Project description:Cellular directed migration is critical to invasion-metastasis cascade of cancer cells. We used in vitro transwell model to screen two esophageal cancer cell lines (KYSE30/180) and obtained two pairs of subpopulations with distinc motiliyt ability. Then we used microarrays to detail the differentially expressed genes and microRNAs between these two cell sublines (30U/D and 180U/D) to identify those responsible for ESCC motility.
Project description:Cellular directed migration is critical to invasion-metastasis cascade of cancer cells. We used in vitro transwell model to screen two esophageal cancer cell lines (KYSE30/180) and obtained two pairs of subpopulations with distinct motility ability. Then we used microarrays to detail the differentially expressed genes and microRNAs between these two cell sublines (30U/D and 180U/D) to identify those responsible for ESCC motility.
Project description:Cellular directed migration is critical to invasion-metastasis cascade of cancer cells. We used in vitro transwell model to screen two esophageal cancer cell lines (KYSE30/180) and obtained two pairs of subpopulations with distinc motiliyt ability. Then we used microarrays to detail the differentially expressed genes and microRNAs between these two cell sublines (30U/D and 180U/D) to identify those responsible for ESCC motility. KYSE30/180 cells were subject to four successive selections using transwell (CORNING, USA). Subpopulations penetrated through membrane (D) or not (U) were harvested respectively for RNA extraction and hybridization on Affymetrix genome and LC Sciences microRNA microarrays
Project description:Cellular directed migration is critical to invasion-metastasis cascade of cancer cells. We used in vitro transwell model to screen two esophageal cancer cell lines (KYSE30/180) and obtained two pairs of subpopulations with distinct motility ability. Then we used microarrays to detail the differentially expressed genes and microRNAs between these two cell sublines (30U/D and 180U/D) to identify those responsible for ESCC motility. KYSE30/180 cells were subject to four successive selections using transwell (CORNING, USA). Subpopulations penetrated through membrane (D) or not (U) were harvested respectively for RNA extraction and hybridization on Affymetrix genome and LC Sciences microRNA microarrays simultaneously.
Project description:In vivo and in vitro analyses revealed distinct and shared characteristics of the metastatic D2A1-m1 and D2A1-m2 sublines. In particular, D2A1-m1 cells are more aggressive in experimental metastasis assays, while D2A1-m2 cells are more efficient at disseminating from the primary tumour in spontaneous metastasis assays. Surprisingly, classical metastasis-associated in vitro phenotypes such as enhanced proliferation, migration and invasion are reduced in the sublines compared to the parental cell line. Further, evasion of immune control cannot fully explain their enhanced metastatic properties. By contrast, both sublines show increased resistance to apoptosis when cultured in non-adherent conditions and, for the D2A1-m2 subline, increased 3D tumour spheroid growth. Moreover, the enhanced spontaneous metastatic phenotype of the D2A1-m2 sublines is associated with the ability to recruit an activated tumour stroma and promote directional migration of fibroblasts. Gene expression profiling revealed that the two metastatic sublines are distinct but more closely related to each other than the parental D2A1 cells.
Project description:Esophageal cancer, one of the most prevalent cancers worldwide, frequently exhibits distant metastases. The adipokine visfatin has been implicated in cancer progression and metastasis. However, the mechanisms by which visfatin regulates motility in esophageal cancer remain unclear. Here, we found that visfatin levels are higher in metastatic esophageal cancer patients than in primary esophageal cancer patients. Visfatin stimulation enhances migration and invasion in esophageal cancer cells. miRNA sequencing results revealed that miR-3613-5p controls visfatin-induced cell motility. Visfatin promotes esophageal cancer cell migration by reducing miR-3613-5p expression and subsequently increasing VEZF1/VCAN production. The visfatin/miR-3613-5p axis exhibits a promising target for inhibiting esophageal cancer metastasis.