Enrichment of cancer stem-like cells by the induction of epithelial-mesenchymal transition using lentiviral vector carrying E-cadherin shRNA in HT29 cell line.

A better understanding of cancer stem cells (CSCs) may facilitate the prevention and treatment of cancers. Epithelial-mesenchymal transition (EMT) is a process activated during invasion and metastasis of tumors. EMT induction in normal and tumor cells makes them more resistant to chemotherapy. E-cadherin is a membrane protein and plays a role in tumor invasion, metastasis, and prognosis. Downregulation of E-cadherin is a hallmark of EMT. Here, we created a model of cancer stem-like cells enrichment via EMT induction using E-cadherin downregulation in HT29 cell line using a lentiviral vector carrying shRNA. We aimed to evaluate cancer and anti-CSC chemotherapeutics screening. The markers of EMT and CSCs were assessed and compared with control cells using flow cytometry, real-time PCR, immunocytochemistry, western blot, migration assay, invasion assay, and colony formation assay. The transduced cells showed a mesenchymal morphology. High levels of EMT-related proteins were also expressed. These results confirmed that the transduced cells underwent EMT. In addition, we observed an increased population of E-cadherin-downregulated HT29 cell line among the cells expressing colon CSC markers (CD133+ and CD44+ ) after EMT induction. E-cadherin-downregulated cells were morphologically like mesenchymal cells, and the number of CD133+ - and CD44+ -cells (CSC-like cells) increased. These cells can be used as stable models to study cancer cells and screening of antitumor therapeutics.

Saltanatpour Z ，Johari B ，Alizadeh A ，Lotfinia M ，Majidzadeh-A K ，Nikbin B ，Kadivar M ... -  《-》

Bmi-1 promotes the invasion and migration of colon cancer stem cells through the downregulation of E-cadherin.

Zhang Z ，Bu X ，Chen H ，Wang Q ，Sha W ... -  《-》

Effect of CD133 overexpression on the epithelial-to-mesenchymal transition in oral cancer cell lines.

Moon Y ，Kim D ，Sohn H ，Lim W ... -  《-》

Identification of a subpopulation of long-term tumor-initiating cells in colon cancer.

Long-term tumor-initiating cells (LT-TICs) are viewed as a quantifiable target for colon cancer therapy owing to their extensive self-renewal and tumorigenic and metastatic capacities. However, it is unknown which subpopulation of colon cancer cells contains LT-TICs. Here, based on the methods for isolating and identifying cancer stem cells (CSCs) and the functional features of LT-TICs, we aimed to identify a subpopulation of LT-TICs. Among the six cell lines assessed, our results showed that CD133 and CD44 coexpression was only detected in HCT116 and HT29 cell lines. In HCT116 and HT29 cells, CD133+CD44+ cells not only shared the extensive tumorigenic potential of LT-TICs but also functionally reproduced the behaviors of LT-TICs that drive tumor metastasis (TM) formation, suggesting that CD133+CD44+ cells are a typical representation of LT-TICs in colon cancer. Mechanistically, the enhanced capacity of CD133+CD44+ cells to drive metastasis involves the up-regulated expression of Wnt-, epithelial-mesenchymal transition (EMT)-, and metastasis-related genes in these cells. Additionally, CD133+CD44+ cells presented significant chemoresistance compared with corresponding nontumorigenic CD133-CD44- cells following exposure to oxaliplatin (OXLP) or 5-fluorouracil (5-FU). Accordingly, CD133+CD44+ cells contained lower reactive oxygen species (ROS) levels than CD1133-CD44- cells, and the low ROS levels in CD133+CD44+ cells were related to the enhancement of antioxidant defense systems. More importantly, CD133+CD44+ cells developed less DNA damage after exposure to chemotherapeutics than CD133-CD44- cells. In conclusion, we identified a subpopulation of LT-TICs in colon cancer.

Peng L ，Xiong Y ，Wang R ，Xiang L ，Zhou H ，Gu H ... -  《-》

Overexpression of microRNA-194 suppresses the epithelial-mesenchymal transition in targeting stem cell transcription factor Sox3 in endometrial carcinoma stem cells.

Gong B ，Yue Y ，Wang R ，Zhang Y ，Jin Q ，Zhou X ... -  《-》