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Purpose: To investigate the role of serum CYR61 as a biomarker for the diagnosis of breast cancer and to analyze the association between serum CYR61 levels and the clinicopathological features in breast cancer patients. Methods: Serum CYR61 was measured in breast cancer patients and healthy controls by ELISA. Results: The serum levels of CYR61 in breast cancer patients were higher than those in healthy controls. The area under the receiver operating characteristic curve for CYR61 was higher than that for carcinoembryonic antigen and carbohydrate antigen 15-3. The increased CYR61 levels were correlated with menopausal status and Ki67 expression. Conclusion: Serum CYR61 might be a novel biomarker to assist the diagnosis and clinicopathological status assessment of breast cancer.

Although the clinical application of oxaliplatin (L-OHP) has improved the survival of colorectal cancer (CRC) patients, approximately half of patients with CRC fail to achieve good clinical outcomes, indicating resistance to L-OHP therapy. Cysteine-rich protein 61 (Cyr61), a multifunctional extracellular matrix protein, is highly expressed in a variety of tumors; increased Cyr61 expression is known to be closely involved in the chemotherapeutic resistance of many tumors, but its role in the L-OHP resistance of CRC cells has not been studied. In this study, we aimed to investigate the role of Cyr61 in the L-OHP resistance of CRC cells and examine the underlying mechanism. Our findings showed that the mRNA and protein levels of Cyr61 in L-OHP-resistant cells were significantly increased compared with those in nonresistant cells. Knockdown of Cyr61 enhanced the chemosensitivity of L-OHP-resistant cells to L-OHP. Mechanistically, we found that overexpression of Cyr61 decreased L-OHP-induced apoptosis in drug-resistant CRC cells through the regulation of Bcl-xL. Collectively, our results revealed for the first time that Cyr61 plays a crucial role in the resistance of CRC cells to L-OHP and indicated that targeting Cyr61 may be a promising therapeutic strategy to overcome L-OHP resistance in CRC.

Background: Acute lymphoblastic leukemia（ALL）is the second most common hematologic malignancy worldwide with B-acute lymphoblastic leukemia（B-ALL）accounting for 70%-80%. Cysteine‐rich protein 61 (Cyr61), a potential tumor-promoting factor, is increased in both serum and bone marrow of B-ALL patients in our previous study. We aimed to elucidate the role of Cyr61 in B-ALL as well as to explore the source of Cyr61 in the bone marrow of B-ALL patients.Methods: The human B-ALL cell line Nalm-6 was used. Cyr61 expression levels were measured by using quantitative real-time PCR (qRT-PCR), enzyme-linked immunosorbent assay (ELISA) and western blot analysis. The biological functions of Cyr61 in regulating B-ALL cell chemosensitivity to DNR and VCR was detected by cell viability assay and flow cytometry analysis. The production mechanisms of Cyr61 in the bone marrow were measured by qRT-PCR and western blot analysis.Results: Knockdown of Cyr61 increased the chemosensitivity of Nalm-6 cells to DNR and VCR, and overexpression of Cyr61 decreased the chemosensitivity of Nalm-6 cells to DNR and VCR. Mechanistically, we found that Cyr61 attenuated chemotherapeutic drug-induced apoptosis by the upregulation of Bcl-2. Importantly, Cyr61 can be up-regulated by the chemotherapeutic drug DNR through the ATM-dependent NF-κ B pathway, however, VCR has no effect on the expression of Cyr61 in B-All cells.Conclusions: In conclusion, our study revealed that DNR can induce the production of Cyr61 in B-ALL cells; further, increasing Cyr61 decreased the chemosensitivity of B-ALL cells to chemotherapeutic drugs. Thus, targeting Cyr61 may be a promising therapeutic strategy to increase the chemotherapy sensitivity in patients with B-ALL.

Background Colorectal cancer (CRC) is the third most common cancer and it is a worldwide challenge. Neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) had been suggested as markers of CRC, but the role of monocyte-to-lymphocyte ratio (MLR) in CRC patients before surgery and chemotherapy is unclear. The study aimed to compare the diagnosis and prognosis value of MLR, NLR, and PLR in CRC. Methods A retrospective study was conducted on 783 patients with histologically confirmed colorectal cancer between 2015 and 2017 in Fujian Medical University Union Hospital. A total of 1,232 healthy age-matched participants were eligible for the study. Receiver-operating characteristic (ROC) analysis was performed to compare the area under the ROC curve (AUC) of MLR, NLR, PLR, carcinoembryonic antigen (CEA), and carbohydrate antigen 19-9 (CA19-9). Furthermore, chi-squared test was conducted to determine the prognostic values of MLR, NLR, and PLR. Results The levels of MLR, NLR, and PLR in CRC patients were significantly higher than those in 1,232 healthy participants. The area under the ROC curves (AUCs) of MLR, CEA, PLR, NLR, and CA19-9 were 0.739, 0.726, 0.683, 0.610, and 0.603, respectively. Moreover, the combined marker of CEA + MLR with an AUC of 0.815 acted as a superior diagnostic marker compared to the other combined markers, including the combined marker of CEA + CA19-9. Furthermore, the level of MLR was associated with tumor size (p = 0.001), and a high level of NLR was significantly correlated with pT stage (p = 0.048) and tumor size (p = 0.004). Conclusions The present study shows for the first time that MLR rather than NLR and PLR is the better diagnostic marker for colorectal cancer, and NLR may be a better prognostic marker for CRC patients.

