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The long noncoding RNA HOX transcript antisense RNA (HOTAIR) has been found to be overexpressed in many human malignancies and involved in tumor progression and metastasis. Although the downstream target through which HOTAIR modulates tumor metastasis is not well known, evidence suggests that microRNA-197 (miR-197) might be involved in this event. In the present study, the significance of HOTAIR and miR-197 in the progression of colorectal cancer was detected in vitro and in vivo. We found that HOTAIR expression was significantly increased in colorectal cancer cells and tissues. In contrast, the expression of miR-197 was obviously decreased. We further demonstrated that HOTAIR knockdown promoted apoptosis and inhibited cell proliferation, migration, and invasion in vitro and in vivo. Moreover, HOTAIR modulated the progression of colorectal cancer by competitively binding miR-197. Taken together, our study has identified a novel pathway through which HOTAIR exerts its oncogenic role and provided a molecular basis for potential applications of HOTAIR in the prognosis and treatment of colorectal cancer.

As important regulators of gene expression long noncoding RNAs (lncRNAs) are implicated in various physiological and pathological processes, including cancer. An oncogenic role of MNX1 antisense RNA 1 (MNX1-AS1) lncRNA has been suggested in cervical cancer and glioblastoma. In this study, we investigated the clinicopathological significance and biological function of MNX1-AS1 in gastric cancer (GC). The expression of MNX1-AS1 was analyzed by qRT-PCR in 96 GC and adjacent non-tumor tissues in relation to clinicopathological features and overall survival (OS) of patients, and in five human GC cell lines compared to a normal gastric epithelial cell line. Loss-of-function experiments using small interfering RNA (siRNA) targeting MNX1-AS1 (si-MNX1-AS1) were carried out in AGS and MGC-803 GC cell lines. Cell proliferation (CCK-8 assay), migration (Transwell) and invasion (Transwell Matrigel), and protein expression of proliferating cell nuclear antigen (PCNA), E-cadherin, N-cadherin, vimentin and matrix metallopeptidase 9 (MMP-9) were analyzed in transfected GC cells. Expression of MNX1-AS1 was significantly higher in GC vs. adjacent non-tumor tissues. Higher MNX1-AS1 expression was significantly associated with tumor size, TNM stage and lymph node metastasis. Kaplan–Meier analysis showed that GC patients with higher MNX1-AS1 expression had worse OS compared to patients with lower MNX1-AS1 expression. Multivariate analysis showed that MNX1-AS1 is an independent poor prognostic factor in GC. Knockdown of MNX1-AS1 significantly inhibited proliferation, migration and invasion of AGS and MGC-803 cells, and resulted in increased E-cadherin and decreased PCNA, N-cadherin, vimentin and MMP-9 expression. Taken together, these results suggest that MNX1-AS1 has an oncogenic function in GC and potential as a molecular target in GC therapy.

Auricularia auricula‐judae is an edible fungus with high nutritional value due to abundant polysaccharides, and is acknowledged as traditional food and medicine in Asia. Polysaccharides from A. auricula (AAPs) are typically fungal polysaccharides and have a wide range of biological activities. It has been shown the potential of AAPs to improve diabetes as an effective adjuvant, but the underlying mechanism remains unclear. In this study, we explored the effects and potential mechanism of AAPs on type 2 diabetes (T2D) using a high‐fat diet and streptozotocin (STZ) induced C57BL/6J mice. The results indicated that 50 and 100 mg/kg AAPs significantly decreased inflammation, liver injury, and insulin resistance. In addition, AAPs improved glycolipid metabolism disorders by activating the AKT and adenosine 5`monophosphate‐activated protein kinase (AMPK) signaling pathways in T2D mice. Furthermore, we investigated the association between changes of gut microbiota and AAPs effects using high‐throughput sequencing of 16S rDNA for fecal samples. In our study, AAPs elevated gut microbiota diversity and optimized microbial composition and function in T2D mice, characterized by increased Lactobacillus and Bacteroides abundance and decreased Clostridium and Allobaculum abundance. Particularly, AAPs intervention mainly affected the amino acid metabolism and glycolipid metabolism pathways. Overall, this study confirms that AAPs can improve type 2 diabetes by regulating the AKT and AMPK pathways and modulating intestinal microbiota. Practical Application The article systematically verified the positive effects of AAPs on insulin resistance, glycolipid metabolism disorder, inflammation, and liver injury, key factors closely related to T2D. Furthermore, our study firstly determined the specific underlying mechanism that AAPs ameliorates T2D through regulating AKT/AMPK pathways and modifying the gut microbiota. These results could offer a full explanation and a potential option for the adjuvant therapy of diabetes with AAPs.

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Nonalcoholic fatty liver disease (NAFLD) is a metabolic syndrome, whose main characteristics are excessive lipid accumulation and oxidative stress. Major royal jelly proteins (MRJPs) is a kind of water‐soluble protein, which is abundant in royal jelly (RJ). The aim of this study was to evaluate the effect of MRJPs on lipid accumulation and oxidative stress of liver cells. Here, we first optimized the conditions for extracting MRJPs from RJ and identified the extraction effect and product by SDS‐PAGE. Then, we used oleic acid (OA) of 1.0 mM to induce hepatocytes for 24 hr to establish a stable cell models of lipid accumulation, and we found that pre‐administration (24 hr) of MRJPs (0.2, 0.5, and 1.0 g/L) could significantly reduce the lipid drop content and triglyceride level in the model cells, and simultaneously reduce the alanine aminotransferase and aspertate aminotransferase levels in the cell culture supernatant. In addition, pre‐incubation (24 hr) with MRJPs (0.2, 0.5, and 1.0 g/L) could restore superoxide dismutase (SOD) level and mitochondrial membrane potential as compared with OA group. Furthermore, MRJPs administration significantly upregulated the expression of Silent Information Regulator 2 Associated Protein 3, mitochondrial superoxide dismutase (SOD2), and cytochrome c oxidase subunit IV in OA‐treated HepG2 cells. The study for the first time provides evidences on the lipid‐lowering effect of MRJPs at the cellular level, which can further provide support for the development and application of polypeptide drugs in the future, and can also provide a choice for the prevention and treatment of liver metabolic diseases represented by NAFLD. Practical Application Our study proved that MRJPs had substantial preventing effect on OA‐induced lipid accumulation and mitochondrial dysfunction in HepG2 cells. This research can further provide theoretical support for the development and application of peptide drugs in the future. Besides, it can not only further broaden our understanding of NAFLD and other diseases, but also provide ideas for research on oxidative stress and lipid accumulation in the body.