exp Lung Res ; 42(7): 346-353, 2016 09.
Artigo em Inglês | MEDLINE | ID: mdl-27607135

RESUMO

BACKGROUND: Lung cancer is one of the most common and a lethal malignancy in the world and non-small cell lung cancer (NSCLC) is the most usual type. H19 long non-coding RNA (lncRNA) plays essential roles in tumor development. But its role in tumor metastasis is still unclear. MATERIALS AND METHODS: MACC1 RNAi and Lentivirus-mediated H19-specific shRNA was used to establish H19 stable knocking-down A549 cells. Transwell assays were performed to examine the effect of H19 knocking-down on A549 cells migration and invasion. The downstream signaling proteins targeted by H19 were also examined by western blot. AG1478 and U0126 were used as the inhibitor of EGFR and ERK1/2, respectively. RESULTS: The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), ß-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). Inhibited the expression of EGFR or ERK1/2 significantly decreased the migration and invasion of tumor cells. CONCLUSION: Our findings showed that H19 functions as a suppressor of NSCLC and plays an important role in the migration and invasion of NSCLC. More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, ß-catenin and ERK1/2. These results put forward our understanding of the detailed mechanism of H19 lncRNA regulating the process of NSCLC metastasis.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/patologia , Movimento Celular/efeitos dos fármacos , Neoplasias Pulmonares/patologia , Interferência de RNA , RNA Longo não Codificante/farmacologia , Células A549 , Linhagem Celular Tumoral , Humanos , Lentivirus , Sistema de Sinalização das MAP Quinases , Invasividade Neoplásica , Metástase Neoplásica , Fatores de Transcrição/metabolismo , beta Catenina/metabolismo
2.
Nan Fang Yi Ke Da Xue Xue Bao ; 35(3): 446-9, 2015 Mar.
Artigo em Chinês | MEDLINE | ID: mdl-25818798

RESUMO

OBJECTIVE: To compare the efficacy of the erlotinib versus gefitinib in the first-line treatment of patients with advanced EGFR mutation-positive NSCLC. METHODS: Fifty patients with untreated advanced EGFR mutation- positive NSCLC were randomly divided into gefitinib group (n=27) and erlotinib group (n=23). The progression-free survival, objective response rate and disease control rate were evaluated to compare the efficacy of gefitinib and erlotinib. RESULTS: There were no significant differences in the objective response rate (P=0.711) and disease control rate (P=0.861) between the two groups. The progression-free survival of gefitinib group and erlotinib group was 8.0 months and 10.0 months, respectively. The efficacy of the two drugs was similar (P=0.293). CONCLUSION: There is no significant differences between gefitinib and erlotinib in the first-line treatment of patients with advanced EGFR mutation-positive NSCLC.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Neoplasias Pulmonares/tratamento farmacológico , Quinazolinas/uso terapêutico , Intervalo Livre de Doença , Receptores ErbB/metabolismo , Cloridrato de Erlotinib , Gefitinibe , Humanos , Mutação
3.
J Huazhong Univ Sci Technolog Med Sci ; 33(6): 840-844, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-24337845

RESUMO

Our previous study demonstrated that BM-cyclin 1, a traditional anti-mycoplasma drug, could effectively reverse the multidrug resistance (MDR) of C-A120 cells. The present study aims to explore the reversal effect of BM-cyclin 1 on MDR and its mechanisms in BALB/C nude mice bearing C-A120 cells. Immunoblotting analysis and reverse transcription-polymerase chain reaction (RT-PCR) were used to study the change in multidrug resistance-associated protein 2 (MRP2) induced by BM-cyclin 1. We found that the expression levels of MRP2 protein and mRNA in C-A120 cells treated with BM-cyclin 1 were reduced significantly. Chemical colorimetry revealed no significant change in the level of glutathione (GSH). In the xenograft model, the inhibitory rate of C-A120 cells growth in BM-cyclin 1 plus adriamycin (ADM) group was 52%, which was significantly higher than in control group (P<0.01). The immunoblotting and RT-PCR results conclusively demonstrated that BM-cycin 1 could significantly reduce the expression of MRP2 in transplanted tumor. In conclusion, BM-cyclin 1 could effectively reverse the MDR of C-A120 cells in vivo by suppressing the expression of MRP2.


