Notes

Advertisements the actual Roles regarding Astrocytes as well as Hedgehog Signaling in Medulloblastoma.
When only FBC was considered, several cancer-associated pathways were among the most enriched KEGG pathways of differentially methylated genes when the BRCA2 group was compared with the BRCAX or BRCA1+BRCAX groups. The comparison between the BRCA1 and BRCA2+BRCAX groups comprised the molecular function term 'cytoskeletal protein binding'. Finally, the functional annotation of differentially methylated genes between the BRCAX and BRCA1+BRCA2 groups indicated that the most enriched molecular function terms were associated with GTPase activity. In conclusion, to the best of our knowledge, the present study was the first to compare the global DNA methylation profile of familial FBC and MBC. The results may provide useful insights into the epigenomic subtyping of BC and shed light on a possible novel molecular mechanism underlying BC carcinogenesis.The extent of lymph node (LN) dissection has been a topic of interest in gastric cancer (GC) surgery. D2 lymphadenectomy is considered the standard surgical procedure for most resectable advanced GC cases. The value and indications of more extended lymphadenectomy than D2 remain unclear. Currently, the controversial stations beyond the D2 range are mainly focused on no. 14v, no. find more 16a2/b1 and no. 13 LN stations. The metastatic rate of no. 14v LN is relatively high in advanced distal GC, particularly in patients with suspicious no. 6 LN metastasis. D2 plus no. 14v LN dissection may be attributed to improved survival outcomes for patients with obvious no. 6 LN metastasis. Although GC with para-aortic lymph node (PALN) metastases is considered an M1 disease beyond surgical cure, patients with limited PALN metastases may benefit from the treatment strategy of adjuvant chemotherapy followed by D2 plus no. 16a2-b1 LN dissection. In addition, D2 plus no. 13 LN dissection may be an option in a potentially curative gastrectomy for GC with duodenal invasion. The present review discusses the current status and future perspectives of D2 plus lymphadenectomy.Recent studies have revealed that colorectal cancer (CRC) displays intratumor genetic heterogeneity, and that the cancer microenvironment plays an important role in the proliferation, invasion and metastasis of CRC. The present study performed genomic analysis on paired primary CRC and synchronous colorectal liver metastasis (CRLM) tissues collected from 22 patients using whole-exome sequencing, cancer gene panels and microarray gene expression profiling. In addition, immunohistochemical analysis was used to confirm the protein expression levels of genes identified as highly expressed in CRLM by DNA microarray analysis. The present study identified 10 genes that were highly expressed in CRLM compared with in CRC, from 36,022 probes obtained from primary CRC, CRLM and normal liver tissues by gene expression analysis with DNA microarrays. Of the 10 genes identified, five were classified as encoding 'matricellular proteins' [(osteopontin, periostin, thrombospondin-2, matrix Gla protein (MGP) and glycoprotein nonenvironment. This finding may lead to novel diagnostic and therapeutic targets in the era of genome-guided personalized cancer treatment.Smoking is a major cause of lung cancer, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the most important carcinogens in cigarette smoke. NNK modulates the expression of peroxiredoxin (Prdx) I in lung cancer. Prdx1 is upregulated in lung squamous cell carcinoma and lung adenocarcinoma, and considered a potential biomarker for lung cancer. The current article reviewed the role and regulatory mechanisms of Prdx1 in NNK-induced lung cancer cells. Prdx1 protects erythrocytes and DNA from NNK-induced oxidative damage, prevents malignant transformation of cells and promotes cytotoxicity of natural killer cells, hence suppressing tumor formation. In addition, Prdx1 has the ability to prevent NNK-induced lung tumor metabolic activity and generation of large amount of reactive oxygen species (ROS) and ROS-induced apoptosis, thus promoting tumor cell survival. In contrast to this, Prdx1, together with NNK, can promote the epithelial-mesenchymal transition and migration of lung tumor cells. The signaling pathways associated with NNK and Prdx1 in lung cancer cells have been discussed in present review; however, numerous potential pathways are yet to be studied. To develop novel methods for treating NNK-induced lung cancer, and improve the survival rate of patients with lung cancer, further research is needed to understand the complete mechanism associated with NNK.The present study aimed to determine the expression of the long non-coding RNA PTPRG-AS1 in patients with osteosarcoma, and to explore its role on the prognosis of patients and the process of osteosarcoma cell metastasis. Reverse transcription quantitative-PCR was performed to detect PTPRG-AS1 expression in osteosarcoma tumor tissues and cells (U2OS, SJSA1 and Saos-2), and normal tissues and cells (hFOB1.19). In addition, qPCR and western blotting were also used to detect mRNA and protein expression, respectively, whereas fluorescence in situ hybridization was used to locate the position of PTPRG-AS1 in osteosarcoma cells. Transwell assay was used to determine the migratory and invasive abilities of osteosarcoma cells. The results demonstrated that PTPRG-AS1 was highly expressed in osteosarcoma cells and tissues, which was compared with normal bone cells and adjacent healthy tissues. Furthermore, PTPRG-AS1 expression level in patients with osteosarcoma and lymph node metastasis or distal metastasis was elevatosteosarcoma cell metastasis.[This retracts the article DOI 10.3892/ol.2017.6945.].