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Analysis of differentially expressed genes in endothelial cells following tumor cell adhesion and role of PRKAA2 and miR-124-3p

ABSTRACT: Tumor cell adhesion to endothelium is one pattern of tumor-endothelium interaction and one key step during tumor metastasis. The endothelium integrity is an important barrier to prevent tumor invasion and metastasis. Changes happened in ECs according to tumor cells adhesion provide important signaling mechanisms for the angiogenesis and metastasis of tumor cells. However, it is unclarified by now. In this present study we used Affymetrix Gene Chip Human Transcriptome Array 2.0. and quantitative real-time PCR (qPCR) to clarify the detailed genes alteration in endothelial cell adhered by prostate tumor cells PC-3M. A total of 504 differentially expressed mRNAs and 444 lncRNAs were obtained through chip data analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE162957 | GEO | 2020/12/10

REPOSITORIES: GEO

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Project description:Although 80% of AML patients can initially achieve a complete remission, the long-term disease-free survival is only 40% at 6 years with a 10% 5-year survival rate from first relapse. Most patients do not achieve a second remission. Therefore, relapse after initial response to chemotherapy remains a serious clinical challenge requiring new therapeutic strategies. Annual relapse rates have been calculated 40%, 17%, and 2% in years 1-3, respectively. One of the issues hindering the successful treatment of AML patients, and contributing to disease relapse, is leukaemic cell adhesion and retention in the protective niche of the BMME. Here, the leukaemic cells are surrounded by other cell types that promote their survival, by enabling them to evade destruction by both the immune system and intra-vascular therapies, ultimately leading to the emergence of drug resistance. Given the dependence of AML cells on the BMME, a better understanding of the biological interactions between the leukaemic cells and the haematopoietic niche is needed. In addition, the identification and development of therapies to target these adhesive interactions will enable AML cells to be forced out of their BMME protective niche, into the peripheral circulation, where they will be more susceptible to conventional drug regimens. We have developed and optimised a robust, reproducible, in vitro co-culture model of the AML-BMME. Using the optimised model, several adhesion blocking agents were tested to reduce the number of adhered AML cells. Anti-CD44 treatment was established as the most effective in preventing AML adhesion of OCI-AML3, KG1a and primary AML cells. However, even with maximum dose of the most promising blocking agent, some AML cells still adhered. Following this observation, KG1a and OCI-AML3 cells were treated in co-culture and monoculture. Subsequently paired adhered, non-adhered and monoculture cells were isolated and sent for RNA sequencing in order to perform comparative transcriptomic analysis. The results from these experiments helped us identify novel targets from the persistently adhered AML cells in order to more effectively block their adhesion on our model.

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Analysis of differentially expressed genes in endothelial cells following tumor cell adhesion and role of PRKAA2 and miR-124-3p

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