MicroRNAs (miRNA) are a class of small, noncoding RNA molecules that regulate the expression of target genes. miRNA dysregulation is involved in carcinogenesis and tumor progression. In this study, we identified microRNA-1253 (miR-1253) as being significantly down-regulated in non-small-cell lung carcinoma (NSCLC) tissues and associated with advanced clinical stage, lymph node metastasis, and poor survival. The enhanced expression of miR-1253 significantly inhibited the proliferation, migration, and invasion of NSCLC cells in vitro. Bioinformatics analyses showed that miR-1253 directly targeted WNT5A (long isoform), which was confirmed using the dual-luciferase reporter assay. The inhibitory effects of miR-1253 on the growth and metastasis of NSCLC cells were attenuated and phenocopied by WNT5A (long) overexpression and knockdown, respectively. Consistent with the in vitro results, subcutaneous tumor and metastatic NSCLC mouse models showed that miR-1253 functions as a potent suppressor of NSCLC in vivo. Taken together, our findings indicated that miR-1253 inhibited the proliferation and metastasis of NSCLC cells by targeting WNT5A (long isoform) and provided new evidence of miR-1253 as a potential therapeutic target in NSCLC.

We retrospectively enrolled 825 breast cancer patients, who was primarily diagnosed in our hospital between January 2009 and December 2014 and explored the relationship between red blood cell distribution width (RDW) and long-term prognosis in patients with breast cancer. There were 412 patients with high RDW (RDW > 13.82) and 413 patients with low RDW (RDW ≤ 13.82). Compared with low RDW group, the high w group has large tumor size (the rate of tumor size >2 cm: 60.7 vs 44.8%, P=0.013). The rate of lymph node metastases was higher in the high RDW group thaten that in the low RDW group (62.1 vs 45.8%, P=0.000). RDW was positively associated with tumor stage. The high RDW tended to be advanced stage (P=0.000). Compared with low RDW group, the high RDW group tended to be higher lymphocyte count (P=0.004), elevated fibrinogen (P=0.043), and elevated high-sensitivity C-reactive protein (P=0.000). The Kaplan–Meier analysis indicated elevated RDW was positively associated with disease-free survival (DFS) (P=0.004) and overall survival (OS) (P=0.011). The multivariate Cox regression analysis indicated that the high RDW group had poorer OS (Hazard risk [HR] = 2.43; 95% CI: 1.62–3.21; P=0.024) and DFS (HR = 1.89; 95% CI: 1.28–3.62; P=0.000) compared with low RDW group. The present study found that high pretreatment RDW levels in breast cancer patients were associated with poor OS and DFS. RDW could be a potential predictive factor in differential diagnosis of poor prognosis from all patients.

MCF-7 cell proliferation was increased, invasion and migration were enhanced, with upregulated expression of HIF-1α mRNA and miR-210 in the hypoxic and anaerobic group following time extension.

Triple-negative breast cancer (TNBC) is a type of breast cancer that is characterized by the lack of expression of estrogen and progesterone receptors, and epidermal growth factor receptor 2. Therefore, there is an absence of a specific target for effective therapy in TNBC. Cisplatin is usually employed as a first-line chemotherapy agent for patients with TNBC. However, resistance remains an obstacle for cisplatin-based chemotherapy, due to its elusive underlying mechanism. Previously, abnormal expression of Islet 1 (ISL1) was demonstrated to be closely associated with cancer development and progression. The present study revealed that (ISL1) was significantly upregulated in TNBC tissues in comparison with adjacent normal tissues. Overexpression of ISL1 markedly promoted the proliferation and invasion of the TNBC MDA-MB-231 and MDA-MB-468 cell lines, while knockdown of ISL1 inhibited cell invasion and proliferation in these cell lines. In addition, overexpression of ISL1 reversed cisplatin-induced cell apoptosis, while knockdown of ISL1 enhanced apoptosis following cisplatin treatment in MDA-MB-231 and MDA-MB-468 cells. Furthermore, the levels of the anti-apoptotic proteins, phosphorylated-protein kinase B and B-cell lymphoma-2 (Bcl-2), were significantly decreased, while the levels of the pro-apoptotic protein Bcl-2-associated X protein were remarkably increased in response to cisplatin treatment. The present study revealed that ISL1 overexpression reversed the protein expression profile of p-Akt, Bcl-2 and Bax, while ISL1 knockdown promoted cell apoptosis. Therefore, the data of the present study demonstrated that ISL1 contributes to TNBC progression and reverses cell sensitivity towards cisplatin in TNBC cells, suggesting that ISL1 is a potential therapeutic target for the treatment of TNBC.

Objective: Breast cancer (BC) is a common malignant tumor in females. The combined assay of multiple molecular markers benefits the diagnosis and prognostic prediction. Human epidermal growth factor receptor 2 (HER2) facilitates the proliferation and differentiation of cancer cells through ligand binding. Ki67 is a tumor proliferation-related gene, whereas GSTP1 is a DNA repair-related gene. This study thus investigated the significance of HER2 and Ki67/GSTP1 gene combined assay in the diagnosis and prognosis of BC. Materials and Methods: A total of 86 breast tumor tissues and adjacent tissues were collected. Gene expression and protein levels of HER2 and Ki67 were quantified by real-time polymerase chain reaction (PCR) and Western blot, respectively. Methylation frequency of GSTP1 was analyzed by methylation-specific PCR. The correlation between HER2 and Ki67/GSTP1 and clinical/pathological features of BC was analyzed. Results: Gene and protein expression levels of HER2 and Ki67 in tumor tissues were increased (p < 0.05 compared with adjacent tissues). Methylation frequency of GSTP1 gene was 37.2%, which was significantly higher in breast tumor tissues than in adjacent tissues (12.79%, p < 0.05). HER2 expression was positively correlated with TNM stage, tumor size, and lymph node metastasis, and negatively correlated with tissue grade and estrogen receptor (ER)/progesterone receptor (PR) expression (p < 0.05). GSTP1 methylation was positively correlated with TNM stage and tumor size, and negatively correlated with ER/PR expression (p < 0.05). Conclusions: HER2, Ki67, and GSTP1 methylation were correlated with clinical and pathological features of BC. The combined assay benefits the early diagnosis and prognostic prediction of cancer.