Any Multicenter Study to guage Harmonization associated with Assays for C-Terminal Telopeptides invo

Author : Niemann Klavsen | Published On : 19 Jan 2025

Background This study aimed to investigate the prognostic value of tumor marker index (TMI) based on preoperative cytokeratin 19 fragment (CYFRA 21-1) and squamous cell carcinoma antigen (SCC-Ag) and the relationship between preoperative TMI and treatment effectiveness of postoperative adjuvant chemotherapy for patients with esophageal squamous cell carcinoma (ESCC). Patients and methods Between January 2009 and December 2014, a total of 267 patients with ESCC who underwent radical resection were retrospectively enrolled. The TMI was defined as the geometric mean of normalized CYFRA 21-1 and SCC-Ag levels. The clinical and prognostic values of TMI were determined using univariate and multivariate survival analyses. Results Preoperative TMI level was associated with age, tumor size, pT stage, pN stage, and CYFRA 21-1, SCC-Ag, neutrophil-lymphocyte ratio (NLR), and platelet-lymphocyte ratio (PLR) levels. The 5-year overall survival rate of patients with high TMI was significantly lower than that of patients with low TMI (P less then 0.001). Univariate and multivariate analyses revealed that TMI (P = 0.031) was an independent prognostic factor. Patients with ESCC with high TMI level who underwent surgery combined with postoperative chemotherapy had a significantly better prognosis than those who underwent surgery alone (P = 0.015). However, no significant difference was observed in patients with low TMI level (P = 0.682). Conclusion TMI as a prognostic indicator of ESCC is superior to CYFRA 21-1 and SCC-Ag. The TMI might be useful in predicting the therapeutic effectiveness of postoperative chemotherapy and selecting patients who may benefit from postoperative chemotherapy.Introduction The clinical significance, biological roles and potential mechanism of Rab18 remain unknown in most human cancers, including head and neck squamous cell carcinoma (HNSCC). Methods We used immunohistochemistry to examine Rab18 protein expression in 112 cases of HNSCC specimens. We overexpressed and knockdown Rab18 in FaDu and Detroit562 cancer cell lines. Biological roles and mechanisms of Rab18 were examined using MTT, colony formation, Matrigel invasion assay, Western blotting, Annexin V and JC1 staining. Results Rab18 was upregulated in 45/112 (40.2%) cases of HNSCC tissues, which correlated with advanced T classification, positive nodal metastasis and tumor node metastasis (TNM) stage. The Oncomine and The Cancer Genome Atlas (TCGA) analyses indicated that Rab18 was elevated in human HNSCC tissues and correlated with poor patient survival. Functionally, Rab18 overexpression increased growth rate, colony numbers, cell cycle progression and invading ability in FaDu cells. Rab18 downregulated cisplatin-induced apoptosis and upregulated the mitochondrial membrane potential (Δψm). Western blot revealed that Rab18 overexpression induced epithelial-to-mesenchymal transition, with downregulation of E-cadherin and upregulation of N-cadherin, Vimentin and Twist. Rab18 overexpression also upregulated Survivin protein and Rab18 knockdown showed the opposite effects on these proteins. Treatment of STAT3 inhibitor, SH-4-54, inhibited cell invasion, increased E-cadherin and downregulated N-cadherin, Twist and Survivin. SH-4-54 also abolished the effects of BCAT1 on these proteins, as well as cell invasion. Conclusion In summary, our data showed that Rab18 was overexpressed in human HNSCC and functioned as an oncoprotein. find more Rab18 regulated HNSCC cell proliferation, invasion and cisplatin sensitivity through STAT3 signaling in HNSCC.Introduction Bruton's tyrosine kinase (BTK) inhibitors have long been known in the treatment of B-cell malignancies. Recently, BTK inhibitors have also become promising novel treatment reagents for prostate cancer. The current study was designed to investigate expression of BTK in prostate cancer tissues in comparison with benign hyperplasia and effect of BTK inhibitor on prostate cancer cell proliferation, migration and invasion. Methods BTK expression was assessed by immunohistochemistry; migration and invasion prostate cancer cell lines (DU145 and PC3) were assessed by Transwell migration and wound-healing assay; cancer cell proliferation was assessed using MTT assay kit; expression of matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) was assessed by immunoblotting. Results Strong expression of BTK was detected in the prostate cancer tissues, especially in the tumors from prostate cancer patients with bone metastasis. BTK inhibitor (Ibrutinib) significantly inhibited cell proliferation, migration and invasion of prostate cancer cells as well as protein synthesis of MMP-2 and MMP-9 by the tumor cells. Overexpressing BTK could partially but significantly block the inhibitory effect of Ibrutinib on cell proliferation, migration and invasion, and protein synthesis of MMP-2 and MMP-9 of the cancer cells. Conclusion These findings suggested that BTK could serve as not only a biomarker but also a therapeutic target for the prostate cancer and that Ibrutinib may be applied as a therapeutic drug for the prostate cancer.Purpose This study aimed to investigate the regulatory role and mechanism of microRNA-766 (miR-766) on cutaneous squamous cell carcinoma (CSCC) cells. Methods The expression of miR-766 and programmed cell death 5 (PDCD5) was detected in CSCC tissues and CSCC cell lines (A431, SCL-1 and DJM-1 cells) by qRT-RCR. The proliferation, colony-forming ability, apoptosis, migration and invasion of A431 and SCL-1 cells was measured by MTT, colony formation, flow cytometry, wound healing and transwell assay, respectively. The interaction between miR-766 and PDCD5 was detected by dual-luciferase reporter gene assay. The expression of matrix metalloproteinase 2 (MMP-2), MMP-9 and PDCD5 was measured by Western blot. In addition, A431 cells were subcutaneously injected into mice, and the tumor volume and weight were measured. Results MiR-766 was upregulated, and PDCD5 was downregulated in CSCC tissues and cells. MiR-766 significantly promoted the proliferation, migration and invasion, and inhibited the apoptosis of A431 and SCL-1 cells. MiR-766 also significantly increased the expression of MMP-2 and MMP-9 in A431 and SCL-1 cells. PDCD5 was a target gene of miR-766. PDCD5 significantly reversed the tumor-promoting effect of miR-766 on A431 and SCL-1 cells. In addition, miR-766 inhibitor inhibited the tumor growth in mice. Conclusion MiR-766 inhibitor inhibited the proliferation, migration and invasion, and promoted the apoptosis of CSCC cells via downregulating PDCD5.