An increasing number of studies have indicated that red blood cell distribution width (RDW) may be a novel biomarker for the diagnosis and prognosis of various malignancies. However, to date, data on the association of RDW with non-small cell lung cancer (NSCLC) are unclear. Our present study aimed to explore the value of RDW in NSCLC patients. A total of 338 NSCLC patients, 109 small cell lung cancer (SCLC) patients, and 302 healthy participants were retrospectively analyzed between January 2016 and December 2018. In the present study, we found that RDW was significantly increased in NSCLC patients. Receiver-operating characteristic (ROC) analysis showed that the area under the ROC curve (AUC) of RDW was 0.753 in discriminating NSCLC patients from healthy participants, the optimal cut-off value of RDW was 12.95, and the specificity and sensitivity were 76.33% and 76.16%, respectively. Further analysis found that RDW can enhance the diagnostic performance of Cyfra21-1 and NSE in discriminating NSCLC patients from healthy participants or SCLC patients. Among NSCLC patients, RDW was significantly correlated with TNM stage, T stage, N stage, M stage, and Cyfra21-1, indicating that RDW may be helpful for predicting the prognosis of NSCLC patients. Our findings suggest that RDW can be used as an auxiliary marker for the diagnosis and prognosis of NSCLC.

Background SCARA5 has been demonstrated to be a tumor suppressor gene, with its expression downregulated in many cancer types. However, only few studies have investigated its role in colorectal cancer (CRC). The current study evaluated SCARA5 expression levels in CRC and its potential value as a diagnostic biomarker for CRC. Methods Data were downloaded from the TCGA, GEO, and Oncomine databases to evaluate SCARA5 mRNA expression levels in CRC. The prognosis value of SCARA5 was assessed using the online tool Cutoff Finder via the Kaplan-Meier plotter (n = 484). Immunohistochemistry was performed to analyze and compare the SCARA5 protein expression levels in CRC and normal tissues from 67 CRC clinical specimens. Relevant CRC CNV data were downloaded from TCGA and cBioPortal for Cancer Genomics databases to assess the associated genetic alterations. GSEA was used to explore the underlying molecular mechanisms of SCARA5. The correlation between SCARA5 mRNA levels and cell cycle-associated genes was explored using GEPIA database. Results SCARA5 mRNA levels were found to be downregulated in CRC tissues compared with normal tissues. Survival analysis showed that low SCARA5 expression was associated with poor prognosis. These results were validated in clinical specimens, wherein the SCARA5 protein levels were significantly downregulated in CRC tissues compared with paracarcinoma tissues. Deep deletion was the most common genetic alteration and was consistent with the downregulated SCARA5 expression in CRC tissues. GSEA indicated that the gene sets of CELL CYCLE, G2M CHECKPOINT, and E2F TARGETS were negatively related to SCARA5 mRNA expression. GEPIA indicated that the mRNA expression of some cell cycle-associated genes was negatively correlated with that of SCARA5 in CRC. Conclusions Thus, SCARA5 may act as a human cancer suppressor gene in CRC, and its expression level may be a reliable adjuvant parameter to diagnose CRC and predict tumor metastasis and prognosis.

Background. S100 family genes exclusively encode at least 20 calcium-binding proteins, which possess a wide spectrum of intracellular and extracellular functions in vertebrates. Multiple lines of evidences suggest that dysregulated S100 proteins are associated with human malignancies including colorectal cancer (CRC). However, the diverse expression patterns and prognostic roles of distinct S100 genes in CRC have not been fully elucidated. Methods. In the current study, we analyzed the mRNA expression levels of S100 family genes and proteins and their associations with the survival of CRC patients using the Oncomine analysis and GEPIA databases. Expressions and mutations of S100 family genes were analyzed using the cBioPortal, and protein-protein interaction (PPI) networks of S100 proteins and their mutation-related coexpressed genes were analyzed using STRING and Cytoscape. Results. We observed that the mRNA expression levels of S100A2, S100A3, S100A9, S100A11, and S100P were higher and the level of S100B was lower in CRC tissues than those in normal colon mucosa. A high S100A10 levels was associated with advanced-stage CRC. Results from GEPIA database showed that highly expressed S100A1 was correlated with worse overall survival (OS) and disease-free survival (DFS) and that overexpressions of S100A2 and S100A11 were associated with poor DFS of CRC, indicating that S100A1, S100A2, and S100A11 are potential prognostic markers. Unexpectedly, most of S100 family genes showed no significant prognostic values in CRC. Conclusions. Our findings, though still need to be ascertained, offer novel insights into the prognostic implications of the S100 family in CRC and will inspire more clinical trials to explore potential S100-targeted inhibitors for the treatment of CRC.