Background and aim: Serum fibrinogen and albumin are two important factors in systemic inflammation and these two factors are related to tumor progression. This study aimed to comprehensively reveal the prognostic value of the ratio of fibrinogen and albumin in malignant tumors. Methods: We systematically searched relevant studies in PubMed, Web of Science and Embase up to November 21, 2018. Hazard ratios (HRs) or odds ratio (ORs) for overall survival (OS)/disease-free survival (DFS), as well as relevant clinical data, were collected for analysis; all data analyses were performed by using STATA/SE 14. Results: Twelve cohort studies were included in this meta-analysis, with a total of 5,088 cases including 9 different kinds of tumors recruited. The pooled results showed that high albumin/fibrinogen ratio (FAR) and low fibrinogen/albumin ratio (AFR) were significantly associated with poor OS (HR=1.50, 95% CI: 1.30–1.70). Subgroup analyses for OS were also performed based on the disease type, detection method, follow-up time and treatment. Similarly, high FAR or low AFR indicated a worse DFS in cancer patients (HR=1.86; 95% CI: 1.41–2.31). In addition, high FAR or low AFR was statistically significant in relation to deeper tumor infiltration (OR=2.81, 95%CI: 1.67–4.72), positive lymph node metastasis (OR=1.57, 95%CI: 1.23–2.02) and distant metastasis (OR=2.30, 95% CI: 1.36–3.89) as well as advanced clinical stage (OR=2.02, 95% CI: 1.17–3.47). Conclusions: The ratio of fibrinogen and albumin could act as a promising prognostic marker in human malignant tumors. It might assist physicians to select optimal treatments by identifying the current status of the patient. Future multicenter clinical trials are needed to validate its applications.

Background: Numerous studies have reported that systemic immune-inflammation index (SII) and C-reactive protein-to-albumin ratio (CAR) correlate with tumor progression and prognosis in various types of human cancer. The aim of this study is to systematically investigate the clinical significance of SII and CAR in esophageal cancer (EC). Methods: We searched a number of databases for articles reporting the effect of pretreatment SII and CAR on the survival of EC patients. Review Manager 5.3 and STATA/SE 14.1 were applied in this meta-analysis. The multivariable-adjusted hazard ratio (HR) was used for calculating the relationship between SII and CAR and overall survival (OS), and the odds ratio (OR) was applied for the clinical pathology. Results: Five original studies for SII and seven original datasets for CAR were included for analysis. Increased SII showed a significant association with shorter OS in EC patients after surgery (HR: 1.34, 95% CI: 1.15–1.53, P <0.001) and high CAR indicated worse long-term OS in EC (HR: 1.60, 95% CI: 1.29–1.90, P <0.001). Different subgroup analyses were also confirmed the prognostic roles in EC patients. Furthermore, the adverse impacts of elevated SII and CAR on tumor progression were revealed in the infiltration depth, lymph node metastasis, and clinical stage. Conclusions: Both pretreatment SII and CAR might be promising predictors of cancer survival and tumor progression in EC. Further studies are warranted to verify the clinical usefulness in patients with EC.

Background Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer death in the world, and has a relatively low survival rate. Long non-coding RNAs (lncRNAs) have been demonstrated to modulate cancer progression through a variety of molecular mechanisms. We sought to investigate the role and potential mechanism of MYC-induced long non-coding RNA (MINCR) in NSCLC. Methods Expression levels of MINCR was first identified using The Cancer Genome Atlas (TCGA), further confirmed with specimens from 29 NSCLC patients and three cell lines using qRT-PCR. Overexpression and knockdown of MINCR were performed in NSCLC cell lines through MINCR overexpression vectors and synthesized siRNAs, respectively. The roles of MINCR in NSCLC cell lines, such as cell proliferation, cell cycle arrest, and apoptosis, were identified by MTT, flow cytometry, and Western blot. The modulation of MINCR-regulated genes, including c-Myc and its downstream effectors, as well as apoptosis-associated genes, was analyzed using Western blot. Results MINCR expression was increased in NSCLC patients from TCGA datasets, and was also significantly increased in our collected specimens from NSCLC patients and NSCLC cell lines. Knocking down of MINCR greatly inhibited the growth of NSCLC cell lines PC9 and A549. In addition, silencing of MINCR induced cell cycle arrest and apoptosis. Furthermore, silencing of MINCR reduced the expression levels of oncogene c-Myc and its downstream cyclin A, cyclin D, CD4, and CDK2, as well as apoptosis-associated Bcl-2, while significantly increased the expression levels of cleaved PARP-1. In the meantime, overexpression of MINCR remarkably enhanced cell proliferation of PC9 cells and activated c-Myc and its downstream effectors. Conclusion MINCR exerted inhibitory effects on the cell cycle arrest and apoptosis of NSCLC cells by activating c-Myc and its downstream effectors, suggesting that this lncRNA could be used as a potential therapeutic target for the treatment of NSCLC. Electronic supplementary material The online version of this article (10.1186/s12931-019-1174-z) contains supplementary material, which is available to authorized users.

