LINC00365 inhibited lung adenocarcinoma progression and glycolysis via sponging miR-429/KCTD12 axis.

This study researched the function of long non-coding RNA LINC00365 in lung adenocarcinoma (LAD) progression. LINC00365, miR-429, and KCTD12 expression in the LAD clinical tissues and cells were detcetd by qRT-PCR and Western blot. LINC00365, miR-429, and KCTD12 effects on H1975 cells malignant phenotype were detected by cell counting kit-8 assay, clone formation experiment, Transwell experiment, and glycolysis. Dual luciferase reporter gene assay and RNA pull-down assay were implemented. LINC00365 effect on H1975 cells in vivo growth was detected. LINC00365 was low expressed in the LAD patients and cells, associating with poor outcome. LINC00365 up-regulation attenuated H1975 cells proliferation, migration, invasion, glycolysis and in vivo growth. LINC00365 inhibited KCTD12 expression by sponging miR-429. miR-429 up-regulation and KCTD12 down-regulation partial reversed LINC00365 inhibition on H1975 cells malignant phenotype. Thus, LINC00365 inhibited LAD progression and glycolysis via targeting miR-429/KCTD12 axis. LINC00365 might be a potential candidate for LAD target treatment clinically.

Preoperative computed tomography diagnosis of non-recurrent laryngeal nerve in patients with esophageal carcinoma.

BACKGROUND: The non-recurrent laryngeal nerve (NRLN) is a rare but potentially serious anomaly that is commonly associated with the aberrant right subclavian artery (ARSA). It is easy to damage during surgical resection of esophageal cancer, leading to severe complications. METHODS: Preoperative enhanced thoracic computed tomography (CT) scans of 2697 patients with esophageal carcinoma treated in our hospital between January 2010 and December 2013 were examined. We classified the positional relationship between the right subclavian artery and the membranous wall of the trachea into two types and used this method to predicate NRLN by identifying ARSA. RESULTS: Twenty-six patients (0.96%) were identified with ARSA, all of which were cases of NRLN by CT. NRLN was identified during surgery in the 26 patients, and a normal right recurrent laryngeal nerve was observed in 2671 patients. The ARSA was detected on the dorsal side of the membranous wall of the trachea in all 26 NRLN cases, while it was detected on the ventral side in all 2671 recurrent laryngeal nerve cases. CONCLUSION: Enhanced CT scanning is a reliable method for predicting NRLN by identifying ARSA. Preoperative recognition of this nerve anomaly allows surgeons to avoid damaging the nerve and abnormal vessels during esophagectomy.

[An experimental study on chemoprevention of esophageal adenocarcinoma by celecoxib, a selective cyclooxygenase-2 inhibitor].

OBJECTIVE: To study the feasibility of chemoprevention of esophageal adenocarcinoma by celecoxib, a selective cyclooxygenase-2(COX-2) inhibitor using a rat model. METHODS: Rats were divided into 3 groups: model group, celecoxib group, and control group. The rat surgical model was established by performing a gastrojejunostomy plus an esophagojejunostomy 5 mm distal to the gastrojejunal anastomosis. Twenty-eight weeks after surgery, all the animals were sacrificed and the pathological changes in the esophagus were examined macroscopically. COX-2 expression was analyzed by immunohistochemistry. Prostaglandin E2(PGE2) level was measured by enzyme-linked immunosorbent assay(ELISA). RESULTS: The incidence of Barrett's esophagus and esophageal adenocarcinoma in the model group was 84% and 57% respectively, significantly higher than those in the control group(P<0.01). The incidence of esophageal adenocarcinoma in the celecoxib-treated group was significantly lower than that in the model group(P<0.01), and no esophageal adenocarcinoma was detected in the control group. COX-2 expression was detected in 100% of reflux esophagitis, Barrett esophagus and esophageal adenocarcinoma, but not found in the normal tissue from the esophagus and the jejunum(P<0.01). The PGE2 level in the esophageal tissue in the model group was significantly higher than that in the control group(P<0.01). Rats in the celecoxib-treated group had significantly lower PGE2 level than that in the model group(P<0.01). The PGE2 levels were significantly higher in rats with cancer than those without cancer(P<0.01). CONCLUSION: Celecoxib successfully prevents the development of esophageal adenocarcinoma in a rat surgical model with mixed reflux of acid and duodenal juice and significantly decreases the risk of Barrett esophagus developing esophageal adenocarcinoma. COX-2 maybe an effective selective target of chemoprevention for esophageal adenocarcinoma.