Assuntos
Antiprotozoários/farmacologia , Regulação para Baixo , Resistência a Múltiplos Medicamentos/efeitos dos fármacos , Proteínas Associadas à Resistência a Múltiplos Medicamentos/metabolismo , Animais , Linhagem Celular Tumoral , Diterpenos/farmacologia , Doxorrubicina/farmacologia , Humanos , Camundongos , Camundongos Nus , Minociclina/farmacologia , Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ensaios Antitumorais Modelo de Xenoenxerto
4.
Nan Fang Yi Ke Da Xue Xue Bao ; 30(5): 1024-7, 2010 May.
Artigo em Chinês | MEDLINE | ID: mdl-20501384

RESUMO

OBJECTIVE: To observe SHP-1 protein expression in breast cancer cell line MDA-MB-231 before and after SHP-1 gene transfer and its effect on the proliferation of MDA-MB-231 cells. METHODS: The eukaryotic expression vector pEGFP-C3-SHP-1 was constructed and transfected into breast cancer cell line MDA-MB-231 via Lipofectamine 2000, and the positive clones were selected using G418. SHP-1 expression in MDA-MB-231 cells was detected with immunocytochemistry and Western blotting, and the cell growth curve was observed using MTT assay. RESULTS: SHP-1 was highly expressed in transfected MDA-MB-231 cells, whose proliferation was significantly inhibited (P<0.05). CONCLUSION: SHP-1 gene transfer into MDA-MB-231 cells results in inhibition of the cell proliferation.


Assuntos
Neoplasias da Mama/patologia , Proliferação de Células , Técnicas de Transferência de Genes , Proteína Tirosina Fosfatase não Receptora Tipo 6/genética , Neoplasias da Mama/genética , Linhagem Celular Tumoral , Feminino , Humanos , Proteína Tirosina Fosfatase não Receptora Tipo 6/metabolismo
5.
Nan Fang Yi Ke Da Xue Xue Bao ; 29(5): 902-5, 2009 May.
Artigo em Chinês | MEDLINE | ID: mdl-19460704

RESUMO

OBJECTIVE: To construct a retrovirus-mediated expression system carrying human SHP-1 gene to transfer SHP-1 gene in human breast cancer MDA-MB-231 cells. METHODS: The full-length SHP-1 gene fragment was amplified by RT-PCR from the total RNA extracted from human breast cancer cell line MCF-7 over-expressing SHP-1 protein. The gene fragment was inserted into the vector pLNCX2 to construct the recombinant retroviral plasmid, which was transfected into the packaging cell PT67 via Lipofectamine2000. A cell line stably producing the virus was selected with G418. MDA-MB-231 cells was infected with the virus, and the expression of SHP-1 gene in the positive cell clone was detected with Western blotting. RESULTS: A 1.8 kb cDNA fragment of SHP-1 gene was obtained from MCF-7 cells and successfully inserted into the pLNCX2. A stable cell clone PT67/SHP-1 and virus supernatant were obtained. Expression of SHP-1 protein was detected in the cells infected with the virus. CONCLUSION: The recombinant retroviral vector carrying SHP-1 gene has been successfully constructed and MDA- MB-231/SHP-1 cell line expressing SHP-1 has been obtained to allow further functional study of SHP-1 in breast cancer.


Assuntos
Neoplasias da Mama/genética , Neoplasias da Mama/metabolismo , Proteína Tirosina Fosfatase não Receptora Tipo 6/biossíntese , Retroviridae/genética , Neoplasias da Mama/patologia , Linhagem Celular Tumoral , Clonagem Molecular , Vetores Genéticos/genética , Humanos , Proteína Tirosina Fosfatase não Receptora Tipo 6/genética , Proteínas Recombinantes/biossíntese , Proteínas Recombinantes/genética , Retroviridae/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transfecção
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