Background: Previous researches have reported that tripartite motif-containing 44 (TRIM44) is related to the prognosis of multiple human tumors. This study was designed to systematically assess the prognostic value of TRIM44 in human malignancies and summarize its possible tumor-related mechanisms. Methods: The available databases were searched for eligible studies that evaluated the clinicopathological and prognostic roles of TRIM44 in patients with malignancies. The hazard ratios (HR) and odds ratios (OR) were combined to assess the predictive role of TRIM44 using Stata/SE 14.1 software. Results: A total of 1740 patients from thirteen original studies were finally included in this study. The results of the combined analysis showed that over-expression of TRIM44 protein was significantly correlated with shorter overall survival (OS) (HR = 1.94, 95% CI: 1.60-2.35) and worse disease-free survival (DFS) (HR = 2.13, 95% CI: 1.24-3.65) in cancer patients. Additionally, the combined ORs indicated that elevated expression level of TRIM44 protein was significantly associated with lymph node metastasis (OR = 2.69, 95% CI: 1.71-4.24), distant metastasis (OR = 10.35, 95% CI: 1.01-106.24), poor tumor differentiation (OR = 1.78, 95% CI: 1.03-3.09), increased depth of tumor invasion (OR = 2.72, 95% CI: 1.73-4.30), advanced clinical stage (OR = 2.75, 95% CI: 2.04-3.71), and recurrence (OR = 2.30, 95% CI: 1.34-3.95). Furthermore, analysis results using Gene Expression Profiling Interactive Analysis (GEPIA) showed that the expression level of TRIM44 mRNA was higher in most tumor tissues than in the corresponding normal tissues, and the relationship between TRIM44 mRNA level and prognosis in various malignant tumors also explored in GEPIA and OS analysis webservers. Conclusions: TRIM44 may serve as a valuable prognostic biomarker and a potential therapeutic target for patients with malignancies.

Proliferation and metastasis are important malignant features of pancreatic cancer (PC), but the underlying molecular mechanism is unclear. ZC3HAV1, a PARP family member of proteins-enzymes, has been considered to play a significant part in a variety of biological processes. Nonetheless, the functions of ZC3HAV1 in developing PC are still unknown. This research aims to explore the biological function and the expression of ZC3HAV1 shown in PC. In our study, PCR analysis suggested that ZC3HAV1 was expressed at a high level in PC tissues and cell lines, and high ZC3HAV1 expression was remarkably related to poor prognosis. The functional assays indicated that upregulated ZC3HAV1 accelerated PC cell proliferation along with colony formation capacities in vitro . Subsequently, ZC3HAV1 could upregulate cyclin D1 and CDK2 and also promote G1/S transition in cells of PC. What’s more, we also discovered that ZC3HAV1 promotes the migration and the invasion of PC cells. It upregulates the expression of EMT (epithelial-mesenchymal transition) relevant markers. Conversely, the functional assays showed that ZC3HAV1 knockdown significantly reduced tumorigenesis. Using bioinformatics analysis and immunoprecipitation assays we found that ZC3HAV1 could directly bind to KRAS and positively regulate its expression. Furthermore, ZC3HAV1 overexpression activated MAPK signaling by increasing p-ERK levels. Conversely, knockdown of KRAS attenuated ZC3HAV1-mediated promotion of proliferation and invasion in cells of PC. The result indicated that ZC3HAV1 was in relation to poor prognosis and accelerated the proliferation and metastasis of PC cells by regulation of KRAS. Our research may offer brand-new evidence to diagnose and treat PC in clinic.