A mechanistic study of chestnut starch retrogradation and its effects on in vitro starch digestion.

Starch retrogradation is a mechanism that is associated with the quality of starch-based food products. A thorough understanding of chestnut starch retrogradation behavior plays an important role in maintaining the quality of chestnut foods during processing and storage. In this study, we investigated the effects of storage time on the structural properties and in vitro digestibility of gelatinized chestnut starch by using X-ray diffraction (XRD), Fourier transform infrared (FTIR) spectroscopy, and solid-state 13C nuclear magnetic resonance (NMR). The results showed that the long-range crystallinity and short-range molecular order of retrograded chestnut starch first rapidly increased from 3 h to 3 d and then decreased from 3 d to 7 d, followed by a slight increase from 7 d to 14 d with retrogradation. With the extension of storage time at 4 °C, there were generally obvious increases in single and double helical structures, which were stacked into long-term ordered structure, resulting in increased enthalpy changes as detected by differential scanning calorimetry spectroscopy (DSC) and reduction of the digestion rate of retrograded chestnut starch. Overall, this study may provide important implications for manipulating and improving the quality of chestnut foods.

Identification of potential prognostic markers associated with lung metastasis in breast cancer by weighted gene co-expression network analysis.

Breast cancer (BC) is an aggressive cancer with a high percentage recurrence and metastasis. As one of the most common distant metastasis organ in BC, lung metastasis has a worse prognosis than that of liver and bone. Therefore, it's important to explore some potential prognostic markers associated with the lung metastasis in BC for preventive treatment. In this study, transcriptomic data and clinical information of BC patients were downloaded from The Cancer Genome Atlas (TCGA) database. Co-expression modules constructed by weighted gene co-expression network analysis (WGCNA) found the royal blue module was significantly associated with lung metastasis in BC. Then, co-expression genes of this module were analyzed for functional enrichment. Furthermore, the prognostic value of these genes was assessed by GEPIA Database and Kaplan-Meier Plotter. Results showed that the hub genes, LMNB and CDC20, were up-regulated in BC and had a worse survival of the patients. Therefore, we speculate that these two genes play crucial roles in the process of lung metastasis in BC, which can be used as potential prognostic markers in lung metastasis of BC. Collectively, our study identified two potential key genes in the lung metastasis of BC, which might be applied as the prognostic markers of the precise treatment in breast cancer with lung metastasis.

The Expression Profile and Prognostic Values of EPHA Family Members in Breast Cancer.

BACKGROUND: EphAs are a class of ephrin receptors that belong to the membrane-bound receptor tyrosine kinases group. Accumulating experimental evidence has shown that the EphA family is involved in tumor progression, namely in cell proliferation, invasiveness, and metastasis. EphAs are a promising target for anticancer therapy. However, their role in breast cancer (BC) is still not well understood. MATERIALS AND METHODS: We used a series of bioinformatic approaches to analyze the expression of the EphA family members and investigate their prognostic value in BC. RESULTS: Lower expression levels of EphA2, EphA3, EphA4, EphA5, and EphA7 and higher expression levels of EphA10 were found in BC tissues compared to those in normal tissues. The expression levels of the EphA family genes were correlated with molecular subtyping but not with tumor stage. High expression levels of most EphAs indicated a better prognosis in BC. CONCLUSIONS: This study suggested that EphA2, EphA3, EphA4, and EphA5 can act as tumor-inhibiting factors as well as biomarkers for the prognosis of BC.

N3ICD with the transmembrane domain can effectively inhibit EMT by correcting the position of tight/adherens junctions.

EMT allows a polarized epithelium to lose epithelial integrity and acquire mesenchymal characteristics. Previously, we found that overexpression of the intracellular domain of Notch3 (N3ICD) can inhibit EMT in breast cancer cells. In this study, we aimed to elucidate the influence of N3ICD or N3ICD combined with the transmembrane domain (TD+N3ICD) on the expression and distribution of TJs/AJs and polar molecules. We found that although N3ICD can upregulate the expression levels of the above-mentioned molecules, TD+N3ICD can inhibit EMT more effectively than N3ICD alone. TD+N3ICD overexpression upregulated the expression of endogenous full-length Notch3 and contributed to correcting the position of TJs/AJs molecules and better acinar structures formation. Co-immunoprecipitation results showed that the upregulated endogenous full-length Notch3 could physically interact with E-ca in MDA-MB-231/pCMV-(TD+N3ICD) cells. Collectively, our data indicate that overexpression of TD+N3ICD can effectively inhibit EMT, resulting in better positioning of TJs/AJs molecules and cell-cell adhesion in breast cancer cells. Abbreviations: EMT: Epithelial-mesenchymal transition; TJs: Tight junctions; AJs: Adherens junctions; aPKC: Atypical protein kinase C; Crb: Crumbs; Lgl: Lethal (2) giant larvae; LLGL2: lethal giant larvae homolog 2; PAR: Partitioning defective; PATJ: Pals1-associated TJ protein.

Notch3 overexpression causes arrest of cell cycle progression by inducing Cdh1 expression in human breast cancer cells.

Uncontrolled cell proliferation, genomic instability and cancer are closely related to the abnormal activation of the cell cycle. Therefore, blocking the cell cycle of cancer cells has become one of the key goals for treating malignancies. Unfortunately, the factors affecting cell cycle progression remain largely unknown. In this study, we have explored the effects of Notch3 on the cell cycle in breast cancer cell lines by 3 methods: overexpressing the intra-cellular domain of Notch3 (N3ICD), knocking-down Notch3 by RNA interference, and using X-ray radiation exposure. The results revealed that overexpression of Notch3 arrested the cell cycle at the G0/G1 phase, and inhibited the proliferation and colony-formation rate in the breast cancer cell line, MDA-MB-231. Furthermore, overexpressing N3ICD upregulated Cdh1 expression and resulted in p27(Kip) accumulation by accelerating Skp2 degradation. Conversely, silencing of Notch3 in the breast cancer cell line, MCF-7, caused a decrease in expression levels of Cdh1 and p27(Kip) at both the protein and mRNA levels, while the expression of Skp2 only increased at the protein level. Correspondingly, there was an increase in the percentage of cells in the G0/G1 phase and an elevated proliferative ability and colony-formation rate, which may be caused by alterations of the Cdh1/Skp2/p27 axis. These results were also supported by exposing MDA-MB-231 cells or MCF-7 treated with siN3 to X-irradiation at various doses. Overall, our data showed that overexpression of N3ICD upregulated the expression of Cdh1 and caused p27(Kip) accumulation by accelerating Skp2 degradation, which in turn led to cell cycle arrest at the G0/G1 phase, in the context of proliferating breast cancer cell lines. These findings help to illuminate the precision therapy targeted to cell cycle progression, required for cancer treatment.