Our data indicate that miR-449a may function as a suppressor of lung cancer, and affects the expression of NEAT1 in lung cancer cells.

Tumor-associated inflammation and aberrantly expressed biomarkers have been demonstrated to play crucial roles in the cancer microenvironment. Cyclooxygenase-2 (COX-2), a prominent inflammatory factor, is highly expressed in tumor cells and contributes to tumor growth, recurrence and metastasis. Overexpression of COX-2 may occur at both transcriptional and post-transcriptional levels. Thus, an improved understanding of the regulatory mechanisms of COX-2 can facilitate the development of novel antitumor therapies. MicroRNAs (miRNAs) are a group of small non-coding RNAs that act as translation repressors of target mRNAs, and play vital roles in regulating cancer development and progression. The present review discusses the association between miRNAs and COX-2 expression in different types of cancer. Understanding the regulatory role of miRNAs in COX-2 post-transcription can provide novel insight for suppressing COX-2 expression via gene silencing mechanisms, which offer new perspectives and future directions for the development of novel COX-2 selective inhibitors based on miRNAs. Contents 1. Introduction 2. Roles of COX-2 in cancer 3. Expression of miRNAs in cancer 4. Post-transcriptional COX-2 regulation is mediated by miRNAs 5. Upregulated expression of miRNAs by COX-2 selective inhibitor 6. Conclusions

No abstract

The κ-opioid receptor (KOR) is one of the primary receptors of opioids and serves a vital role in the regulation of pain, anesthesia, addiction and other pathological and physiological processes. KOR is associated with several types of cancer and may influence cancer progression. It has been proposed that KOR may represent a new tumor molecular marker and provide a novel basis for molecular targeted therapies for cancer. However, the association between KOR and cancer remains to be explored comprehensively. The present review introduces KOR and its association with different types of cancer. Improved understanding of KOR may facilitate development of novel antitumor therapies. Contents1. Introduction 2. Discovery, structure and typing of KOR 3. Expression and physiological function of KOR 4. Expression, function and significance of KOR in various types of cancer 5. Potential roles of KOR in cancer 6. Effects of opioids on tumors 7. Conclusion and future prospects

Background: Ischemia-reperfusion injury (IRI) is the main cause of perioperative organ injury, and the morbidity increase constantly in population. Due to a lack of effective treatment, IRI is associated with a high mortality rate. Thus, we need to discover an effective means to alleviate IRI.Methods: HUVECs were treated with different concentrations of H2O2 alone and in combination with Dex to explore the dose-effect relationship of different concentrations of H2O2 and Dex on HUVEC. In order to explore the relationship between Dex and p38MAPK signal pathway, HUVEC was treated with SB202190, an inhibitor of p38MAPK signal pathway. Cell viability was detected by CCK-8 method. ELISA kit was used to detect lactate dehydrogenase (LDH). Fluorescence probe DCFH-DA staining was used to detect ROS level. Flow cytometry analysis with Propidium Iodide (PI) was used to determine the rate of cell apoptosis. And the protein expression of p-p38MAPK, total p38MAPK, p-ERK1/2 and caspase9 was detected by western blot.Results: 1）H2O2 could damage HUVEC and lead to the release of LDH. The higher the concentration of H2O2, the more severe the injury. 2）Dex pretreatment attenuated H2O2-induced oxidative stress injury and apoptosis of HUVEC. The cell activity of HUVEC increase as Dex concentration increase, the release of LDH decreased, the intracellular ROS level and apoptosis rate decreased, the protein expression of p-p38MAPK and caspase9 decreased, while the protein expression of p-ERK1/2 increased. 3）Dex had the same effect as SB202190, an inhibitor of p38MAPK signaling pathway. After the application of SB202190, the activity of HUVECs increased significantly, while LDH, intracellular ROS and apoptosis rate decreased significantly. Western blot showed that the protein expression of p-p38MAPK and caspase9 decreased significantly, while the protein levels of p-ERK1/2 increased significantly.Conclusion: 1）Dex attenuates H2O2-induced oxidative stress injury and apoptosis of HUVEC in a concentration-dependent. 2）Dex may attenuate H2O2-induced oxidative stress injury and apoptosis of HUVEC by inhibiting p38MAPK signal pathway.