Long noncoding RNAs (lncRNAs) have been discovered as significant regulators in a wide range of human cancers. Among them, lncRNA MNX1-AS1 has been proved to be an oncogene in ovarian cancer and glioblastoma. However, the regulatory mechanism of MNX1-AS1 in cervical cancer remains to be understood. Therefore, this study planned to explore the role of MNX1-AS1 in cervical cancer. In the beginning, we found that the expression of MNX1-AS1 was obviously upregulated in cervical cancer tissues and cell lines. Kaplan-Meier survival analysis revealed that patients with higher MNX1-AS1 expression level suffered from shorter overall survival time than those with lower MNX1-AS1 level. Moreover, by loss-of-function and gain-of-function assay, the effect of MNX1-AS1 on cell proliferation and apoptosis was examined on cellular level. Results showed that the proliferation of Hela cells was significantly inhibited and apoptosis enhanced by the transfection of shMNX1-AS1, while overexpressing MNX1-AS1 in E6E7 cells presented the contrary results. As for mechanism investigation, it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK. Taken together, it was identified that MNX1-AS1 promoted proliferation and inhibited apoptosis of cervical cancer cells through MAPK pathway. Highlights 1. Expression of MNX1-AS1 is upregulated in cervical cancer tissues and cell lines.2. MNX1-AS1 expression is of important clinical significance and it is a novel prognosis biomarker in cervical cancer. 3. MNX1-AS1 regulates cell survival, proliferation, and apoptosis in cervical cancer cells. 4. MNX1-AS1 affects the progression of cervical cancer via MAPK pathway. K E Y W O R D S apoptosis, cervical cancer, MAPK pathway., MNX1-AS1, proliferation J Cell Biochem. 2019;120:4268-4277. wileyonlinelibrary.com/journal/jcb 4268 |
Purpose
Nanomaterial-based drug-delivery systems allowing for effective targeted delivery of smallmolecule chemodrugs to tumors have revolutionized cancer therapy. Recently, as novel nanomaterials with outstanding physicochemical properties, boron nitride nanospheres (BNs) have emerged as a promising candidate for drug delivery. However, poor dispersity and lack of tumor targeting severely limit further applications. In this study, cancer cell–membrane biomimetic BNs were designed for targeted anticancer drug delivery.
Methods
Cell membrane extracted from HeLa cells (HM) was used to encapsulate BNs by physical extrusion. Doxorubicin (Dox) was loaded onto HM-BNs as a model drug.
Results
The cell-membrane coating endowed the BNs with excellent dispersibility and cytocompatibility. The drug-release profile showed that the Dox@HM-BNs responded to acid pH, resulting in rapid Dox release. Enhanced cellular uptake of Dox@HM-BNs by HeLa cells was revealed because of the homologous targeting of cancer-cell membranes. CCK8 and live/dead assays showed that Dox@HM-BNs had stronger cytotoxicity against HeLa cells, due to self-selective cellular uptake. Finally, antitumor investigation using the HeLa tumor model demonstrated that Dox@HM-BNs possessed much more efficient tumor inhibition than free Dox or Dox@BNs.
Conclusion
These findings indicate that the newly developed HM-BNs are promising as an efficient tumor-selective drug-delivery vehicle for tumor therapy.
Preeclampsia (PE) is characterized by the impaired invasive ability of trophocytes, which can be modulated by microRNAs (miRs). In the current study, the effects of rhynchophylline (Rhy) on the viability and invasive ability of trophocytes were explored by focusing on miR-141-3p/ZEB1 axis. The level of miR-141-3p was modulated in human trophocytes and the changes in cell viability, apoptosis, invasive ability, and ZEB1 level were detected. Then the trophocytes with miR-141-3p overexpression were treated with Rhy and the effects on trophocyte phenotypes were assessed. The induced miR-141-3p level suppressed cell viability, induced apoptosis, and inhibited invasion and ZEB1 level in trophocytes. The treatment of Rhy restored the viability and invasive ability of trophocytes under the overexpression of miR-141-3p, indicating the protective effects of Rhy on trophocytes. The findings in the current study highlighted the protective effects of Rhy on trophocytes during PE progression, which was associated with the inhibition of miR-141-3p.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.