HTR1E and neoplasm: However, either the extrinsic serotonin or the specific HTR1E agonist is not able to reduce the stress-promoted formation of peritoneal metastatic nodules and malignant ascites to the level comparable to that in mice without stress stimulation (Figures 7B-7D), possibly due to the dramatically reduced HTR1E expression (Figures 1E-1I, Figures 1F-1G). These results suggest that the blockage of HTR1E-mediated tumor-suppressive signaling is a prerequisite for OC metastasis.