Background: Recently, NCAPH (non-SMC condensin I complex subunit H), a regulatory subunit of the condensin complex, has captured our attention in various cancer studies. However, the function of NCAPH in endometrial cancer (EC) remains unclear. Our study aims to investigate the role of NCAPH in EC. Methods: The expression of NCAPH in EC tissues and normal tissues was predicted by The Cancer Genome Atlas (TCGA). The Kaplan-Meier analysis was performed to evaluate the impact of NCAPH expression on EC patients' survival. Logistic regression was used to study the correlation of NCAPH expression with clinicopathologic characteristics. Molecular mechanisms behind NCAPH in EC were evaluated by Gene Set Enrichment Analysis, genetic mutations, copy number variation, and DNA methylation level. Results: NCAPH was significantly upregulated in EC (p = 1e−24), and its expression level was significantly related to the more advanced International Federation of Gynecology & Obstetrics (FIGO) stage (stage IV vs. stage I: odd ratio.[OR] = 3.7), higher grade (poor vs. well & moderate: OR = 5.3), serous histology subtype (SEA vs. EEA: OR = 8.5), myometrial invasion (≥50 vs. < 50 invasion: OR = 1.8), metastasis (vs. no metastasis: OR = 2.5), and withtumor status (vs. free of tumor: OR = 2.3) (all p were less than .05). The Gene Set Enrichment Analysis method indicated that MITOTIC_SPINDLE, G2M_CHECKPOINT, MYC_TARGETS_V1, E2F_TARGETS, MYC_TARGETS_ V2, and MTORC1_SIGNALING were involved in the upregulated NCAPH group. NCAPH hypomethylation, amplified copy number variations and genetic mutations; all played a contributive role in NCAPH upregulation. Conclusions: These results reveal NCAPH functions as oncogene and promote the development of EC.
Ovarian cancer (OC) is the leading cause of gynecological cancer deaths. Extraordinary histologic and genetic heterogeneity presents as great hurdle to OC's diagnosis and treatment. MRPS12 (Mitochondrial Ribosomal Protein S12), encoding a 28S subunit protein, controls the decoding fidelity and susceptibility to aminoglycoside antibiotics. Our study aims to investigate the clinical significance and potential mechanism of MRPS12 in OC. Oncomine, Tumor Immune Estimation Resource database (TIMER), and GEPIA databases were utilized to explore the expression level of MRPS12 in OC and normal tissues. Kaplan–Meier plotter was used to evaluate the influence of MRPS12 expression on OC patients’ survival. The potential biologic function and immune infiltration of MRPS12 in OC were analyzed by GSEA (Gene set enrichment analysis) and TIMER database, respectively. MRPS12 was significantly highly expressed in OC (P < .05) compared with normal ovarian tissues. Its overexpression was also significantly related with poor overall survival in advanced FIGO stage (III+IV) patients, in serous OC and in those patients with TP53 mutation (P < .05). GSEA showed that HALLMARK_G2M_CHECKPOINT, BIOCARTA_CELLCYCLE_PATHWAY, HALLMARK_PI3K_AKT_MTOR_SIGNALING, BIOCARTA_P53_PATHWAY were significantly enriched in high-MRPS12-expression phenotype. MRPS12 expression was positively correlated with the infiltration of macrophages and neutrophils in OC. These results reveal that MRPS12 could function as a potential oncogene and serve as a promising prognostic candidate in OC.
