MiR-106b-5p regulates esophageal squamous cell carcinoma progression by binding to HPGD.

BACKGROUND: Several studies have documented the key role of microRNAs (miRNAs) in esophageal squamous cell carcinoma (ESCC). Although the expression of the 15-hydroxyprostaglandin dehydrogenase (HPGD) gene and miR-106b-5p are reportedly linked to cancer progression, their underlying mechanisms in ESCC remain unclear. METHODS: mRNA and miRNA expression in ESCC tissues and cells were analyzed using RT-qPCR. Luciferase and RNA pull-down assays were used to identify the interaction between miR-106b-5p and HPGD. Xenograft and pulmonary metastasis models were used to assess tumor growth and metastasis. CCK-8, BrdU, colony formation, adhesion, cell wound healing, Transwell, and caspase-3/7 activity assays, and flow cytometry and western blot analyses were used to examine the function of miR-106-5p and HPGD in ESCC cell lines. RESULTS: The findings revealed that miR-106b-5p expression was upregulated in ESCC tissues and cell lines. miR-106b-5p augmented cellular proliferation, colony formation, adhesion, migration, invasion, and proportion of cells in the S-phase, but reduced apoptosis and the proportion of cells in G1-phase. Silencing of miR-106-5p inhibited tumor growth in vivo and pulmonary metastasis. Although HPGD overexpression suppressed proliferation, colony formation, adhesion, migration, and invasion of ESCC cells, it promoted apoptosis and caused cell cycle arrest of the ESCC cells. The results also indicated a direct interaction of HPGD with miR-106b-5p in ESCC cells. Furthermore, miR-106b-5p inhibited HPGD expression, thereby suppressing ESCC tumorigenesis. CONCLUSION: Our data suggest that miR-106b-5p enhances proliferation, colony formation, adhesion, migration, and invasion, and induces the cycle progression, but represses apoptosis of ESCC cells by targeting HPGD. This suggests that the miR-106b-5p/HPGD axis may serve as a promising target for the diagnosis and treatment of ESCC.

The Improved Mediastinal Drainage Strategy for the Enhanced Recovery System After Esophagectomy.

BACKGROUND: The improved drainage strategy was the transperitoneal placement of a single mediastinal drainage tube after esophagectomy. This study aimed to explore its effect on the incidence of postoperative complications, pain scores, and hospital stay. METHODS: Data from 108 patients who underwent minimally invasive esophagectomy were retrospectively analyzed. Patients were divided into 2 groups: those in group A were treated with transthoracic placement of mediastinal drain and those in group B were treated with transperitoneal placement. The incidence of postoperative complications, pain scores, and postoperative hospital stay were compared. RESULTS: The maximum pain scores in group B were significantly lower than those in group A from the first to the fourth postoperative days (PODs): POD1, 3.9 ± 0.7 vs 2.3 ± 0.7; POD2, 3.5 ± 0.8 vs 2.1 ± 0.7; POD3, 3.3 ± 0.8 vs 1.7 ± 0.8; and POD4, 3.1 ± 0.7 vs 1.7 ± 0.8 (all P < .001). Compared with group A, there were fewer postoperative analgesic drug users in group B (44.6% vs 17.9%; P = .005), fewer cases of pleural effusion (10.7% vs 0%; P = .045), and fewer cases of closed thoracic drainage due to pleural effusion or pneumothorax (14.3% vs 0%; P = .014). There were no significant differences in the incidence of anastomotic leakage, mediastinitis, major pulmonary complications, major abdominal complications, surgical site infection, and total postoperative complications, without statistical differences in postoperative hospital stay and 30-d mortality (all P > .05). CONCLUSIONS: The transperitoneal placement of a single mediastinal drain can reduce postoperative pain and the incidence of pleural effusion, without increasing the incidence of other major postoperative complications and postoperative hospital stay.

MicroRNA-217 modulates inflammation, oxidative stress, and lung injury in septic mice via SIRT1.

