Objective To investigate the effect of resveratrol (RSV) on epithelial-mesenchymal transition of MDA-MB-231 cells by down-regulating POLD1 expression. Methods CCK-8 was used to detect the effect of RSV on the activity of MDA-MB-231 cells. POLD1-OE and POLD1-NC cell lines were constructed by transfecting MDA-MB-231 cells with recombinant lentivirus. Western blot was used to detect the expression of POLD1, E-cadherin, N-cadherin and Vimentin after RSV treatment. Transwell invasion experiment and the scratch test were used to detect the cells invasion and migration abilities of each experimental group. Results RSV could significantly inhibit the survival of MDA-MB-231 cells, reduce the expression of POLD1, N-cadherin and Vimentin, increase the expression of E-cadherin, and inhibit the abilities of cell invasion and migration. Increasing the POLD1 expression could reduce the above-mentioned biological effects of RSV on MDA-MB-231 cells. Conclusion RSV could significantly inhibit the viability and EMT of MDA-MB-231 cells by down-regulating the expression of POLD1.

Objective: To investigate the role of HIV-1 envelope protein gp120 in cognitive impairment induced by neuronal damage. Methods: Western blot and immunofluorescence assay were used to detect microglia activation, inflammatory factor expression and neuronal damage after gp120 treatment. Neuronal damage and neurocognitive performance in gp120-transgenic mice were evaluated using immunohistochemical staining and behavioral analysis, respectively. Results: In vivo and in vitro experiments showed that HIV-1 gp120 significantly induced the expression of caspase-1 and IL-1β, and indirectly caused neuronal synaptic shortening and neuronal damage (P<0.05). Compared with wild-type mice, gp120-transgenic mice showed significant cortical and hippocampal glial activation, neuronal loss, dendritic damage and neurocognitive disorders. Conclusions HIV-1 gp120 might cause neuronal damage through activating the release of inflammatory factor by microglia and involve in neurocognitive impairment.

Radiation-induced lung injury is a common complication of thoracic malignant tumor radiotherapy and severe nuclear accident injury. Currently, there is no effective treatment on this injury. Mesenchymal stem cells (MSCs) are a group of cells with multi-directional differentiation potential and they can protect lung tissue from radiation damage by homing to the injured site and differentiating to the damaged tissues, secreting cytokines and immune regulation. Further, the genetically modifying mesenchymal stem cells have not only the main characteristics of MSCs, but also can efficiently and stably express or knock down a certain of target genes, thereby enhancing or reducing the sensitivity of mesenchymal stem cells to various physiological stimulus and enhancing its therapeutic effect in radiation-induced lung injury, providing new ideas and new strategies for clinical treatment. This paper reviewed the relevant research progress in recent years.

With the improved understanding of driver mutations in non-small cell lung cancer (NSCLC), expanding the targeted therapeutic options improved the survival and safety. However, responses to these agents are commonly temporary and incomplete. Moreover, even patients with the same oncogenic driver gene can respond diversely to the same agent. Furthermore, the therapeutic role of immune-checkpoint inhibitors (ICIs) in oncogene-driven NSCLC remains unclear. Therefore, this review aimed to classify the management of NSCLC with driver mutations based on the gene subtype, concomitant mutation, and dynamic alternation. Then, we provide an overview of the resistant mechanism of target therapy occurring in targeted alternations ("target-dependent resistance") and in the parallel and downstream pathways ("target-independent resistance"). Thirdly, we discuss the effectiveness of ICIs for NSCLC with driver mutations and the combined therapeutic approaches that might reverse the immunosuppressive tumor immune microenvironment. Finally, we listed the emerging treatment strategies for the new oncogenic alternations, and proposed the perspective of NSCLC with driver mutations. This review will guide clinicians to design tailored treatments for NSCLC with driver mutations.
Humans ; Carcinoma, Non-Small-Cell Lung/genetics* ; Lung Neoplasms/genetics* ; Mutation ; Tumor Microenvironment/genetics*