Project description:Bladder cancer stem cells (CSCs) contribute to tumorigenesis, recurrence and chemoresistance of bladder cancer. However, the molecular mechanisms underlying their self-renewal are poorly unknown. Long noncoding RNAs (lncRNAs) act as crucial regulators in a lot of human cancers, yet their potential roles and molecular mechanisms in bladder CSCs are poorly understood. The goal of this study is to identify the differentially expressed lncRNAs in bladder CSCs (UM-UC-3 4th spheres), its two differentiation sublines and bladder non-CSCs (UM-UC-3). Our study reveals that deregulation of lncRNAs is involved in the bladder CSCs.
Project description:Lung cancer is the malignant tumor with the highest incidence in the world. Cancer stem cells (CSCs) has the characteristics of immortal proliferation, self-renewal, differentiation of stem cells and high invasion and migration capabilities. In recent years, the function of non-coding RNA (ncRNA) that is regarded as transcription noise has been gradually discovered which can participate in the occurrence and development of tumors by regulating the stemness of cancer stem cells. Herein, we detected the differential expressed lncRNAs in A549 NANOG+ (CSCs) and A549 NANOG- (non-CSCs) cells. Our finding suggest the profiles of lncRNAs changed in CSCs compared with non-CSCs and provide new insight into molecular mechanism that may account for the lung adenocarcinoma.
Project description:To explore non-coding and coding expression profiling and their biological functions in bladder cancer, we surveyed the lncRNA and mRNA expression signature of bladder cancer and para-cancer tissues using microarray for four patients. Thousands of significantly changed lncRNAs and mRNAs were identified. Our findings provide a novel perspective on transcriptional group and lay the foundation for future research of potential roles of lncRNAs in bladder carcinoma.
Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest and most metastatic cancers in human. PDACs respond poorly to therapies, partly due to cancer stem cells (CSCs) that self-renew, survive chemotherapies, metastasise and replenish the tumor. Factors secreted by tumor cells mediate autocrine/paracrine crosstalk with surrounding cells contributing to the stem cell niche but are still insufficiently characterised. Here we used quantitative SILAC proteomics to identify secreted factors enriched in CSC secretome compared to non-CSCs. Our data uncovered factors that mediate the crosstalk between CSCs and non-CSCs as well as genes mediating the gene expression circuitries regulating CSC proliferation.
Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest and most metastatic cancers in human. PDACs respond poorly to therapies, partly due to cancer stem cells (CSCs) that self-renew, survive chemotherapies, metastasise and replenish the tumor. Factors secreted by tumor cells mediate autocrine/paracrine crosstalk with surrounding cells contributing to the stem cell niche but are still insufficiently characterised. Here we used quantitative SILAC proteomics to identify secreted factors enriched in CSC secretome compared to non-CSCs. Our data uncovered factors that mediate the crosstalk between CSCs and non-CSCs as well as genes mediating the gene expression circuitries regulating CSC proliferation.