Background Long-chain acyl-CoA synthetase-4 (ACSL4) is involved in fatty acid metabolism, and aberrant ACSL4 expression could be either tumorigenic or tumor-suppressive in different tumor types. However, the function and clinical significance of ACSL4 in lung adenocarcinoma remain elusive. Results ACSL4 was frequently downregulated in lung adenocarcinoma when analyzing both the TCGA database and the validation samples, and the lower ACSL4 expression was correlated with a worse prognosis. Using gene set enrichment analysis, we found that high ACSL4 expression was frequently associated with the oxidative stress pathway, especially ferroptosis-related proteins. In vitro functional studies showed that knockdown of ACSL4 increased tumor survival/invasiveness and inhibited ferroptosis, while ACSL4 overexpression exhibited the opposite effects. Moreover, high-fat treatment could also inhibit erastin-induced ferroptosis by affecting ACSL4 expression. The anti-tumor effects of ferroptosis inducers and the anti-ferroptosis effects of the high-fat diet were further validated using the mouse xenograft model. Conclusions ACSL4 plays a tumor-suppressive role in lung adenocarcinoma by suppressing tumor survival/invasiveness and promoting ferroptosis. Our study provided a theoretical reference for the application of ferroptotic inducers and dietary guidance for lung adenocarcinoma patients.
There has been a controversy as to whether or not the non-pathological flat foot and high-arched foot have an effect on human walking activities. The 3D foot scanning system was employed to obtain static footprints from subjects adopting a half-weight-bearing stance. Based upon their footprints, the subjects were divided into two groups: the flat-footed and the high-arched. The plantar pressure measurement system was used to measure and record the subjects' successive natural gaits. Two indices were proposed: distribution of vertical ground reaction force (VGRF) of plantar and the rate of change of footprint areas. Using these two indices to compare the natural gaits of the two subject groups, we found that (1) in stance phase, there is a significant difference (p<0.01) in the distributions of VGRF of plantar; (2) in a stride cycle, there is also a significant difference (p<0.01) in the rate of change of footprint area. Our analysis suggests that when walking, the VGRF of the plantar brings greater muscle tension to the flat-footed while a smaller rate of change of footprint area brings greater stability to the high-arched.
Background: Bilateral synchronous multiple primary lung adenocarcinoma (BSMPLA) is a rapidly increasing disease for which timely and accurate treatment is required. We describe our experience which we hope to establish optimal therapeutic options for patients with BSMPLA. Methods: This study aimed to explore the feasibility and safety of simultaneous bilateral video-assisted thoracoscopic surgery (VATS) in 56 patients who received histological diagnoses of BSMPLA at our hospital between January 2016 and January 2018. In this retrospective analysis of clinical outcomes, we observed no serious postoperative complications or perioperative death. Results: Four and 28 patients respectively underwent bilateral lobectomy and lobectomy with contralateral sublobar resection, whereas the remaining 24 patients underwent bilateral sublobar resection. Sublobar resection means anatomical segmentectomy or wedge resection. The mean postoperative hospital stay duration was 5.39±2.67 days. Postoperative complications comprising persistent air leakage for more than 5 days was observed in 8 (14.2%) of 56 patients. No severe postoperative complications or deaths occurred. Conclusions: Our results suggest that simultaneous bilateral VATS is feasible, safe, and reproducible. This therapeutic strategy appears to confer considerable benefits on patients with BSMPLA.
Background: Aspirin is a classic anti-inflammatory drug and its anticancer effect has been previously explored in many types of cancer including colorectal cancer therapy. Programmed cell death-ligand 1 (PD-L1) is widely expressed in tumor cells and displays an inhibitory role in antitumor immunity. This study aimed to clarify the role of PD-L1 in aspirin-suppressed lung cancer. Methods: The inhibitory effect of aspirin on lung cancer cell proliferation was assessed using an MTT cell viability assay. The role of aspirin in the modulation of PD-L1 expression was analyzed by western blot or RT-PCR assays. In lung cancer cells, the influence of aspirin on PD-L1 promoter activity was detected using a luciferase reporter assay. The interaction of TAZ with PD-L1 promoter in the cells, with or without aspirin administration, was tested via chromatin immunoprecipitation (ChIP) analysis. The function of PD-L1 in aspirinmediated growth inhibition of lung cancer was examined using a cell viability assay. Results: Following treatment with aspirin, lung cancer cell growth was markedly suppressed. Aspirin was able to markedly decrease the expression of PD-L1 at the mRNA and protein levels in lung cancer cells. For the mechanism study, we found that the promoter of PD-L1 was inactivated by aspirin via TAZ transcriptional coactivator in the cells. With regard to the functional investigation, aspirin was capable of resisting cell proliferation and PD-L1 overexpression abolished aspirin-depressed cell proliferation in lung cancer. Conclusions: Aspirin suppressed the growth of lung cancer cells via targeting the TAZ/PD-L1 axis.
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