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1.
Kaohsiung J Med Sci ; 37(8): 699-708, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34042256

RESUMO

Cervical cancer is the fourth highest mortality cancer among women worldwide. Many researchers have discovered the major anticancer role of miR-192-5p. However, no study has revealed the effect of miR-192-5p on cervical cancer and its molecular mechanism. Therefore, in this study, we aimed to explore the role of miR-192-5p in proliferation, invasion of cervical cancer, and its regulatory mechanism. Firstly, the expression level of miR-192-5p was examined by real-time quantitative polymerase chain reaction. Cell counting kit-8 analysis was applied to detect the proliferation of transfected Caski and SiHa cells. Flow cytometry assay was applied to detect the apoptosis of transfected Caski and SiHa cells. Our result showed that miR-192-5p restrained cervical cancer cell proliferation and induced apoptosis. Then we employed wound healing and transwell assays to analyze the migration and invasion abilities of Caski and SiHa cells in vitro. The results showed that miR-192-5p had an inhibitory effect on cervical cancer migration and invasion. The results of in vivo experiment demonstrated that miR-192-5p also inhibited tumor development in nude mice. We further detected that the binding of transient receptor potential melastatin-subfamily member 7 (TRPM7) to miR-192-5p using bioinformatic methods and dual-luciferase reporter assay. Finally, we found that TRPM7 overexpression reversed the inhibitory effects of miR-192-5p on proliferation, migration, and invasion on cervical cancer cells. In conclusion, the findings of the present study revealed that miR-192-5p performs an inhibitory role in cervical cancer proliferation and invasion by targeting TRPM7.


Assuntos
Proliferação de Células/fisiologia , Genes Supressores de Tumor , MicroRNAs/metabolismo , Invasividade Neoplásica/fisiopatologia , Proteínas Serina-Treonina Quinases/metabolismo , Canais de Cátion TRPM/metabolismo , Neoplasias do Colo do Útero/patologia , Animais , Linhagem Celular Tumoral , Feminino , Xenoenxertos , Humanos , Camundongos , Camundongos Nus , MicroRNAs/fisiologia , Ligação Proteica , Neoplasias do Colo do Útero/metabolismo
2.
Zhonghua Fu Chan Ke Za Zhi ; 41(2): 88-90, 2006 Feb.
Artigo em Chinês | MEDLINE | ID: mdl-16640854

RESUMO

OBJECTIVE: To evaluate the efficacy of floxuridine, actinomycin D, etoposide, vincristine (FAEV) regimen in treatment of high-risk drug-resistant gestational trophoblastic tumor (GTT). METHODS: From October 2001 to May 2004, 11 cases of high-risk drug-resistant GTT were treated with FAEV regimen. The International Federation of Gynecology and Obstetrics (FIGO) prognosis score (2000) was 7 to 13 (median 9). All patients were referred to Peking Union Medical College Hospital because of failure of chemotherapy previously. After the FAEV treatment, they were followed up for 15 to 42 months. RESULTS: Seven cases (64%, 7/11) were cured by FAEV regimen. The median treatment course for serum human chorionic gonadotropin reaching normal level was 3. Four cases (36%, 4/11) showed drug-resistant to FAEV regimen. The major side effect of FAEV regimen was myelosuppression. Granulocyte colony stimulating factor support was needed after 98% (63/64) of the courses. CONCLUSION: For those high-risk drug-resistant GTT cases, FAEV regimen could be considered as an effective choice of treatment.


Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Doença Trofoblástica Gestacional/tratamento farmacológico , Adulto , Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos , Gonadotropina Coriônica Humana Subunidade beta/sangue , Dactinomicina/administração & dosagem , Resistencia a Medicamentos Antineoplásicos , Etoposídeo/administração & dosagem , Feminino , Floxuridina/administração & dosagem , Seguimentos , Doença Trofoblástica Gestacional/patologia , Doença Trofoblástica Gestacional/cirurgia , Humanos , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Gravidez , Resultado do Tratamento , Vincristina/administração & dosagem
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