RESUMO
Cancer remains one of the major cause of death in the Western world. Although, it has been demonstrated that new therapies can improve the outcome of cancer patients, still many patients relapse after treatment. Therefore, there is a need to identify novel factors involved in cancer development and/or progression. Recently, neutrophil gelatinase-associated lipocalin (NGAL) has been suggested as a key player in different cancer types. Its oncogenic effect may be related to the complex NGAL/MMP-9. In the present study, NGAL was analyzed at both transcript and protein levels in different cancer types by analysing 38 public available microarray datasets and the Human Protein Atlas tool. NGAL transcripts were significantly higher in the majority of solid tumors compared to the relative normal tissues for every dataset analyzed. Furthermore, concordance of NGAL at both mRNA and protein levels was observed for 6 cancer types including bladder, colorectal, liver, lung, ovarian, and pancreatic. All metastatic tumors showed a decrease of NGAL expression when compared to matched primary lesions. According to these results, NGAL is a candidate marker for tumor growth in a fraction of solid tumors. Further investigations are required to elucidate the function of NGAL in tumor development and metastatic processes.
Assuntos
Proteínas de Fase Aguda/genética , Proteínas de Fase Aguda/metabolismo , Perfilação da Expressão Gênica , Lipocalinas/genética , Lipocalinas/metabolismo , Neoplasias/genética , Neoplasias/metabolismo , Proteínas Proto-Oncogênicas/genética , Proteínas Proto-Oncogênicas/metabolismo , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Biologia Computacional , Conjuntos de Dados como Assunto , Humanos , Lipocalina-2 , Metástase Neoplásica , Neoplasias/classificação , Análise de Sequência com Séries de OligonucleotídeosRESUMO
Cutaneous melanoma is the most aggressive skin cancer. Beside surgery, it is treated with chemotherapy and immunotherapy. However, many patients relapse after adjuvant therapy. The recent identification of several key molecular pathways implicated in the pathogenesis of melanoma is spreading development of a number of new translational targeted therapies which could play an important role in overcoming or minimizing resistance to chemotherapeutic drugs and proapoptotic therapies. This review summarizes environmental factors and the most significant molecular events involved in melanoma pathogenesis, disclosing mechanisms responsible for drug resistance and pointing out the clinical view for emerging targeted therapies. Standard therapies and an update on the current clinical trials are also described.
Assuntos
Resistencia a Medicamentos Antineoplásicos , Melanoma/terapia , Neoplasias Cutâneas/terapia , Antineoplásicos/uso terapêutico , Apoptose , Antígeno CTLA-4/metabolismo , Proteínas de Choque Térmico HSP90/antagonistas & inibidores , Humanos , Terapia de Alvo Molecular , Inibidores de Proteassoma , Inibidores de Proteínas Quinases/uso terapêuticoRESUMO
MicroRNAs (MiRNAs) are small non-coding RNAs able to regulate gene expression at a posttranscriptional level. Recent evidence indicates that they play a crucial role in the initiation and progression of human cancers. In this review we briefly describe microRNA biogenesis and function, giving a more detailed account of the current state of knowledge concerning the role of microRNAs in brain tumors and stem-like tumor cells. MicroRNAs control brain tumor development by regulating multiple biological characteristics such as proliferation, invasion, differentiation and angiogenesis. Research in this field is rapidly spreading and encourages potential applications of microRNAs as diagnostic and prognostic tools, in addition to therapeutic targets and tools, to grant clinical benefits to patients suffering of brain tumors.
