Assuntos
Adenocarcinoma de Pulmão/genética , Ataxina-7/genética , Crizotinibe/farmacologia , Neoplasias Pulmonares/genética , Proteínas de Fusão Oncogênica/genética , Proteínas Proto-Oncogênicas c-met/genética , Fatores de Transcrição/genética , Adenocarcinoma de Pulmão/diagnóstico , Adenocarcinoma de Pulmão/tratamento farmacológico , Adenocarcinoma de Pulmão/patologia , Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Biópsia , Crizotinibe/uso terapêutico , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Resistencia a Medicamentos Antineoplásicos/genética , Feminino , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/patologia , Pessoa de Meia-Idade , Resultado do TratamentoRESUMO
Recent studies have shown an indirect link between platelet count and blood vessel metastasis, but this association with lymphatic vessels metastasis has not been established in NSCLC. So we investigated whether an association exists between preoperative platelet count and lymph node metastasis in NSCLC patients. Between January 2001 and January 2011, platelet counts were obtained from 883 NSCLC patients who were resistant to chemotherapy, radiotherapy, and surgery. The preoperative platelet counts, tumor metastasis, and overall survival of NSCLC patients were analyzed for correlations via statistical analysis. Upon considering patients according to their TNM lymph node metastasis stage (N0-N3), multiple comparison analyses revealed that the mean preoperative platelet count of the N0 group was significantly lower than that of the N1-N3. Analysis of variance showed that the preoperative platelet count of patients in stage I was significantly lower than that of those in stages II, III, and IV, with no significant difference among the latter three stages. According to the Kaplan-Meier survival analysis, the overall survival of patients with platelet counts <214.5 × 109/L was significantly longer than that of those with platelet counts ≥214.5 × 109/L. Cox regression analysis indicated that, besides preoperative platelet count, patient age, gender, and TNM stage were independent prognostic factors. In conclusion, preoperative platelet count was significantly associated with metastasis of lymph nodes in NSCLC patients. Preoperative platelet count may be a reliable biomarker of lymph node metastasis possibility and an independent prognostic factor of overall survival in patients with NSCLC.
Assuntos
Carcinoma Pulmonar de Células não Pequenas/sangue , Neoplasias Pulmonares/sangue , Contagem de Plaquetas , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Carcinoma Pulmonar de Células não Pequenas/mortalidade , Carcinoma Pulmonar de Células não Pequenas/patologia , Feminino , Humanos , Neoplasias Pulmonares/mortalidade , Neoplasias Pulmonares/patologia , Metástase Linfática , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Prognóstico , Modelos de Riscos ProporcionaisRESUMO
OBJECTIVE: Aberrant activation of (Wingless and mouse homolog Int-1) Wnt/ß-catenin signaling pathways closely involved in the occurrence and progression of several types of human malignancies. This research was undertaken to elucidate the important role of (Wingless and mouse homolog Int-1) in lung cancer. PATIENTS AND METHODS: Wnt3 expression in lung cancers and their respective normal tissues were examined by immunoblotting and immunohistochemistry. Then, Wnt3 was regulated with RNA interference (RNAi) technology in human lung cancer A549 cells, and the cell proliferation, cell cycle, cell invasion/metastasis, and apoptosis were evaluated. RESULTS: In all cases, Wnt3 expression was significantly elevated in lung cancers compared with normal tissues. Knocking down Wnt3 in A549 lung cancer cells by small interfering RNAs transfection led to a distinct reduction of Wnt3 in both transcript and protein levels. Knockdown of Wnt3 expression in lung cancer cells inhibited the expression of ß-catenin and cyclin D1 genes in Wnt/ß-catenin pathway. It also significantly blocked cellular proliferation, delayed cell cycle and suppressed cell invasion/metastasis, accompanied by a higher apoptosis rate. CONCLUSIONS: We conclude that the upregulation of Wnt3 plays a crucial role in lung tumorigenesis by inducing proliferation, migration, and invasion and inhibiting apoptosis of cancer cells. Wnt3 might be a potential target for the treatment of lung cancer.