[This corrects the article DOI 10.3892/ol.2018.7987.].Oral tongue squamous cell carcinoma (OTSCC) is a highly malignant type of tumor. The 5-year survival rate of patients with advanced tongue squamous cell carcinoma is only ~50%. Pyruvate kinase M2 (PKM2) is the key rate-limiting enzyme of glycolysis, maintaining the Warburg effect in tumor cells. The present study aimed to investigate the relationship between PKM2 expression and the poor prognosis of patients with OTSCC and to determine oral squamous carcinoma tumor cell proliferation and apoptosis. Reverse transcription-quantitative (RT-q) PCR, western blotting and immunohistochemistry were used to analyze the expression levels of PKM2 in OTSCC, and the clinicopathological characteristics and prognosis of patients with OTSCC were further analyzed by statistical analysis. The results from RT-qPCR and immunohistochemistry demonstrated that PKM2 was upregulated in OTSCC tissues and highly expressed in advanced stage OTSCC tissues compared with paired adjacent tissues and lower stage OTSCC tissues. Patients with OTSCC and high PKM2 expression had shorter overall survival (OS) compared with those with low PKM2 expression. Furthermore, high expression of PKM2 was significantly associated with Tumor-Node-Metastasis (TNM) stage. TNM stage and PKM2 expression were independent predictive factors for OS in patients with OTSCC. In addition, PKM2 knockdown inhibited the proliferation and increased the apoptosis of oral squamous carcinoma tumor cells. Furthermore, PKM2 knockdown could regulate the expression of cell cycle and apoptosis-related proteins by activating Hippo signaling pathway, as confirmed by the decreased expression of yes-associated protein 1 (YAP), Bcl-2 and Ki-67 and the increased expression of large tumor suppressor kinase 1, phosphorylated YAP and Bax. Taken together, the findings from this study demonstrated that PKM2 may be considered as a potential target for the diagnosis and treatment of OTSCC.Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor, whose canonical pathway mainly regulates the genes involved in xenobiotic metabolism. However, it can also regulate several responses in a non-canonical manner, such as proliferation, differentiation, cell death and cell adhesion. AhR plays an important role in central nervous system tumors, as it can regulate several cellular responses via different pathways. The polymorphisms of the AHR gene have been associated with the development of gliomas. In addition, the metabolism of tumor cells promotes tumor growth, particularly in tryptophan synthesis, where some metabolites, such as kynurenine, can activate the AhR pathway, triggering cell proliferation in astrocytomas, medulloblastomas and glioblastomas. Furthermore, as part of the changes in neuroblastomas, AHR is able to downregulate the expression of proto-oncogene c-Myc, induce differentiation in tumor cells, and cause cell cycle arrest and apoptosis. Collectively, these data suggested that the modulation of the AhR pathway may downregulate tumor growth, providing a novel strategy for applications for the treatment of certain tumors through the control of the AhR pathway.Numerous studies have suggested that non-coding RNAs mediate tumorigenesis via the epithelial-mesenchymal transition (EMT). However, whether the long non-coding RNA (lncRNA) HOXA transcript at the distal tip (HOTTIP) plays a role in the EMT of small cell lung cancer (SCLC) remains unclear. The results of the present study suggest that HOTTIP-knockdown may lead to a significant increase in E-cadherin expression and a decrease in vimentin (VIM) expression; these proteins are two key markers of EMT. Furthermore, a notable morphological change in SCLC cells with HOTTIP-knockdown was observed After upregulation of microRNA (miR)-574-5p, the cells exhibited a long, fusiform morphology. Investigating these phenomena further revealed that HOTTIP may participate in EMT by binding to miR-574-5p. In addition, using bioinformatics technology and a dual luciferase reporter assay, it was found that miR-574-5p inhibited VIM expression via direct binding and interaction. In summary, the present results indicate that HOTTIP may be involved in the EMT of SCLC by binding to miR-574-5p, and that miR-574-5p may act through VIM, which is a key marker of EMT.Cryoablation is an emerging type of treatment for cancer. The sensitization of tumors using cryosensitizing agents prior to treatment enhances ablation efficiency and may improve clinical outcomes. Water efflux, which is regulated by aquaporin channels, contributes to cancer cell damage achieved through cryoablation. An increase in aquaporin (AQP) 3 is cryoprotective, whereas its inhibition augments cryodamage. The present study aimed to investigate aquaporin (AQP1, AQP3 and AQP5) gene expression and cellular localization in response to cryoinjury. Cultured breast cancer cells (MDA-MB-231 and MCF-7) were exposed to freezing to induce cryoinjury. RNA and protein extracts were then analyzed using reverse transcription-quantitative PCR and western blotting, respectively. Localization of aquaporins was studied using immunocytochemistry. Additionally, cells were transfected with small interfering RNA to silence aquaporin gene expression and cell viability was assessed using the Sulforhodamine B assay. Cryoinjury did not influence gene expression of AQPs, except for a 4-fold increase of AQP1 expression in MDA-MD-231 cells. There were no clear differences in AQP protein expression for either cell lines upon exposure to frozen and non-frozen temperatures, with the exception of fainter AQP5 bands for non-frozen MCF-7 cells. The exposure of cancer cells to freezing temperatures altered the localization of AQP1 and AQP3 proteins in both MCF-7 and MDA-MD-231 cells. The silencing of AQP1, AQP3 and AQP5 exacerbated MDA-MD-231 cell damage associated with freezing compared with control siRNA. This was also observed with AQP3 and AQP5 silencing in MCF-7 cells. Inhibition of aquaporins may potentially enhance cryoinjury. This cryosensitizing process may be used as an adjunct to breast cancer cryotherapy, especially in the border area targeted by cryoablation where freezing temperatures are not cold enough to induce cellular damage.
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