Background:Several studies were conducted to investigate the prognostic value of pretreatment serum lactate dehydrogenase (LDH) level in pancreatic cancer (PC), but the results were inconsistent. This study aims to comprehensively assess the prognostic value of pretreatment serum LDH level in PC patients by combining the data of the published literatures on this topic.Methods:Embase, PubMed, and Web of Science were completely retrieved until June, 2018. The observational studies focusing on the prognostic value of pretreatment serum LDH level in PC patients were eligible. STATA version 12.0 was used to undertake the statistical analysis.Results:Eighteen studies with a total of 3345 patients were included in this meta-analysis. The meta-analysis was conducted to generate pooled hazard ratios (HRs) and 95% confidence interval (CI) for overall survival (OS). Our analysis results suggested that high serum LDH level predicted worse OS (HR 1.57, 95% CI 1.30–1.90, P < .001) in PC patients. Moreover, for patients with advanced PC, the prognostic relevance of pretreatment serum LDH level not only existed in those receiving palliative chemotherapy (HR 1.72, 95% CI 1.35–2.18, P < .001), but also in those who were precluded from chemotherapy (HR 1.91, 95% CI 1.4219–2.58, P < .001).Conclusion:The meta-analysis results demonstrated that pretreatment serum LDH level is closely associated with OS, and it may be a useful biomarker for assessing the prognosis of PC patients.
Background:The expression levels and detailed functions of LINC00265 in gastric cancer (GC) have not yet been explored. This study aimed to measure LINC00265 expression in GC tissues and cell lines, investigate its specific roles in the aggressive characteristics of GC cells in vitro and in vivo, and elucidate the regulatory mechanisms of LINC00265 action.Materials and methods: The qRT-PCR was performed to test the RNA expression levels in GC tissues and cell lines. Cell proliferation was detected by CCK-8 and colony formation assays. Western blot assay was used to measure relevant protein expression. Luciferase reporter assays were performed to investigate the association between LINC00265 and microRNA-144-3p and CBX4.Results: LINC00265 expression was high in GC tissue samples and cell lines; LINC00265 overexpression correlated with shorter overall survival of the patients. A LINC00265 knockdown inhibited GC cell proliferation in vitro and slowed tumor growth in vivo. Mechanism investigation revealed that LINC00265 acts as a competing endogenous RNA on microRNA-144-3p (miR- 144) in GC cells. Chromobox 4 (CBX4) mRNA was identified as a direct target of miR-144-3p in GC cells. The knockdown of miR-144-3p counteracted the reduction in the malignant characteristics of GC cells by the downregulation of LINC00265.Conclusion: In conclusion, LINC00265 functions as a competing endogenous RNA targeting miR-144-3p and increases the malignancy of GC cells in vitro and in vivo by upregulating CBX4.
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