Background: Endometrial carcinoma (EC) is the most common cancer of female reproductive system, thus requiring for new effective biomarkers which could predict the onset of EC and worse prognosis. Cell Division Cycle Associated (CDCA) family plays indispensable roles in cell cycle process. However, no study has been focused on the role of CDCAs in EC. Our study aims to investigate the clinical relevance, potential biologic functions and molecular mechanisms of CDCAs in EC. Methods: GEPIA, cBioPortal, GeneMANIA, Networkanalyst, TCGA-UCEC cohort were utilized in this study. Results: NUF2 and CDCA2/3/4/5/7/8 were significantly highly expressed in EC compared with normal tissues. The patients with high NUF2 and CDCA2/3/4/5/8 expression tended to develop to advanced FIGO stages, poor differentiation and worse prognosis(in both OS and RFS analyses) than those with low expression. By contrast, elevated CDCA7 was significantly associated with better prognosis. CBX2 exerted no significant prognostic impact on EC patients. Distinct patterns of the genetic alterations of CDCAs were observed in various histological subtypes of EC. The biological functions of NUF2 and CDCA2/3/4/5/8 were mainly related with the activation of the following pathway: cell cycle, DNA replication, base excision repair, mismatch repair, nucleotide excision repair, cellular senescence and p53 signaling pathway. Conclusions: Our study provides new insight into the onset and progression of EC and proposes NUF2 and CDCA2/3/4/5/8 could act as oncogenes and have shown great diagnostic and prognostic promise in improving EC patient detection and survival prediction with accuracy.
Aims: This study was designed to investigate the mechanisms and suppressive effects of matrine on the development of urinary bladder cancers induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in rats. Methods: Male Sprague-Dawley rats were given BBN (200 mg/rat) twice a week for a period of 8 weeks. Oral administration of matrine (50 and 100 mg/kg) was started 1 week before BBN exposure for 35 weeks. Half of each bladder was histopathologically analyzed and the remainder was extracted for protein analysis by Western blot. Results: The bladders of BBN-treated rats demonstrated progression from epithelial hyperplasia to papillary urothelial neoplasia and even poorly differentiated invasive cancer. Matrine (50 and 100 mg/kg) treatment decreased the formation of large bladder tumors by 31.6 and 21.1%, respectively. An incidence of cancer cells was detected in rats given BBN [70% (14/20)] and matrine [50 mg/kg: 68.4% (13/19) and 100 mg/kg: 57.9% (11/19), respectively]. The frequency of invasive tumors in the matrine treatment groups [50 mg/kg: 15.4% (2/13), 100 mg/kg: 9.1% (1/11)] was significantly lower than in the BBN-alone group [57% (8/14)]. Furthermore, oral administration of matrine (50 and 100 mg/kg) markedly attenuated the BBN-induced upregulation of bladder cyclooxygenase-2 (COX-2) expression and the elevation of bladder cytosolic phospholipase A2 (cPLA2) levels. Although the contents of 15-prostaglandin dehydrogenase (PGDH), which degrades PGE2, were dramatically reduced by BBN, matrine exerted no effects on reduced PGDH contents. Conclusion: Our results suggest that matrine suppressed bladder tumor invasion in a rat model, and this might be primarily mediated through regulation of the protein contents, COX-2 and cPLA2 in the bladder.
Bone infection is one of the common complications of orthopedic surgery. After bone trauma occurs in the human body, the infection of Staphylococcus aureus and Gram-negative bacteria into the fracture area can lead to double infection of the soft tissue and bone tissue at the fracture site, leading to a variety of complications, mostly in the lower extremities. Bone infection easily causes bone destruction, bone nonunion, and bone defect, seriously affecting the quality of life of patients. The traditional treatment method of bone infection is to control the infection first and then repair the bone graft, but this method has a long course, poor efficacy, and high disability rate. In this study, anti-infective reconstituted bone xenograft (ARBX) combined with external fixation was used to treat patients with posttraumatic bone infections of the long bones of the lower extremities, to explore its efficacy, and to analyze its effects on serum CRP, PCT levels, and prognosis. Our results showed that ARBX combined with the external fixator had a good effect on the treatment of patients with bone infection after lower extremity long bone trauma, which could effectively enhance the repair and functional recovery of the limb bone, significantly alleviate the infection degree of patients, reduce the inflammatory response of the body, and have a good prognosis.
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