Anthropogenic Sex Microenvironment Of Anthropogenic Regulation Function Research Of Tumor Cells

During the past decades, many efforts have been made in mimicking the clinicalprogress of human cancer in mouse models. Previously, we have developed a humanbreast tissue-derived (HB) mouse model, which may mimic the interactions betweenhuman mammary microenvironment and human breast cancer cells. However,detailed evidences are absent. In the present study, in vivo, cellular and molecularexperiments were conducted to explore the regulatory role of human mammarymicroenvironment in the progress of human breast cancer cells. Subcutaneous (SUB),mammary fat pad (MFP) and HB mouse models were developed for in vivocomparisons. Then the orthotopic tumor masses from3different mouse models werecollected for primary culture. Finally, the biology of primary cultured human breastcancer cells were compared by cellular and molecular experiments. Results of in vivomouse models indicated that human breast cancer cells grew better in humanmammary microenvironment. Cellular and molecular experiments confirmed thatprimary cultured human breast cancer cells from HB mouse model showed a betterproliferative and anti-apoptotic biology than those from SUB and MFP mouse models.Meanwhile, primary cultured human breast cancer cells from HB mouse model alsoobtained the migratory and invasive biology for human tissue metastasis.Comprehensive analyses of all the evidences above suggested that human mammarymicroenvironment better regulated the biology of human breast cancer cells in ourhumanized mouse model of breast cancer, which was more consistent with theclinical progress of human breast cancer. During the past decades, many efforts have been made in mimicking the clinicalprogress of human cancer in mouse models. Previously, we have developed a humanbreast tissue-derived (HB) mouse model, which may mimic the interactions betweenhuman mammary microenvironment and human breast cancer cells. At first part ofthis study, in vivo, cellular and molecular experiments were conducted to explore theregulatory role of “human” mammary microenvironment in the progress of humanbreast cancer cells.In this part of study, gene expression profiles were generated bymicroarray to screen the changed genes in the primary breast cancer cells, which wereregulated by human mammary microenvironment and subcutaneousmicroenvironment respectively. Furthermore, differentially expressed genes werevalidated by quantitative reverse transcriptase-PCR (qRT-PCR) and analyzedcompared with several databases. The results showed that94genes differentiallyexpressed between the two study groups (p<0.05). Gene ontology analysis showedsignificant enrichment of16molecular functions,6distinct biological processes and2cellular components (p<0.05). Kyoto Encyclopedia of Genes and Genomes (KEGG)yielded7pathways with significant differences (p<0.05). Through further analysis ofthese genes, we realized the correlation between genotypes and tumor phenotypes. Italso further validated the regulation effect of human mammary microenvironment tohuman breast cancer cells and confirmed the superiority of our new model. It alsoprovides clues to explore the function of subsequent unknown genes which regulatedby human mammary microenvironment. Mouse models play an irreplaceable role in the in vivo research of human gastriccancer. In this study, we developed a novel human Gastric tissue-derived Orthotopicand Metastatic (GOM) mouse model of human gastric cancer, in which the humannormal gastric tissues were implanted subcutaneously into immunodeficient mice tocreate a human gastric microenvironment. Then, human gastric cancer cells wereinjected into the implants. The novel gastric mouse model was compared with theclassical subcutaneous model. The outhotopic tumor formation and distant metastasiswere detected. Furthermore, the orthotopic tumor masses from different mousemodels were collected for primary culture. Finally, the biology of primary cultured“human” gastric cancer cells were compared by cellular experiments and molecularexperiments. GOM model could mimic the interactions between human gastricmicro-environment and human gastric cancer cells, which help exhibit the realcharacteristics of tumor cells,and finally mimic the clinical-like tumor proliferationand metastases of human beings.