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Background: The role of Sm-like 5 (LSM5) in colon cancer has not been determined. In this study, we investigated the role of LSM5 in progression of colon cancer and the potential underlying mechanism involved., Aim: To determine the role of LSM5 in the progression of colon cancer and the potential underlying mechanism involved., Methods: The Gene Expression Profiling Interactive Analysis database and the Human Protein Atlas website were used for LSM5 expression analysis and prognosis analysis. Real-time quantitative polymerase chain reaction and Western blotting were utilized to detect the expression of mRNAs and proteins. A lentivirus targeting LSM5 was constructed and transfected into colon cancer cells to silence LSM5 expression. Proliferation and apoptosis assays were also conducted to evaluate the growth of the colon cancer cells. Human GeneChip assay and bioinformatics analysis were performed to identify the potential underlying mechanism of LSM5 in colon cancer., Results: LSM5 was highly expressed in tumor tissue and colon cancer cells. A high expression level of LSM5 was related to poor prognosis in patients with colon cancer. Knockdown of LSM5 suppressed proliferation and promoted apoptosis in colon cancer cells. Silencing of LSM5 also facilitates the expression of p53, cyclin-dependent kinase inhibitor 1A (CDKN1A) and tumor necrosis factor receptor superfamily 10B (TNFRSF10B). The inhibitory effect of LSM5 knockdown on the growth of colon cancer cells was associated with the upregulation of p53, CDKN1A and TNFRSF10B., Conclusion: LSM5 knockdown inhibited the proliferation and facilitated the apoptosis of colon cancer cells by upregulating p53, CDKN1A and TNFRSF10B., Competing Interests: Conflict-of-interest statement: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Aim: To investigate the rate of spontaneous passage of single and symptomatic common bile duct (CBD) stones ≤ 10 mm in diameter in 4 wk with or without a 2-wk course of anisodamine., Methods: A multicenter, randomized, placebo-controlled trial was undertaken. A total of 197 patients who met the inclusion criteria were enrolled. Ninety-seven patients were assigned randomly to the control group and the other 100 to the anisodamine group. The anisodamine group received intravenous infusions of anisodamine (10 mg every 8 h) for 2 wk. The control group received the same volume of 0.9% isotonic saline for 2 wk. Patients underwent imaging studies and liver-function tests every week for 4 wk. The rate of spontaneous passage of CBD stones was analyzed., Results: The rate of spontaneous passage of CBD stones was significantly higher in the anisodamine group than that in the control group (47.0% vs 22.7%). Most (87.2%, 41/47) stone passages in the anisodamine group occurred in the first 2 wk, and passages in the control group occurred at a comparable rate each week. Factors significantly increasing the possibility of spontaneous passage by univariate logistic regression analyses were stone diameter (< 5 mm vs ≥ 5 mm and ≤ 10 mm) and anisodamine therapy. Multivariate logistic regression analyses revealed that these two factors were significantly associated with spontaneous passage., Conclusion: Two weeks of anisodamine administration can safely accelerate spontaneous passage of single and symptomatic CBD stones ≤ 10 mm in diameter, especially for stones < 5 mm.

AIM:To investigate the age-related alterations of cytoskeleton system in liver Kupffer cell and their relation to the changed phagocytic function.METHODS: The phagocytic function of Kupffer cells from rats of various ages (6mo, 12mo,18mo and 24mo) were quantitatively evaluated by phagocytosis of polystyrene beads. The actin distribution and measurement of Kupffer cell were determined by a phalloidin-TRITC method; and the myosin and vimentin distribution and measurement with indirect immunochemical staining.RESULTS: Aging resulted in significant alterations of actin, myosin and vimentin distributions and reductions in Kupffer cell; the 3 cytoskeleton components of 24-mo-old Kupffer cell were significantly decreased to 68.0%, 84.9% and 75.5%, respectively of these of 6-mo-old Kupffer cell(P < 0.01,0.01 and 0.01). And these decreases had significant positive relations with the damaged phagocytosis of the aged Kupffer cell.gammavalues were 0.96(P < 0.05), 0.99(P < 0.01) and 0.95 (P < 0.05) respectively.CONCLUSION: The cytos-keleton system of the aged Kupffer cell presents an evident state of senescence, which may be an important mechanism of decreased phagocytosis of the aged Kupffer cell.

Aim: To investigate the mechanism of age-related reduction of Kupffer cell (KC) phagocytic capacity and the protective management., Methods: Using rhodamine 123 fluorescence density and rate of glucose utilization as parameters, we measured the mitochondrial energy metabolism status in vitro and the glucose utilization capacity of isolated rat liver Kupffer cells (KCs) from rats of various ages (6 mo, 12 mo, 18 mo and 24 mo) and the effect of vitamin E (VE) pretreatment (500 mg/kg/wk × 13 wk)., Results: The rate of KC glucose utilization and the rhodamine fluorescence density of KC mitochondria of 18 mo-old untreated rats (NVEG) were significantly lower than that of 6 mo-old NVEG by 19.3% (4.0 nmol·h ± 0.4 nmol·h(-1) 10.6 cells(-1) vs 5.7 nmol·h ± 0.6 nmol·h(-1) 10(6) cells(-1), P < 0.05) and 19.5% (80.5 ± 6.3 vs 100.0 ± 4.7, P < 0.01) respectively; Rate of KC glucose utilization and the rhodamine fluorescence density of KC mitochondria of 6 mo-old rats were also lower than the 24 mo-old NVEG by 35.1% (3.7 nmol·h ± 0.6 nmol·h(-1)10(6) cells(-1) vs 5.7 nmol·h ± 0.6 nmol·h(-1) 10(6) cells(-1), P < 0.01) and 32.1% (67.9 ± 7.4 vs 100.0 ± 4.7, P < 0.01) respectively. The two parameters of 18 mo-old VE pretreated rats (VEG) were significantly higher than those of 18 mo-old NVEG, and statistically comparable to those of 6 mo-old VEG. The two parameters of the 24 mo-old VEG were significantly higher in comparison with those of 24 mo-old NVEG, but still significantly lower than those of 6 mo-old VEG., Conclusion: Aging has a significantly negative effect on KC energy metabolism, which can be alleviated by VE pretreatment.