Surgical timing for primary encapsulating peritoneal sclerosis: A case report and review of literature.

BACKGROUND: Primary encapsulating peritoneal sclerosis (EPS) is a rare but devastating disease that causes fibrocollagenous cocoon-like encapsulation of the bowel, resulting in bowel obstruction. The pathogenesis, prevention, and treatment strategies of EPS remain unclear so far. Since most patients are diagnosed during exploratory laparotomy, for the non-surgically diagnosed patients with primary EPS, the surgical timing is also uncertain. CASE SUMMARY: A 44-year-old female patient was referred to our center on September 6, 2021, with complaints of abdominal distention and bilious vomiting for 2 d. Physical examination revealed that the vital signs were stable, and the abdomen was slightly distended. Computerized tomography scan showed a conglomerate of multiple intestinal loops encapsulated in a thick sac-like membrane, which was surrounded by abdominal ascites. The patient was diagnosed with idiopathic EPS. Recovery was observed after abdominal paracentesis, and the patient was discharged on September 13 after the resumption of a normal diet. This case raised a question: When should an exploratory laparotomy be performed on patients who are non-surgically diagnosed with EPS. As a result, we conducted a review of the literature on the clinical manifestations, intraoperative findings, surgical methods, and therapeutic effects of EPS. CONCLUSION: Recurrent intestinal obstructions and abdominal mass combined with the imaging of encapsulated bowel are helpful in diagnosing idiopathic EPS. Small intestinal resection should be avoided.

MORF4L1 suppresses cell proliferation, migration and invasion by increasing p21 and E-cadherin expression in nasopharyngeal carcinoma.

Mortality factor 4-like 1 (MORF4L1) is a member of a subgroup of histone acetyltransferases and belongs to the mortality factor on chromosome 4 (MORF4) class of proteins. However, the role of MORF4L1 in cancers is largely unknown. Using reverse transcription-quantitative polymerase chain reaction and published datasets, the present study demonstrated that the expression of MORF4L1 is decreased in several cancers, including nasopharyngeal carcinoma (NPC). Additionally, the methylation rate of the promoter of MORF4L1 was identified to be significantly higher in tumour cells than in normal cells. The ectopic expression of MORF4L1 was also revealed to inhibit cell proliferation, colony formation, migration and invasion in NPC, whereas the knockdown of MORF4L1 promoted cell proliferation, colony formation, migration and invasion. Mechanistically, the present study demonstrated that MORF4L1 functions as a tumour suppressor by increasing p21 and E-cadherin levels. These findings may be useful novel targets for treating patients with NPC.

miR-429 promotes capecitabine-resistance in pancreatic cancer PANC-1 cells by down-regulating PTEN and activating PI3K/AKT signaling pathway / 中国肿瘤生物治疗杂志

@# Objective: To explore the mechanism of miR-429 targeting PTEN to affect capecitabine-resistance in pancreatic cancer PANC-1 cells though the PI3K/AKT signaling pathway. Methods: Capecitabine-resistant pancreatic cancer cell line PANC-1/CAP was constructed, and the expression of miR-429 and PTEN were detected by quantitative Real-time polymerase chain reaction (qRT-PCR) and Western blotting. The effect of miR-429 knock-down on cell proliferation viability, apoptosis and capecitabine-resistance was measured by colony formation assay, CCK-8 assay andAnnexin V-FITC/PI double staining flow cytometry assay, respectively. Subsequently, dual luciferase reporter assay verified that PTEN was a target gene of miR-429. Furthermore, the effect of miR-429 on PTEN-PI3K/ AKT signaling pathway was measured by Western blotting. Results: miR-429 was found to be up-regulated in PANC-1 cells and PANC-1/CAP cells compared with the non-malignant pancreatic ductal cell line (HPDE6-C7) (P<0.05 or P<0.01). Moreover, silencing of miR-429 significantly decreased cell proliferation viability, capecitabine-resistance and enhanced apoptosis of PANC-1/CAP cells; additionally, dual luciferase reporter assay confirmed that PTEN was a target of miR-429 (P<0.05 or P<0.01). Suppression of miR-429 up-regulated PTEN and blocked the PI3K/AKT signaling pathway to decrease cell proliferation viability and further reduce the capecitabine-resistance of PANC-1/CAP cells (P<0.05 or P<0.01). Conclusion: miR-429/PTEN-PI3K/AKT signaling pathway plays a certain role in regulating the capecitabine-resistance of pancreatic cancer, and inhibition of miR-429 expression may reverse the resistance of PANC-1/CAPto capecitabine.

SUN2 exerts tumor suppressor functions by suppressing the Warburg effect in lung cancer.

SUN2, a key component of LINC (linker of nucleoskeleton and cytoskeleton) complex located at the inner nuclear membrane, plays unknown role in lung cancer. We found that SUN2 expression was decreased in lung cancer tissue compared with paired normal tissues and that higher SUN2 levels predicted better overall survival and first progression survival. Overexpression of SUN2 inhibits cell proliferation, colony formation and migration in lung cancer, whereas knockdown of SUN2 promotes cell proliferation and migration. Additionally, SUN2 increases the sensitivity of lung cancer to cisplatin by inducing cell apoptosis. Mechanistically, we showed that SUN2 exerts its tumor suppressor functions by decreasing the expression of GLUT1 and LDHA to inhibit the Warburg effect. Finally, our results provided evidence that SIRT5 acts, at least partly, as a negative regulator of SUN2.Taken together, our findings indicate that SUN2 is a key component in lung cancer progression by inhibiting the Warburg effect and that the novel SIRT5/SUN2 axis may prove to be useful for the development of new strategies for treating the patients with lung cancer.