To investigate the SOX9 expression and its effects on promoting invasion and metastasis in the primary gastric adenocarcinomas. One hundred and eighty six patients with primary gastric adenocarcinomas who underwent surgery between 2002 and 2006 were classified as low, intermediate, and high SOX9 expression groups by immunohistochemistry (IHC). Our IHC performance showed that SOX9 was lowly expressed in lower crypt of the normal epithelium adjacent to the tumor, and SOX9 expression was also observed in the intestinal metaplastic epithelium, but no SOX9 expression was detected in the surface epithelium. The stronger SOX9 expression was observed in the T3-T4 group than in the T1-T2 group, and there was a significant difference between the two groups (P < 0.0005). The SOX9 expression was correlated with the lymph node metastasis, and it showed significant between N0, N1, N2, and N3 groups (P < 0.0005). Similar to the lymph node metastasis classification, the SOX9 expression was also related to the tumor staging. From the stage Ia-Ib to stage II-IIIa and stage IIIb-IV, the SOX9 expression was elevated and the difference was significant (P < 0.0005). On the contrary, the SOX9 expression was not related to the histological classification (P > 0.05). Also the SOX9 expression showed no significance in patient age (P > 0.05). The SOX9 is overexpressed in the advanced stage of gastric carcinoma. SOX9 is related to the tumor progression though promoting invasion and metastasis, probably via enhancing the adhesion between the tumor cells and matrix or vessels which facilitates the tumor cells metastasis.

Colorectal cancer (CRC) is the third most common type of cancer and the second leading cause of cancer-related death around the word. 1 Although advances have been made over the past several decades in the treatment of patients with CRC, the 5-y survival rate remains at 50%-55%. While metastatic CRC (mCRC) occurs in only 11.7% of patients with CRC, mortality results mainly in patients with tumor metastasis. 2 Tumor metastasis is a complex process involving multiple gene interactions. The lack of effective biomarkers to predict metastasis and guide diagnosis and therapy is one of the primary causes of poor prognosis. Accordingly, there is a need for identifying novel metastasis-associated biomarkers and clarifying their mechanisms to improve the prognosis of patients with CRC.

Our results showed that during the development of NAFL and NASH, F2-isoPG levels increased and Nrf2 expression was upregulated. Our findings suggest Nrf2 may play a key role during liver steatosis, and activation of Nrf2 may protect liver from inflammation damage induced by oxidative stress.

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ER achieves the same positive results as MIE in the treatment of early esophageal cancer and is associated with a lower complication rate, a shorter recovery time, and a similar survival rate. However, multiple ER procedures were required for several patients in this study.

H2S is produced mainly by two enzymes:cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE), using L-cysteine (L-Cys) as the substrate. In this study, we investigated the role of H2S in gastric accommodation using CBS+/− mice, immunohistochemistry, immunoblot, methylene blue assay, intragastric pressure (IGP) recording and electrical field stimulation (EFS). Mouse gastric fundus expressed H2S-generating enzymes (CBS and CSE) and generated detectable amounts of H2S. The H2S donor, NaHS or L-Cys, caused a relaxation in either gastric fundus or body. The gastric compliance was significantly increased in the presence of L-Cys (1 mM). On the contrary, AOAA, an inhibitor for CBS, largely inhibited gastric compliance. Consistently, CBS+/− mice shows a lower gastric compliance. However, PAG, a CSE inhibitor, had no effect on gastric compliances. L-Cys enhances the non-adrenergic, non-cholinergic (NANC) relaxation of fundus strips, but AOAA reduces the magnitude of relaxations to EFS. Notably, the expression level of CBS but not CSE protein was elevated after feeding. Consistently, the production of H2S was also increased after feeding in mice gastric fundus. In addition, AOAA largely reduced food intake and body weight in mice. Furthermore, a metabolic aberration of H2S was found in patients with functional dyspepsia (FD). In conclusion, endogenous H2S, a novel gasotransmitter, involves in gastric accommodation.

Long non‐coding RNAs have important roles in the occurrence and progression of various cancers. However, the molecular mechanism of lncRNAs in colorectal cancer (CRC) is not well illustrated. Thus, we used bioinformatics methods to find potential lncRNAs associated with CRC progression, and chose SH3PXD2A‐AS1 as a candidate for further analysis. The roles of SH3PXD2A‐AS1 in CRC cells were determined by CCK‐8, transwell invasion, wound healing and flow cytometry assays. Besides, we established the CRC tumor models in nude mice to study the effect of SH3PXD2A‐AS1 on the tumor growth. Based on the ceRNA hypothesis, we used miRDB and miRTarBase websites to identify the SH3PXD2A‐AS1‐related ceRNA regulatory network, and measured the roles of this network in CRC cells. The results revealed that the expression profiles of SH3PXD2A‐AS1 from GEO and TCGA databases showed an aberrant high level in CRC tissues compared with colorectal normal tissues. SH3PXD2A‐AS1 over‐expression was also found in CRC cells. SH3PXD2A‐AS1 knockdown inhibited the CRC cellular proliferation, invasion and migration but induced apoptosis. Besides, SH3PXD2A‐AS1 knockdown also suppressed the growth of CRC tumors. Furthermore, SH3PXD2A‐AS1 could function as a ceRNA of miR‐330‐5p. Additionally, UBA2 was proved to be a target gene of miR‐330‐5p. Moreover, SH3PXD2A‐AS1 knockdown downregulated UBA2 expression through sponging miR‐330‐5p to inactivate the Wnt/β‐catenin signaling pathway, thereby inhibiting the cell growth and promoting apoptosis. Therefore, the SH3PXD2A‐AS1/miR‐330‐5p/UBA2 network could regulate the progression of CRC through the Wnt/β‐catenin pathway. These findings offer new sights for understanding the pathogenesis of CRC and provide potential biomarkers for CRC treatment.