An intratumoral hypoxic microenvironment is frequently observed in solid tumors, including breast cancer. Lutein, a plant-derived compound and non-vitamin A carotenoid, has been demonstrated to possess multiple protective properties including anti-inflammation, anti-oxidative stress and antitumor effects. The main objective of the present research was to elucidate the involvement of lutein in the production of reactive oxygen species (ROS) under hypoxia, the activation of hairy and enhancer of split 1 (HES1), and the proliferation, invasion and migration of breast cancer cells. The human breast cancer cell lines MDA‑MB‑157 and MCF‑7 were exposed to hypoxic conditions and various concentrations of lutein. An MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay was performed to examine cell proliferation, and Annexin V-fluorescein isothiocyanate/propidium iodide staining was performed to analyze the apoptosis ratio. The levels of hypoxia inducible factor-1α (HIF‑1α), NOTCH signaling molecules, HES1 and epithelial-mesenchymal transition (EMT)-associated factors were examined by reverse transcription-quantitative polymerase chain reaction and western blot analysis. Wound healing and Transwell invasion assays were used to detect the invasion and migration of breast cancer cells. Intracellular ROS levels were examined using 2,7-dichlorodihydrofluorescein-diacetate and flow cytometry. The results revealed that cell proliferation was inhibited by lutein in a dose-dependent manner, and the apoptosis ratio gradually increased with lutein treatment under hypoxia as evident from flow cytometry-based analysis. Exposure to lutein inhibited hypoxia-mediated activation of HIF‑1α, NOTCH signaling and HES1 expression, and suppressed the hypoxia-induced expression of EMT-associated factors. Lutein markedly inhibited the invasion and migration of breast cancer cells under hypoxia. Hypoxia-induced production of ROS was also decreased by lutein. Furthermore, the ROS scavenger N‑acetylcysteine also suppressed hypoxia inducible factor 1α and HES1 expression in breast cancer cells during hypoxia, but hydrogen peroxide (H2O2) levels were increased. Taken together, the results of the present study suggested that lutein may be a novel candidate for the chemoprevention of breast cancer. Furthermore, HES1 may be crucial in mediating the involvement of lutein in the suppression of hypoxia-driven ROS-induced breast cancer progression.

Invertases catalyze the hydrolysis of sucrose into fructose and glucose and can be employed as an alternative in producing high fructose syrup. In this study, we reported the heterologous expression of an invertase gene (GspInv) of Gongronella sp. w5 in Komagataella pastoris. GspInv activity reached 147.6 ± 0.4 U/mL after 5 days of methanol induction. GspInv is invertase with a high specific activity of 2,776.1 ± 124.2 U/mg toward sucrose. GspInv showed high tolerance to sucrose (IC 50 = 1.2 M), glucose (IC 50 > 2 M), fructose (IC 50 = 1.5 M), and a variety of metal ions that make it an ideal candidate for high fructose syrup production. A carbohydratebinding module was sequence-optimized and fused to the N-terminus of GspInv. The fusion protein had the highest immobilization efficiency at room temperature within 1 h adsorption, with 1 g of cellulose absorption up to 8,000 U protein. The celluloseimmobilized fusion protein retained the unique properties of GspInv. When applied in high fructose syrup preparation by using 1 M sucrose as the substrate, the sucrose conversion efficiency of the fused protein remained at approximately 95% after 50 h of continuous hydrolysis on a packed bed reactor. The fused protein can also hydrolyze completely the sucrose in sugarcane molasses. Our results suggest that GspInv is an unusual invertase and a promising candidate for high fructose syrup preparation.

Despite being one of the most prevalent and fatal types of cancer worldwide, the biological details of esophageal squamous cell carcinoma (ESCC) remain unknown. Recent studies have demonstrated the crucial roles of long non-coding RNAs (lncRNAs) in diverse biological processes including cancer initiation, progression and metastasis. The aim of the present study was to assess the expression profile of distal-less homeobox 6 antisense RNA 1 (DLX6-AS1) in ESCC tissues and its contributions to ESCC cell proliferation, apoptosis and invasion. The expression of DLX6-AS1 in a series of ESCC samples and paired adjacent noncancerous tissues was evaluated by reverse transcription-quantitative polymerase chain reaction. Cell proliferation, apoptosis, wound healing and Transwell invasion assays were performed to evaluate the roles of DLX6-AS1 in the ESCC cell lines EC109 and KYSE30 transfected with DLX6-AS1 small interfering RNA (siRNA). Compared with the paired adjacent noncancerous tissues, DLX6-AS1 expression was upregulated in the ESCC tissues and significantly associated with differentiation status, Tumor-Node-Metastasis stage, distant metastasis, and lymph node metastasis. Knockdown of DLX6-AS1 significantly suppressed cell proliferation, invasion and migration abilities, and enhanced the apoptotic rate in the two ESCC cell lines. Furthermore, western blot assays revealed that silencing DLX6-AS1 partly influenced the epithelial-mesenchymal transition process in ESCC cells. These results imply that the oncogenic function of DLX6-AS1 may be a novel candidate target for treating human ESCC.