Stomatin-like protein 2 promotes cell proliferation and survival under 5-Fluorouracil stress in hepatocellular carcinoma.

BACKGROUND: The crucial role of STOML2 in tumor progression has been documented recently in various cancers. Previous studies have shown that STOML2 promoted cancer cell proliferation, but the underlying mechanism is not fully illustrated. METHODS AND RESULTS: The expression and clinical relevance of STOML2 in pan-cancer was analyzed by TIMER2 web platform in pan-cancer. The prognostic significance of STOML2 in HCC was evaluated utilizing KM curve and a nomogram model. Signaling pathways associated with STOML2 expression were discovered by GSEA. CCK-8 assay was performed to evaluate the proliferative capacity of HCC cells after manipulating STOML2 expression. Flow cytometry was utilized to analyze cell cycle progression. Results indicated that increased STOML2 expression in HCC linked to unfavorable clinical outcomes. Cell cycle and cell division related terms were enriched under conditions of elevated STOML2 expression via GSEA analysis. A notable decrease in cell proliferation was observed in MHCC97H with STOML2 knocked-down, accompanied by G1-phase arrest, up-regulation of p21, down-regulation of CyclinD1 and its regulatory factor MYC, while STOML2 overexpression in Huh7 showed the opposite results. These results indicated that STOML2 was responsible for HCC proliferation by regulating the expression level of MYC/cyclin D1 and p21. Furthermore, an inverse correlation was found between STOML2 expression and 5-FU sensitivity. CONCLUSIONS: STOML2 promotes cell cycle progression in HCC which is associated with activation of MYC/CyclinD1/p21 pathway, and modulates the response of HCC to 5-FU.

Role of gut microbiota in postoperative complications and prognosis of gastrointestinal surgery: A narrative review.

Gastrointestinal surgery is often challenging because of unexpected postoperative complications such as pouchitis, malabsorption, anastomotic leak, diarrhea, inflammatory responses, and life-threatening infections. Moreover, the gut microbiota has been shown to be associated with the complications described above. Major intestinal reconstruction, such as Roux-en-Y gastric bypass (RYGB) and ileal pouch-anal anastomosis surgery, could result in altered gut microbiota, which might lead to some of the benefits of these procedures but could also contribute to the development of postsurgical complications. Moreover, postsurgical reestablishment of the gut microbiota population is still poorly understood. Here, we review evidence outlining the role of gut microbiota in complications of gastrointestinal surgery, especially malabsorption, anastomotic leak, pouchitis, and infections. In addition, this review will evaluate the risks and benefits of live biotherapeutics in the complications of gastrointestinal surgery.

Linc00511 Indicates A Poor Prognosis Of Liver Hepatocellular Carcinoma.

OBJECTIVE: To uncover the specific function of linc00511 in the progression of liver hepatocellular carcinoma (LIHC) and the underlying mechanism. PATIENTS AND METHODS: GEPIA dataset containing 9736 LIHC samples and 857 normal samples were downloaded from TCGA. Expression pattern and prognostic potential of linc00511 in LIHC were analyzed. Subsequently, expression level of linc00511 in LIHC tissues collected in our hospital and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Differential expressions of linc00511 in LIHC with different tumor grades and metastatic status were compared. After transfection of si-linc00511, proliferative and migratory changes in Huh7 and Hep3B cells were assessed by cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU) and Transwell assay. Lastly, Pearson correlation analysis and qRT-PCR were conducted to investigate the interaction between linc00511 and miR-29c. RESULTS: Linc00511 was upregulated in LIHC tissues and cell lines. Its level was positively correlated to TNM staging, lymphatic metastasis and poor prognosis in LIHC patients. Knockdown of linc00511 attenuated proliferative and migratory abilities in Huh7 and Hep3B cells. In addition, miR-29c was downregulated in LIHC and negatively linked to linc00511 level. A negative interaction between linc00511 and miR-29c could be a regulatory feedback influencing the progression of LIHC. CONCLUSION: Linc00511 accelerates the proliferation and migration in LIHC, thus aggravating tumor progression. Meanwhile, linc00511 could be utilized as a hallmark predicting poor prognosis in LIHC patients.

Fatty liver disease is associated with the severity of acute pancreatitis:A systematic review and meta-analysis.

BACKGROUND: Fatty liver (FL) has been positively associated with the risk of acute pancreatitis (AP), but whether FL is associated with the severity of AP remains unknown. To this, a meta-analysis was conducted to assess the effect of FL on severity and outcomes of AP. METHOD: We searched PubMed, EMBASE and the Cochrane library to identify all eligible studies (up to June 2017). We pooled the odds ratios (ORs) or weighted mean differences (WMD) from individual studies using a random-effects model to investigate associations between FL and the prognosis of AP. RESULT: Four studies were included in the meta-analysis, including a total of 805 patients with fatty liver-related acute pancreatitis (FLAP) and 1026 patients with non fatty liver-related acute pancreatitis (NFLAP). The incidences of moderately severe AP (MSAP) (OR = 2.72, 95%CI: 1.82-4.05, P < 0.001) and severe AP (SAP) (OR = 3.57, 95%CI: 2.06-6.18, P < 0.001) were statistically significantly higher in FLAP group than those in NFLAP group. Taking obesity into consideration, a higher rate of MSAP and SAP were also found in patients with FL, no matter whether they were obese or not. Furthermore, mortality (OR = 4.16, 95%CI: 2.57-6.73, P < 0.001), systemic inflammatory response syndrome (SIRS) (OR = 2.82, 95%CI: 2.3-3.47, P < 0.001) and local complications were also statistically significantly higher in the FLAP group than in NFLAP group. CONCLUSION: Fatty liver is associated with the severity of acute pancreatitis.