More than 25% localized CRC patients died from post-operative metastasis, and risk of metastasis varies among individuals due to the high heterogeneity of CRC. Therefore, figuring out potential biomarkers for disease recurrence would be invaluable to improve the follow-up efficiency and clinical treatment. Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) is a core component of the nuclear receptor corepressor complex, which functions as a repressive coregulatory factor for multiple transcription factors. The clinical significance of TBL1XR1 in CRC hasn’t been fully elucidated. In this study, we investigated the expression of TBL1XR1 in primary CRC tissues and liver metastases from TNM stage IV CRC patients, and found that its expression in primary tumor tissues was an independent prognostic factor for tumor recurrence. Thus, we enrolled another cohort including TNM stage I-III patients to further evaluate the relationship between TBL1XR1 expression and disease recurrence. Accordingly, high TBL1XR1 expression indicates poor disease-free survival of stage I-III CRC patients. Furthermore, we confirmed the importance of β-catenin signaling pathways in TBL1XR1-mediated CRC cell oncogenicity by clinical and cellular results. Our results emphasize the necessity of individual therapy decisions based on clinical biomarkers, especially for localized CRC patients who are not routinely treated with adjunctive chemotherapy.

Starches were isolated from bulbs of seven lily cultivars grown in China and their morphological, structural, and physicochemical properties were investigated. All the isolated starch samples showed triangular, elliptical, less scalloped, round, and irregular shaped granules. The starch of different lily cultivars exhibited B-type crystalline pattern. The median diameters (D50) were found to be in range from 17.79 μm to 45.06 μm and the amylose content in range from 23.63 to 30.38 g/100 g starch. The weight average molar mass (M w) of amylopectin ranged from 4.03 × 10 7 g/mol to 11.00 × 10 7 g/mol and root-mean-square rotation radius (R z) ranged from 203.90 nm to 264.20 nm. HPAEC-PAD chain distribution analysis revealed that the average chain length of amylopectin ranged from DP 23.19-25.29. Starch samples of different lily cultivars showed peak viscosity ranging from 1699.7 cP to 2963.0 cP, and pasting temperature varying from 63.83°C to 71.00°C. Furthermore, the transition temperatures of the starch samples isolated from different lily cultivars were found to be in range from 50.76°C to 57.59°C for onset temperature (T o), 54.57°C to 64.30°C for peak temperature (T p), and 68.07°C to 77.16°C for conclusion temperature (T c). The gelatinization temperature range (ΔT r) was found to be from 16.66°C to 21.65°C and enthalpy (ΔH) was in range from 11.46 J/g to 16.29 J/g. These results indicated that lily starch properties were significantly different depending on lily variety, which could help in understanding the convenience of these starches for the application in different food and non-food industries.

Several studies have shown the tumorigenesis role of transcriptional enhancer associate domain (TEAD) proteins; here, we initially explored expression, function and signalling mechanisms of TEAD4 in lung adenocarcinoma (LAD). Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour‐promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial‐mesenchymal transition (EMT) markers such as E‐cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4‐targeted microRNA, namely miR6839‐3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839‐3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839‐3p mimics as a promising therapeutic direction.