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OBJECTIVE: To explore the relationship between cancer awareness and the survival of the patients with non-small cell lung carcinoma (NSCLC).â© Methods: A total of 865 NSCLC patients were screened for the risk factors, including age, gender, address, tumor/lymph nodes/metastasis (TNM) stage, and cancer awareness. Survival of the patients was calculated by Kaplan-Meier method and Cox regression analysis.â© Results: After an average observation time of 304 d (ranging from 0 to 4 718 d), 62 of the 394 patients in the cancer awareness group survived, whereas 26 of the 471 patients in the cancer concealment group survived. Cancer-specific and all-cause survival was poorer in the cancer concealment group (P<0.001 for each, log-rank test). Cox multivariate regression analysis showed that cancer concealment displayed significantly lower cancer-specific survival [hazard ratio (HR)=1.534, 95% confidence interval (CI) 1.320 to 1.784, P<0.001] and all-cause survival (HR=1.558, 95% CI 1.346 to 1.803, P<0.001).â© Conclusion: Cancer concealment is associated with a poor survival of NSCLC patients, which may prohibit the patients from obtaining the real "right to survival".
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Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Humanos , Metástase Linfática , Prognóstico , Modelos de Riscos ProporcionaisRESUMO
[This retracts the article DOI: 10.3892/etm.2018.6226.].
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Various microRNAs (miRs) have been demonstrated to serve important roles in gastric cancer (GC). miR-153 in particular has been reported to serve a suppressive role in GC; however, the underlying mechanism remains unclear. In the present study Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to examine the mRNA and protein expression of Kruppel-like factor 5. An MTT, wound healing and transwell assay were used to study cell proliferation, migration and invasion, respectively. In the present study, quantitative polymerase chain reaction data indicated that miR-153 was significantly downregulated in GC tissues compared with the adjacent non-tumor tissues. In addition, the reduced expression of miR-153 was significantly associated with GC aggressiveness and poor prognosis of patients. The expression of miR-153 was also reduced in GC cell lines, including KATO III, NCI-N87, SNU-16 and SNU-5, when compared with normal gastric epithelial GES-1 cells. Overexpression of miR-153 in the GC SNU-5 cells by miR-153 mimic transfection significantly inhibited the cell proliferation, migration and invasion. Furthermore, KLF5 was identified as a target gene of miR-153 in SNU-5 cells by bioinformatics prediction. It was observed that KLF5 was significantly upregulated in GC tissues and cell lines, and its expression was negatively regulated by miR-153 in SNU-5 cells. Overexpression of KLF5 impaired the suppressive effects of miR-153 on the proliferation, migration and invasion of SNU-5 cells. In conclusion, the present study demonstrated that miR-153 serves a tumor suppressive role in GC, at least partly, through directly targeting KLF5, thus highlighting the clinical significance of miR-153 in GC.
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Hepatocellular carcinoma (HCC) is the most common primary liver cancer, ranking as the second leading cause of male cancer death worldwide. MicroRNA-29 (miR-29) has been demonstrated to act as a tumor suppressor in HCC. However, the regulatory mechanism of miR-29 underlying HCC growth and metastasis still remains obscure. In the present study, we showed that the expression of miR-29 was significantly reduced in HCC tissues and cell lines, and low miR-29 expression was associated with disease progression and shorter survival time of HCC patients. In vitro experiments showed that restoration of miR-29 expression caused a significant reduction in HCC cell proliferation, migration and invasion. Insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) was identified as a novel target gene of miR-29. The expression of IGF2BP1 was significantly increased in HCC tissues and cell lines. Moreover, IGF2BP1 was negatively regulated by miR-29 at the post-transcriptional levels in HCC cells. Furthermore, overexpression of IGF2BP1 attenuated the suppressive effects of miR-29 on the proliferation, migration, and invasion of HCC cells. According to these above findings, our study suggests that miR-29 may play a suppressive role in HCC growth and metastasis through directly targeting IGF2BP1. Therefore, miR-29 may be used as a potential candidate for the treatment of HCC.