Cyclin genes as potential novel prognostic biomarkers and therapeutic targets in breast cancer.

Cell cycle progression and cell proliferation are tightly controlled processes physiologically; however, in cancerous cells, uncontrolled cell proliferation may be attributed to abnormal expression of the cyclin genes. Therefore, analysis of the expression of the cyclin genes may result in the discovery of biomarkers that can be used to predict a prognosis and help to evaluate the therapeutic efficacy more accurately in several types of cancer, including breast cancer. In this study, 15 subtypes of the cyclin genes in breast cancer from public databases were selected using bioinformatics analysis, the correlation between their transcriptional expression levels and survival rates were analyzed, and the results were further confirmed using reverse transcription-quantitative PCR in vitro in various breast cancer cell lines. The expression of the majority of the cyclin genes in SK-BR-3, a HER2 overexpressing breast cancer cell line, was lower than that in MCF-10A cells. CCNC mRNA expression was higher and CCNH mRNA expression was lower in tumor and tumor-adjacent tissues compared with that in normal tissues; however, CCNC expression was lower and CCNH expression was higher in breast cancer cell lines compared with that in MCF-10A cells. The expression of the 13 other cyclin genes in breast cancer cell lines was generally consistent with the data from the bioinformatics analyses of breast cancer tissue samples, tumor-adjacent tissues, and normal tissues. Low expression of CCNA2, CCNB1/2, CCNC, CCND1, CCNE1/2 and CCNF, and high expression of CCNA1, CCNB3, CCND2/3, CCNG1/2 and CCNH genes was correlated with a higher survival rate for breast cancer patients (P<0.05). In conclusion, CCNA2, CCNB1/2, CCND1/2 and CCNE1/2 may serve as relatively mature and accurate biomarkers, and CCNG1/2 may be used to evaluate the prognosis and therapeutic efficacy of hormone receptor-positive breast cancer. Furthermore, CCNA1, CCNB3, CCNC, CCND3, CCNF and CCNH may serve as promising targets for the management of breast cancer.

Errate: Role of Ca²âº in Inhibiting Ischemia-Induced Apoptosis of Parathyroid Gland Cells in New Zealand White Rabbits.

In Figure 1A, the images of CG 24h group and Sham 72h group are duplicated, where the picture of Sham 72h group is correct, now the authors have corrected the picture of CG 24h group. In Figure 2A, the images of CG 72h and CSG 72h groups are duplicated, the images of CG 168h and CSG 168h groups are duplicated，where the pictures of CG 168h and CSG 72h groups are correct, now the authors have corrected the pictures of CG 72h and CSG 168h groups. In Figure 3B, the images of CG 24h group and CSG 72h group are duplicated, where the picture of CSG 72h group is correct, now the authors have corrected the picture of CG 24h group. Reference: Wei-han Cao, Yan-jun Su, Nian-qiu Liu, Ying Peng, Chang Diao, Ruo-chuan Cheng: Role of Ca²âº in Inhibiting Ischemia-Induced Apoptosis of Parathyroid Gland Cells in New Zealand White Rabbits. Med Sci Monit, 2020; 26: e920546. DOI: 10.12659/MSM.920546.

Exploration of the Potential Biomarkers of Papillary Thyroid Cancer (PTC) Based on RT2 Profiler PCR Arrays and Bioinformatics Analysis.

BACKGROUND: Papillary thyroid carcinoma (PTC) has increased rapidly over recent years, and radiation, hormone effects, gene mutations, and others were viewed as closely related. However, the molecular mechanisms of PTC have not been cleared. Therefore, we intended to screen more accurate key genes and pathways of PTC by combining RT2 profiler PCR arrays and bioinformatics methods in this study. MATERIALS AND METHODS: RT2 profiler PCR arrays were firstly analyzed to identify differential expression genes (DEGs) in PTC. RT-qPCR were performed to verify the most significant differential expression genes. The TCGA database was used to further verify for expanded data. Enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) was analyzed. To construct the protein-protein interaction (PPI) network, we used STRING and Cytoscape to make module analysis of these DEGs. RESULTS: Sixteen differentially expressed genes were presented in RT2 profiler PCR arrays, including 13 down-regulated DEGs (DEGs) and three up-regulated DEGs (DEGs), while 13 stable DEGs were eventually verified. A total of 155 DEGs were presented in the TCGA database, including 82 up-regulated DEGs (DEGs) and 73 down-regulated DEGs (dDEGs). A total of 29 important genes were extracted after integrating these two results, GO and KEGG analyses were used to observe the possible mechanisms of action of these DEGs. The PPI network was constructed to observe hub genes. Prognostic analysis further demonstrated the involvement of these genes in the biological processes of PTC. CONCLUSION: This study identified some potential molecular targets and signal pathways, which might help us raise our awareness of the mechanisms of PTC.

