RESUMEN
More and more evidence shows that long non-coding RNA (lncRNA) plays an important role in the biological behavior of many kinds of malignant tumors, but the specific function of lncRNA Linc00657 in cervical cancer is still unknown. The purpose of this study is to explore the effect of Linc00657 on the malignant progression of cervical cancer and its potential mechanism. In two kinds of cervical cancer cell lines and normal cervical epithelial cells, qRT-PCR showed increased expression of Linc00657 in cervical cancer cells. Through MTT, clone formation test, flow cytometry, wound healing test and Transwell test, it has been found that overexpression of Linc00657 could promote the proliferation,migration and invasion of cervical cancer cellsï¼and inhibit apoptosis. Through the StarBase database, it was found that there may be a mutual regulatory relationship between Linc00657 and Skp2, and Skp2 may be the downstream target of Linc00657. QRT-PCR detection confirmed that the expression of Skp2 was increased in cervical cancer cells with overexpression of Linc00657. TIMER2 database found that Skp2 was associated with lipid metabolic enzymes and immune cell infiltration. It was found that Linc00657 knockdown inhibited tumor growth and metastasis and inhibited the expression of Skp2 in vivo. In short, our research shows that Linc00657 has carcinogenic properties in cervical cancer, and LINC00657 promotes the occurrence of cervical cancer by up-regulating the expression of Skp2. We predict that Linc00657/mir30s/Skp2 axis plays a role in the malignant progression of cervical cancer. In addition, Skp2 may participate in cancer immune response and promote lymph node metastasis of cervical cancer through lipid reprogramming. These findings also provide promising targets for the diagnosis and treatment of cervical cancer.
Asunto(s)
MicroARNs , ARN Largo no Codificante , Neoplasias del Cuello Uterino , Femenino , Humanos , Línea Celular Tumoral , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Neoplasias del Cuello Uterino/genética , Carcinogénesis/genética , Lípidos , Regulación Neoplásica de la Expresión Génica , Proliferación Celular/genética , Movimiento Celular/genética , MicroARNs/metabolismo , Microambiente Tumoral/genéticaRESUMEN
Osteosarcoma is an aggressive form of bone cancer and affects the health in children and adolescents. Although conventional treatment improves the osteosarcoma survival, some patients have metastasis and drug resistance, leading to a worse prognosis. Therefore, it is necessary to explore the molecular mechanism of osteosarcoma occurrence and progression, which could discover the novel treatment for osteosarcoma. Long noncoding RNAs (lncRNAs) have been reported to regulate osteosarcoma occurrence and malignant progression. LncRNA HOXA-AS3 facilitates the tumorigenesis and progression in a variety of human cancers. However, the underlying mechanism of lncRNA HOXA-AS3-induced oncogenesis is poorly determined in osteosarcoma. To address this point, we utilized several cellular biological strategies and molecular approaches to explore the biological functions and mechanisms of lncRNA HOXA-AS3 in osteosarcoma cells. We found that lncRNA HOXA-AS3 facilitates cell proliferation and invasion via targeting miR-218-5p/FOXP1 axis in osteosarcoma. In conclusion, lncRNA HOXA-AS3 could be a promising target for osteosarcoma treatment.
Asunto(s)
Neoplasias Óseas , Proliferación Celular , Factores de Transcripción Forkhead , Regulación Neoplásica de la Expresión Génica , MicroARNs , Osteosarcoma , ARN Largo no Codificante , Proteínas Represoras , Osteosarcoma/genética , Osteosarcoma/patología , Osteosarcoma/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Humanos , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Proliferación Celular/genética , Línea Celular Tumoral , Proteínas Represoras/genética , Proteínas Represoras/metabolismo , Factores de Transcripción Forkhead/genética , Factores de Transcripción Forkhead/metabolismo , Neoplasias Óseas/genética , Neoplasias Óseas/patología , Neoplasias Óseas/metabolismo , Invasividad Neoplásica , Movimiento Celular/genéticaRESUMEN
Osteosarcoma often occurs in children and adolescents and affects their health. The survival rate of osteosarcoma patients is unsatisfactory due to the lack of early detection and metastasis development and drug resistance. Hence, dissection of molecular insight into osteosarcoma initiation and progression is pivotal to provide the new therapeutic strategy. In recent years, long noncoding RNAs (lncRNAs) have burst into stage in osteosarcoma development and malignant behaviors. LncRNA SCAMP1 has been discovered to play an essential role in carcinogenesis and progression. However, the mechanisms of lncRNA SCAMP1-involved tumorigenesis have not been reported in human osteosarcoma. In this study, we utilized multiple cellular biological approaches to determine the function of lncRNA SCAMP1 in osteosarcoma cells. Moreover, we performed several molecular biological approaches to define the mechanism by which lncRNA SCAMP1 regulated cell viability and invasion in osteosarcoma. We dissected that lncRNA SCAMP1 promoted progression of osteosarcoma via modulation of miR-26a-5p/ZEB2 axis. In conclusion, targeting lncRNA SCAMP1 and its downstream targets, miR-26a-5p and ZEB2, might be a useful approach for osteosarcoma therapy.