This study aims to evaluate the changes of phenolic acids, lignans and tocopherols of sesame seeds during 0-6 days of germination by monitoring the activities of phenolic metabolism related enzymes...

Introduction Studies have found that Lnc-HCG11 is an important regulator of cancer. However, the function of Lnc-HCG11 in NSCLC is not known. Therefore, this experimental design was based on Lnc-HCG11 to explore the pathogenesis of NSCLC. Methods RT-qPCR was used to detect the expression of Lnc-HCG11 and miR-224-3p in NSCLC. The effects of Lnc-HCG11 and miR-224-3p on proliferation and apoptosis of NSCLC cells were detected by CCK-8 assay, Edu assay and Annexin V-FITC/PI assay. Target gene prediction and screening, luciferase reporter assays were used to verify downstream target genes for lnc-HCG11 and miR-224-3p. Western blotting was used to detect the protein expression of caspase-3. The tumor changes in mice were detected by in vivo. Results Lnc-HCG11 was significantly reduced in NSCLC. Lnc-HCG11 significantly inhibited cell proliferation of NSCLC cells and induced apoptosis. miR-224-3p was significantly elevated in the NSCLC cell line. Moreover, miR-224-3p significantly increased cell proliferation and inhibited apoptosis of NSCLC cells. Furthermore, Lnc-HCG11 was negatively correlated with miR-224-3p expression. Lnc-HCG11 over-expression was up-regulated the expression levels of c-caspase-3 and caspase-3. Finally, the results of in vivo animal models confirmed that Lnc-HCG11 inhibited tumor growth by modulating the miR-224-3p/c-caspase-3 axis. Conclusion Lnc-HCG11 could inhibit the progression of NSCLC by modulating the miR-224-3p/caspase-3 axis, and Lnc-HCG11 may be a potential therapeutic target for NSCLC.

BackgroundNon-small cell lung carcinoma (NSCLC) with ipsilateral and/or subcarinal mediastinal lymphatic spread (N2) is a heterogeneous disease. The role of surgical resection in patients with N2 NSCLC remains controversial and no survival-based definition of “resectable N2” exists. The purpose of this study is to evaluate the factors that potentially affect the survival of N2 NSCLC patients who receive surgical resection and to define “resectable N2” based on the survival benefits.MethodsData from the open Surveillance, Epidemiology, and End Results (SEER) database from the National Cancer Institute in the United States were used to construct a nomogram. Patients who received surgery between 2010 and 2015 for N2 NSCLC were included. Independent prognostic factors for survival identified through Cox regression analysis were used to create the nomogram. The C-index, receiver operating characteristics (ROC) analyses, calibration curves, and risk stratification were used to evaluate the nomogram. The nomogram was also validated using data from 222 patients from Peking Union Medical College Hospital (PUMCH). Furthermore, lung cancer–related deaths were compared using competitive risk analysis.ResultsIn total, 4267 patients were included in the SEER cohort. Male gender, old age, high T stage and grade, adenosquamous and squamous cell carcinoma, lower lobe and overlapping lesions, extended lobe or bilobectomy and pneumonectomy, no chemotherapy, radiation before and after surgery, positive number of lymph nodes, and lymph node ratio (LNR) were identified as independent risk factors for higher mortality. The nomogram was created using these parameters. The C-index was 0.665 (95% confidence interval (CI), 0.651-0.679) and 0.722 (95% CI, 0.620-0.824) in the SEER and PUMCH cohorts, respectively. The calibration curves showed satisfactory consistency between the predicted and actual survival status in both the SEER and PUMCH cohorts. Competitive risk analysis confirmed that the variables in the nomogram, except radiation, are risk factors for prognosis.Conclusions“Resectable N2” should be assessed by a multidisciplinary team. The novel nomogram developed in this study may help with clinical decision-making for this patient population.

Chicoric acid (CA) can display health benefits as a dietary polyphenol. However, as CA is widely metabolized in vivo, the actual compounds responsible for its bioactivities are not entirely known. Herein, the major methylated metabolites of CA were isolated from an in vitro co-incubation system, and their structures were elucidated. The antioxidant activities of the monomethylated metabolites (M1) and dimethylated metabolites (M2) of CA were evaluated against H2O2-induced oxidative stress damage in HepG2 cells and compared to CA. The results indicated that both M1 and M2 had better antioxidant capacities than CA by increasing cell viability, improving mitochondrial function, and balancing cellular redox status. These compounds also prevented oxidative stress by mediating the Keap1/Nrf2 transcriptional pathway and downregulating enzyme activity. The current research indicates that the methylated metabolites of CA could potentially be the candidates that are responsible for the biological efficacies attributed to CA.