Background Lung cancer is one of the most common malignancies, and there is a trend of increasing incidence in young patients. The preoperative diagnosis of pulmonary nodules is mainly based on the combination of imaging and tumor markers. There is no relevant report on the diagnostic value of tumor markers in young pulmonary nodules. Our study was designed to explore the value of five tumor markers in young patients with pulmonary nodules. Methods We reviewed the medical records of 390 young patients (age ≤45 years) with pulmonary nodules treated at two separate centers from January 1, 2015, to January 1, 2021. Malignant pulmonary nodules were confirmed in 318 patients, and the other 72 patients were diagnosed with benign pulmonary nodules. The gold standard for diagnosis of pulmonary nodules was surgical biopsy. The conventional serum biomarkers included cytokeratin 19 (CYFRA21‐1), pro‐gastrin‐releasing‐peptide (ProGRP), carcinoembryonic antigen (CEA), neuron‐specific enolase (NSE), and squamous cell carcinoma‐associated antigen (SCCA). The diagnostic values of five tumor markers were analyzed by receiver operating characteristic (ROC) curves. Results There were no significant differences in the expression of five tumor markers between the groups (p > 0.05). Single tumor marker (CYFRA21‐1, ProGRP, CEA, NSE, and SCCA) showed a limited value in the diagnosis of malignant pulmonary nodules, with the AUC of 0.506, 0.503 0.532, 0.548, and 0.562, respectively. The AUC of the combined examination was only 0.502~0.596, which did not improve the diagnostic value. Conclusions Five conventional tumor markers had a limited diagnostic value in young patients with pulmonary nodules.

Liver fibrosis and cirrhosis are primarily caused by the activation of hepatic stellate cells (HSCs), regardless of their etiology. Collagen type I (collagen I) and connective tissue growth factor (CTGF) is produced more readily by activated HSCs. Consequently, identifying the molecular and cellular mechanisms responsible for HSCs activation is essential to better understand its mechanism of action and therapeutic potential. Cell death is caused by iron‐dependent lipid peroxidation during ferroptosis. Ferroptosis plays an important role in the survival of activated HSCs and could contribute to the development of innovative prevention and treatment strategies for liver fibrosis. Danshensu (Dan) is a pure molecule extracted from the Salvia miltiorrhiza herb that protects against liver damage. However, Dan's effect on attenuating HSCs activation by regulating ferroptosis remains unclear. The results of this study indicated that lipopolysaccharide (LPS)‐induced LX‐2 and T6 cells activation occurs through the upregulation of collagen I, CTGF, Gpx4, and SLC7A11. Interestingly, Dan attenuated LPS‐induced liver fibrosis in those cells by upregulating collagen I, CTGF, Gpx4, and SLC7A11 and by increasing lipid reactive oxygen species accumulation. Furthermore, the results also showed that the ferroptosis inhibitor liproxstatin attenuated the overproduction of lipid reactive oxygen species in LPS‐activated LX‐2 cells. We conclude that Dan attenuates LPS‐induced HSC activation during liver fibrosis by regulating ferroptosis in LX‐2 and T6 cells.

Background: FoxO3a is a well-studied tumor suppressor gene in the forkhead transcriptional factor O (FoxO) subfamily and its downregulation is correlated with the occurrence of gastric cancer (GC). GC tissues had microRNA (miR)-372 upregulation, which has targeted relationship with 3¢-untranslated region (3¢-UTR) of FoxO3a gene. This study investigated if miR-372 plays a role in modulating FoxO3a expression, and affecting GC cell proliferation, apoptosis, and cisplatin (DDP) resistance. Materials and Methods: Dual luciferase reporter gene assay assessed the targeted regulation between miR-372 and FoxO3a. DDP-resistant cell lines MGC803/DDP and MKN28/DDP were compared for gene expression against parental cells. Cell proliferation was measured by Cell Counting Kit-8 (CCK-8) assay. Cultured cells were transfected with miR-372 mimic or miR-negative control (NC) to measure FoxO3a mRNA and protein expression. Cell apoptosis and proliferation were tested by flow cytometry and 5-Ethynyl-2¢-deoxyuridine (EdU) staining, respectively. Results: miR-372 had a targeted relationship with FoxO3a mRNA. MGC803/DDP and MKN28/DDP cells had significantly elevated miR-372 level than parental cells, while Foxo3a mRNA or protein levels were significantly decreased. CCK-8 assay revealed significantly lower inhibitory activity on cell proliferation in drugresistant cells. Compared with miR-NC group, miR-273 inhibitor transfected DDP-resistant cells had significantly increased Foxo3a expression, enhanced cell apoptosis, reduced proliferation, and drug resistance. Conclusions: miR-372 upregulation is associated with DPP resistance of GC cells. Downregulation of miR-372 can inhibit proliferation, facilitate apoptosis, and suppress DDP resistance of drug-resistant GC cells.

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