The Potential Action of Thomsen-Friedenreich Monoclonal Antibody (A78-G/A7) in Thyroid Cancer.

BACKGROUND: Thomsen-Friedenreich antibody (TF-Ab) is a specific antibody against the Thomsen-Friedenreich antigen (TF-Ag). At present, studies on a number of other tumors have shown that TF-Ab can effectively inhibit metastasis and induce apoptosis in tumor cells. However, the role of TF-Ab in thyroid cancer (TC) remains unclear. MATERIALS AND METHODS: Normal subjects and patients with primary papillary TC with or without lymph node metastasis were tested for TF-Ab expression by enzyme-linked immunosorbent assays (ELISAs). Immunofluorescence was used to assess the expression of TF-Ag in thyroid papillary carcinoma with or without lymph node metastasis and undifferentiated cancer tissues. To evaluate the role of TF-Ab in TC, the effects of TF monoclonal antibody (mAb A78-G/A7) on cell biological function were investigated by MTT assays, flow cytometry, adhesion assays and transwell experiments. RESULTS: Compared with normal individuals, TF-Ab levels in patients with TC were decreased, but no changes were observed with respect to lymph node metastasis. The expression of TF-Ag in TC tissues was relatively higher than that detected in adjacent tissues, but it was not affected by the presence or absence of lymph node metastasis. Upon treatment mAb A78-G/A7 treating, TC cell cycles were affected, meanwhile the abilities to adhere, invade and migrate were also significantly reduced. CONCLUSION: The results of the present study showed that mAb A78-G/A7 could affect the invasion and migration of all assayed TC cell lines. The effects of mAb A78-G/A7 on the cell cycle, adhesion, invasion and migration of TC cells were more significant than those observed for proliferation and apoptosis.

Role of Ca²âº in Inhibiting Ischemia-Induced Apoptosis of Parathyroid Gland Cells in New Zealand White Rabbits.

BACKGROUND Hypoparathyroidism is a common complication after thyroidectomy. Calcium supplementation can relieve these symptoms, but it is not clear whether it can protect the parathyroid glands. This study aimed to verify whether Ca²âº inhibits the apoptosis of parathyroid cells following ischemic injury. MATERIAL AND METHODS A rabbit model of parathyroid gland ischemic injury was established. The blood calcium concentrations were measured by colorimetry. The parathyroid hormone (PTH) levels were measured by enzyme-linked immunosorbent assay (ELISA). The parathyroid tissues were observed by hematoxylin and eosin (H&E) staining and the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Western blotting was used to quantify the levels of the following proteins: caspase-3 and p38 MAP Kinase (p38 MAPK). RESULTS This study demonstrates that apoptosis can be a part of the pathological changes associated with parathyroid ischemic injury. Calcium supplementation inhibited the apoptosis of parathyroid cells following ischemic injury. There were no significant differences among the serum calcium levels from the Sham operation (Sham), the Control group (CG), or the Calcium supplementation group (CSG) after 24 h, 72 h, and 168 h of treatment. PTH levels in the CG were significantly higher than in the CSG at 24 h and 72 h after treatments. The apoptosis rate of parathyroid cells from rabbits in the CSG was significantly lower than that of those from rabbits in the CG at 24 h and 72 h after the treatment. Calcium supplementation inhibited p38 MAPK and caspase-3 expression. CONCLUSIONS This study demonstrates that calcium supplementation inhibited the apoptosis of parathyroid cells following ischemic injury.