Clinical and pathological analyses showed that the low expression of miR-665 was significantly associated with high TNM stage (P = 0.007), distant metastasis (P = 0.031), and poor differentiation (P = 0.029). Endogenic mimics of miR-665 remarkably suppressed GC cell proliferation, migration, invasion, and EMT in in vitro experiments. Inhibition of miR-665 expression induced the opposite effects. The results of the bioinformatics analysis and dual-luciferase assay showed that miR-665 targeted the 3'-UTR of the CRIM1 gene. Rescue assays revealed that overexpression of CRIM1 attenuated the inhibitory effects of miR-665 in GC progression and EMT. Conclusion The overall study results demonstrated that miR-665 inhibits tumor progression and EMT in GC by targeting CRIM1, indicating that miR-665 might be a potential therapeutic target in the treatment of GC patients.The clinical use of selective cyclin-dependent kinase (CDK) 4/6 inhibitors has significantly improved the prognosis of patients with hormone receptor (HR)-positive human epidermal growth factor receptor 2 (HER2)-negative advanced or metastatic breast cancer (ABC/mBC), which almost achieved the double progression-free survival (PFS) in combination with endocrine therapy (ET) compared with ET alone. To date, there are 3 CDK4/6 inhibitors (palbociclib, ribocilcib and abemaciclib) approved by the US Food and Drug Administration (FDA) and European Medicines Agency (EMA) to treat patients with HR+/HER2-ABC/mBC in the first and later lines. The aim of this review is to summarize the current clinical use and ongoing clinical trials of CDK4/6 inhibitors, the published overall survival data, and the potential biomarkers and resistance to CDK4/6 inhibitors.Background Ursolic acid (UA), a primary bioactive triterpenoid, was reported as an anti-cancer agent. However, the current knowledge of UA and its potential anti-cancer mechanisms and targets in breast cancer cells are limited. In this study, we aimed to illustrate the potential mechanisms and targets of UA in breast cancer cells MCF-7. Methods The effect of UA on cell growth was determined in MCF-7 cells by MTT assay. The anti-tumor mechanism of UA was evaluated by microarray, CAMP, and Western blot. Moreover, the molecular docking between UA and potential receptors were predicted by iGEMDOCK software. Results The result of MTT assay demonstrated that UA could inhibit MCF-7 cell growth with IC50 values of 20 μM. find more Microarray and CMAP analysis, validated by Western blot, indicated that UA significantly modulated IKK/NF-κB, RAF/ERK pathways, and down-regulated the phosphorylation level of PLK1 in MCF-7 cells. Conclusion Our data indicated that the anti-tumor effects of UA are due to the inhibited RAF/ERK pathway and IKK/NF-κB pathway. It could also be explained by the reduced phosphorylation of PLK1 in MCF-7 cells. This study provides a new insight for deep understanding of the new anti-cancer mechanisms of UA in MCF-7 breast cancer cells.Background Circular RNAs (circRNAs) function as essential regulators in diverse human cancers, including hepatocellular carcinoma (HCC). However, the function of circ_0000517 in HCC was unknown. We aimed to explore the roles and mechanisms of circ_0000517 in HCC. Materials and methods The levels of circ_0000517, RPPH1 mRNA and microRNA-1296-5p (miR-1296-5p) were measured using quantitative real-time polymerase chain reaction (qRT-PCR). The characteristics of circ_0000517 were explored by RNase R digestion and actinomycin D assays. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell cycle process and cell apoptosis were analyzed by flow cytometry analysis. The function of circ_0000517 in vivo was explored by a murine xenograft model. The association between miR-1296-5p and circ_0000517 or thioredoxin domain containing 5 (TXNDC5) was determined by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The protein level of TXNDC5 was detected by Western blot assay. Results Circ_0000517 was upregulated in HCC tissues and cells. Silencing of circ_0000517 suppressed HCC cell viability and colony formation and promoted cell cycle arrest and apoptosis in vitro and hampered tumor growth in vivo. MiR-1296-5p was a target of circ_0000517 and the effects of circ_0000517 silencing on HCC cell viability, cell cycle, colony formation and apoptosis were abolished by miR-1296-5p inhibition. TXNDC5 functioned as a target gene of miR-1296-5p, and the inhibitory effect of miR-1296-5p on HCC cell progression was rescued by TXNDC5 overexpression. Moreover, circ_0000517 promoted TXNDC5 expression via targeting miR-1296-5p. Conclusion Circ_0000517 accelerated HCC progression by upregulating TXNDC5 through sponging miR-1296-5p.Purpose Small-cell carcinoma of the cervix (SCCC) is a rare type of cervical cancer. This study aimed to investigate the clinicopathological characteristics and survival as well as the optimal local treatment modalities for SCCC. Patients and methods We retrospectively evaluated the data of patients diagnosed with SCCC between 1988 and 2015 in our institution - those included in the Surveillance, Epidemiology, and End Results (SEER) database and those in the Periodical Database. Kaplan-Meier method and Cox regression proportional hazard methods were used to evaluate overall survival (OS). A nomogram that could predict OS was constructed based on the Cox proportional hazard model. Results In total, 695 patients were included in this study. The 5-year overall survival in FIGO stage I-IIA and IIB-IV patients was 45.7% and 14.4%, respectively (P less then 0.01). Univariate and multivariate analyses showed that lymph node status (P less then 0.01) and cancer-directed surgery (P less then 0.01) were independent prognostic factors for FIGO I-IIA stage patients, and age (P less then 0.05), tumor size (P less then 0.01), chemotherapy (P less then 0.01) and radiation (P less then 0.01) were independent prognostic factors for FIGO stage IIB-IV patients. Conclusion Better prognosis was associated with negative lymph node status, no lymphatic vasculature, surgery, and early-stage patients. Furthermore, our data showed that the prognosis and treatment pattern varied depending on the FIGO stage, and that optimal treatment modalities included radical surgery for early-stage SCCC and chemoradiotherapy for advanced-stage SCCC. It is helpful to assess the individual prognosis of SCCC patients and choose personalized treatment modalities.find more