In this study, we investigated the biological roles and mechanisms of SALL4 in the pathogenesis of gastric cancer. We found that the upregulation of SALL4 in STAD was positively correlated with tumor progression. Also, we found that SALL4-B downregulation inhibited, while overexpression enhanced, the pro-angiogenic effect of gastric cancer cells. In addition, we also discovered that SALL4 promoted angiogenesis via the regulation of the VEGF gene.
green on a Bio-Rad CFX96 system. The 2method was used to determine mRNA fold changes. β-actin served as a normalization control. The primer sequences are listed in .The transfected and treated cells were cultured in RPMI-1640 containing 10% FBS and plated on a 6-well plate . The cells were washed after 24 h and changed from normal growth medium to serum-free medium. After 48 h of incubation, cell culture supernatants were collected and centrifuged at 2000 rpm to remove cell debris.
Cs were resuspended in a serum-free medium and placed in the upper chamber . The lower chamber was then incubated with the indicated CMs for 24 h. Penetrated cells were stained with crystal violet, and images were taken under a microscope to count the cells.The level of VEGF-A, B, and C in si-SALL4-B, P-SALL4-B, CRISPR/Cas9-KO-SALL4, MGC-803-Thalidomide or engineered exosomes cells’ conditioned medium were determined using an ELISA kit according to the manufacturer’s protocol .
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Autologous humanized PDX modeling for immuno-oncology recapitulates features of the human tumor microenvironmentBackground Interactions between immune and tumor cells are critical to determining cancer progression and response. In addition, preclinical prediction of immune-related drug efficacy is limited by interspecies differences between human and mouse, as well as inter-person germline and somatic variation. To address these gaps, we developed an autologous system that models the tumor microenvironment (TME) from individual patients with solid tumors. Method With patient-derived bone marrow hematopoietic stem and progenitor cells (HSPCs), we engrafted a patient’s hematopoietic system in MISTRG6 mice, followed by transfer of patient-derived xenograft (PDX) tissue, providing a fully genetically matched model to recapitulate the individual’s TME. We used this system to prospectively study tumor-immune interactions in patients with solid tumor. Results Autologous PDX mice generated innate and adaptive immune populations; these cells populated the TME; and tumors from autologously engrafted mice grew larger than tumors from non-engrafted littermate controls. Single-cell transcriptomics revealed a prominent vascular endothelial growth factor A (VEGFA) signature in TME myeloid cells, and inhibition of human VEGF-A abrogated enhanced growth. Conclusions Humanization of the interleukin 6 locus in MISTRG6 mice enhances HSPC engraftment, making it feasible to model tumor-immune interactions in an autologous manner from a bedside bone marrow aspirate. The TME from these autologous tumors display hallmarks of the human TME including innate and adaptive immune activation and provide a platform for preclinical drug testing. Data are available upon reasonable request.
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