Inflammation and oxidative stress contribute to the initiation and progression of septic lung injury. MicroRNA-217 (miR-217) is proved to be involved in controlling inflammatory response and oxidative stress, yet its role and underlying mechanism in the pathogenesis of septic lung injury remain elusive. Caecal ligation and puncture surgery were performed to generate sepsis in vivo and mice were kept for 12 h to imitate septic lung injury. Next, mice were administrated with miR-217 antagomir or agomir to decrease or increase the expression of miR-217 in lung tissue. Moreover, primary peritoneal macrophages were separated and incubated with lipopolysaccharide (LPS) to further verify the role of miR-217 in vitro. miR-217 was upregulated in septic lungs and primary macrophages. miR-217 antagomir alleviated, whereas miR-217 agomir aggravated inflammation and oxidative stress in septic mice and LPS-stimulated macrophages. Further detection identified SIRT1 was responsible for miR-217 antagomir-mediated anti-inflammatory and anti-oxidant effects, and SIRT1 inhibition abolished the beneficial effects of miR-217 antagomir in vivo and in vitro. Our data defined miR-217 as a therapeutic target for treating septic lung injury.

MicroRNA-499-5p targets SIRT1 to aggravate lipopolysaccharide-induced acute lung injury.

Acute lung injury (ALI) is a life-threatening disease without effective and specific therapeutic strategies except the life-supporting treatments. Inflammation and oxidative stress are essential for the progression of ALI. MicroRNA-499-5p (miR-499-5p) has multiple pathophysiological actions; however, its function and mechanisms in ALI remain elusive. Mice were intravenously injected with miR-499-5p agomir, antagomir or the negative controls for 3 consecutive days and then received a single intratracheal injection of lipopolysaccharide (LPS, 5 mg/kg) to generate ALI model. Twenty four hours prior to LPS injection, EX-527 (1 mg/kg) was applied to inhibit SIRT1 activity. We identified a significant upregulation of miR-499-5p in LPS-treated lung tissues. miR-499-5p antagomir prevented, while miR-499-5p agomir promoted inflammation, oxidative stress and ALI in LPS-treated mice. Further studies indicated that miR-499-5p directly bound to the 3'-untranslated region of Sirtuin 1 (Sirt1) and decreased its protein level. SIRT1 inhibition blocked miR-499-5p antagomir-mediated pulmonary protection against LPS injury. miR-499-5p targets SIRT1 to aggravate LPS-induced ALI and it is a promising therapeutic target for the treatment of ALI.

Factors associated with the costs of hospitalization after esophagectomy: a retrospective observational study at a three-tertiary cancer hospital in China.

BACKGROUND: Esophageal cancer represents a major health threat in China. Esophagectomy is the standard treatment for respectable esophageal cancer. This study aimed to investigate the costs of hospitalization in esophageal cancer patients undergoing esophagectomy, and to analyze the factors influencing these costs. METHODS: A retrospective observational study which enrolled 196 patients who underwent esophagectomy from September, 2018, to April, 2019, in the Affiliated Cancer Hospital of Zhengzhou University were conducted. RESULTS: The median inpatient cost was ï¿¥72,772 (range, ï¿¥49,796-128,771). Materials accounted for 39.7% of the direct medical costs, which was the highest proportion for any of the cost components. Minimally invasive esophagectomy (MIE, OR: 0.031; 95% CI: 0.005-0.209), cardiopathy comorbidity (OR: 0.344; 95% CI: 0.136-0.872), and anastomotic leak (OR: 0.012; 95% CI: 0.001-0.131) were risk factors for higher cost, while early oral feeding (OR: 3.979; 95% CI: 1.430-11.067) was a protective factor. CONCLUSIONS: Understanding the factors associated with high hospitalization costs will help to reduce healthcare expenditure. By controlling complications and promoting early oral feeding, the economic burden on esophagectomy patients can be relieved. Further research based on a longitudinal design is needed to investigate the full costs of hospitalization associated with esophageal cancer.

MicroRNA-326 prevents sepsis-induced acute lung injury via targeting TLR4.

Unrestrained inflammation provokes oxidative stress and contributes to the development of sepsis-induced acute lung injury (ALI). MicroRNA-326 (miR-326) is originally identified as an autoimmunity-associated microRNA, yet its role and potential molecular basis in sepsis-induced ALI remain unclear. Herein, we found that miR-326 was downregulated in murine lungs and macrophages upon lipopolysaccharide (LPS) stimulation. MiR-326 agomir prevented, whereas miR-326 antagomir exacerbated LPS-induced inflammation, oxidative stress, and ALI in mice. Furthermore, we found that miR-326 suppressed LPS-induced inflammation and oxidative stress in macrophages via downregulating toll-like receptor (TLR4), and TLR4 inhibition abolished miR-326 antagomir-mediated deleterious effect in vivo and in vitro. Finally, we proved miR-326 agomir notably alleviated sepsis-induced ALI after caecal ligation and puncture surgery. Our data identified miR-326 as a potential therapeutic target for sepsis-induced ALI.