Acta biochimica Polonica最新文献

Background: Prostate cancer is one of the most common cancers in men worldwide. This study aims to elucidate the roles of c-Jun N-terminal kinase (JNK) in the progression of castration-resistant prostate cancer (CRPC).

Methods: JNK overexpressing and knockdown cell lines were established on the PC-3 prostate cell line. qPCR and Western blotting were performed to determine the mRNA and protein levels of target genes in prostate tissues and cell lines. MTT and Matrigel invasion assays were conducted to evaluate the cell viability and invasive ability, respectively. The Kaplan-Meier estimator was performed to estimate the overall survival rate and second progression-free survival rate. Pearson's correlation coefficient was used to evaluate the relationship between JNK and prostate-specific antigen (PSA).

Results: Relative JNK expression was correlated with Gleason score and PSA value in patients with CRPC. Kaplan-Meier analysis revealed that patients with low JNK expression exhibited high overall survival and second progression-free survival rate. In vitro assays demonstrated that JNK overexpression promoted cell viability and invasion as well as the protein expressions of extracellular signal-regulated kinase (ERK) and matrix metalloproteinase 1 (MMP1) in PC-3 cell lines.

Conclusions: JNK overexpression promotes the development of CRPC via the regulation of ERK and MMP1.

LncRNA MIR31HG is involved in many types of cancers, while its roles in breast cancer are still unknown. The current study aimed to explore the function of lncRNA MIR31HG in breast cancer and the underlying mechanisms. Stable expression cell lines were constructed by using lentivirus particles. MTT assay was used to determine cell viability. Wound healing and Transwell assay were used to determine cell migration and invasion, respectively. The changes in biomarkers were determined by using qPR-PCT and Western blotting, respectively. BALB/c nude mice were used to generate a xenograft mouse model. MIR31HG regulated cell proliferation, migration and invasion in MCF7 cells. Besides, MIR31HG regulated N-Cadherin, Vimentin, and E-Cadherin. MIR31HG positively regulated receptor-interacting serine-threonine kinase 4 (RIPK4), as supported by the fact that knockdown of MIR31HG suppressed RIPK4, and the knockdown of RIPK4 did not affect MIR31HG. Additionally, we found that RIPK4 regulated cell proliferation, migration and invasion in MCF7 cells. The changes in RIPK4 regulated N-Cadherin, Vimentin, and E-Cadherin. Consistently, in vivo studies showed that the knockdown of MIR31HG or RIPK4 reduced tumor size in xenograft animal models. The roles of lncRNA MIR31HG in breast cancer were associated with its regulatory effects against RIPK4.

Background: Chronic obstructive pulmonary disease (COPD) was a risk factor for lung cancer tumorigenesis. This study aimed to discover novel diagnostic biomarkers for COPD patients and determine their underlying pathogenetic mechanisms.

Materials and methods: Differentially expressed genes (DEGs) in COPD samples and normal controls were analyzed and utilized to construct a network associated with a high risk for COPD occurrence. Enrichment analysis was applied on the strength of Gene Ontology (GO) annotations and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The RT-qPCR analysis was performed to determine 10 hub genes in COPD. ELISA assay was utilized to measure IL-1β, IL-6, and IL-10 levels. Spearman's correlation analysis was conducted to detect the correlation between inflammatory cytokines and AHNAK expression. Cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry assays.

Results: AHNAK was significantly increased in COPD serum samples compared with non-COPD smokers and strongly correlated with inflammation. AHNAK level could also discriminate COPD from non-COPD with high accuracy.

Conclusion: AHNAK may be a feasible biomarker playing crucial functions in the diagnosis and progression of COPD.

Objective: To investigate the prognostic value of serum albumin (SA) levels before chemotherapy in patients with diffuse large B-cell lymphoma (DLBCL) after receiving chemotherapy.

Methods: This is a retrospective study, and 127 patients with DLBCL including 71 males (55.9%) and 56 females (44.1%) were included. Patients' gender, age, Ann Arbor staging, eastern cooperative oncology group (ECOG) score, treatment options, international prognostic index, response rate, overall survival (OS), and progression-free survival (PFS) were obtained for statistical analysis.

Results: Univariate analysis showed that SA≤34 g/L, Ann Arbor III-IV, B symptoms, ECOG≥2, and bone marrow involvement suggest a poor prognosis in patients with DLBCL. Patients with persistent SA>34 g/L had significantly longer OS than patients with persistent SA≤34 g/L (P=0.020). Multivariate analysis showed that SA≤34 g/L (HR=0.48, 95% CI=0.26-0.90, P=0.022) and R-CHOP-like treatment regimen (HR=0.43, 95% CI=0.24-0.76, P=0.004) are independent factors that could affect the prognosis of patients with DLBCL.

Conclusion: SA can be used as an indicator of prognosis in patients with DLBCL before the first chemotherapy. DLBCL patients with SA≤34 g/L are associated with short OS and poor prognosis, which may potentially provide guidance for the clinician to pay more attention to this population before the first chemotherapy.

Wound healing is a considerable problem for clinicians. Ever greater attention has been paid to the role of Chinese herbal monomers and compounds on wound healing. This study aims to elucidate the wound healing mechanism of Modified Hongyu Decoction (MHD) in vivo and in vitro. MHD wound healing activity in vivo was evaluated using an excision rat model. H and E staining, Masson's staining and immunofluorescence of wound tissue on days 7 and 14 were performed to evaluate the efficacy of MHD on wound healing. Subsequently, human umbilical vein endothelial cells (HUVECs) were used to evaluate wound healing characteristics in vitro. Cell Counting Kit-8 (CCK-8) and scratch assays were conducted to assess the effects of MHD on the proliferation and migration of HUVECs. The involvement of the VEGF/PI3K/Akt signaling pathway was assessed by western blotting. The rats in the MHD group displayed more neovascularization and collagen fibers. Western blotting of wound tissue showed that VEGF, PI3K, p-Akt and p-eNOS expression were significantly increased (p<0.05) in the MHD group. Cell Counting Kit-8 and scratch assays demonstrated that MHD promoted HUVECs proliferation and migration. MHD treatment significantly increased VEGF, PI3K, p-Akt and p-eNOS expression in HUVECs (p<0.05), which was inhibited by LY294002. Both in vivo and in vitro data indicated that MHD promotes wound healing by regulating the VEGF/PI3K/Akt signaling pathway.

The cell adhesion protein cadherin 19 (CDH19) has been reported to be involved in various types of cancer, but its role in cervical carcinoma remains unknown. We collected and analyzed the patients' data using the GEPIA Kaplan-Meier plotter databases. CDH19 was overexpressed in cervical carcinoma cells to assess its effect on cell proliferation and activation of AKT and NF-κB signaling pathways. A xenograft mouse model was established to study the function of CDH19 in vivo. We found that CDH19 expression was significantly downregulated in cervical carcinoma tissues compared to adjacent normal tissues. Patients with high expression of CDH19 had a significantly better overall survival rate than those with low CDH19 expression. CDH19 expression was negatively correlated with the expression of the proliferation marker Ki-67, and overexpression of CDH19 significantly inhibited cervical carcinoma cell proliferation. Furthermore, overexpression of CDH19 suppressed the activation of the AKT and NF-κB signaling pathways, and CDH19-overexpressing cervical carcinoma tumors exhibited significantly slower growth in vivo. CDH19 plays an important role in cervical carcinoma by suppressing both cell proliferation and the activation of AKT and NF-κB signaling pathways. Therefore, CDH19 may be a potential therapeutic target for cervical carcinoma.