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Background Pneumoperitoneum during laparoscopic surgery has a systemic impact on the renal system and might contribute to acute kidney injury or postoperative renal dysfunction. However, effective preventive strategies are still lacking. We aimed to explore the effects of dexmedetomidine (DEX) on kidney and other organ function in patients undergoing elective laparoscopic surgery for colorectal cancer. Materials and methods Fifty-six patients were randomly enrolled into the Control or DEX group. The DEX group received 1 µg kg−1 DEX intravenously within 10 min followed by a maintenance dose of 0.5 µg kg−1 h−1 infused until 30 min before closing the peritoneum. In the Control group, 0.9% sodium chloride was administered as a placebo. The primary outcome was serum neutrophil gelatinase-associated lipocalin (NGAL) levels reflecting kidney injury. Secondary outcomes included variables reflecting the kidney, intestinal injury and systemic inflammatory response. Results NGAL levels were significantly lower in the DEX group than in the Control group at 1 d and 5 d postoperatively (107.5 ± 55.6 ng mL−1 versus 179.5 ± 78.2 ng mL−1; 70.3 ± 45.8 ng mL−1 versus 135.2 ± 59.6 ng mL−1, P Conclusions Perioperative DEX administration may potentially confer kidney and intestinal protection during laparoscopic surgery for colorectal cancer patients.

Background Endometriosis (EM) is a benign gynecological disease that shares some characteristics with malignancy, such as proliferation and invasion. So far, the pathogenesis of EM is still unclear. In this study, we investigated whether TRIM65 can play a role in the development of EM. Methods TRIM65 expression levels in eutopic, ectopic, and normal endometrium were detected by quantitative real-time PCR and Western blot. Cell proliferation and invasion of primary endometrial stromal (EMS) cells were detected by CCK-8 and Transwell analysis. The interaction between TRIM65 and DUSP6 or C-myc was measured by coimmunoprecipitation, ubiquitylation, dual luciferase, and chromatin immunoprecipitation analysis. Results We found that TRIM65 was identified as an up-regulated gene in ectopic endometrial tissues and EMS cells compared with control groups without EM. TRIM65 expression was positively correlated with the levels of p-ERK1/2, C-myc, matrix metalloproteinase-2, and integrin β1 in ectopic endometrial tissues in patients and mice. TRIM65 promoted the cell proliferation and invasion of EMS cells via the ERK1/2/C-myc pathway through ubiquitination of DUSP6. C-myc promoted TRIM65 expression through inducing TRIM65 promoter activity. Additionally, the increased expression of TRIM65, C-myc, matrix metalloproteinase-2, integrin β1, and p-ERK1/2 and the decreased expression of DUSP6 in ectopic endometrial tissues were significantly suppressed by inhibition of ERK1/2 signaling pathway in ectopic endometrial tissues in experimental mice model. Conclusion In conclusion, TRIM65 promotes invasion of ectopic EMS cells by activating a feedback loop with the ERK1/2/C-myc signaling pathway and may be a potential therapeutic target for EM.

Sal-like protein 4 (SALL4) is overexpressed in breast cancer and might contribute to breast cancer progression, but the molecular mechanism remains unknown. Here, we found that within a group of 371 ethnic Chinese breast cancer patients, SALL4 was associated with lower grade (P = .002) and progesterone receptor positivity (P = .004) for overall cases; lower Ki67 (P = .045) and high vimentin (P = .007) for luminal cases. Patients with high SALL4 expression in lymph node metastasis showed a significantly worse survival than those with low expression. Knockout of SALL4 in a triple-negative breast cancer cell line MDA-MB-231-Red-FLuc-GFP led to suppressed ability in proliferation, clonogenic formation, migration, and mammosphere formation in vitro, tumorigenicity and lung colonization in vivo. On the other hand, overexpression of SALL4 enhanced migration and mammosphere formation in vitro and tumorigenicity in vivo. Mechanistically, there was a positive correlation between SALL4 expression and mesenchymal markers including Zinc finger E-box binding homeobox 1 (ZEB1), vimentin, Slug, and Snail in vivo. Chromatin immunoprecipitation experiment indicated that SALL4 can bind to the promoter region of vimentin (-778 to -550 bp). Taken together, we hypothesize that SALL4 promotes tumor progression in breast cancer by inducing the mesenchymal markers like vimentin through directly binding to its promoter. Increased SALL4 level in metastatic lymph node relative to the primary site is an important poor survival marker in breast cancer.