The increase in bladder carcinoma cell population induced by the free beta subunit of human chorionic gonadotrophin is a result of an anti-apoptosis effect and not cell proliferation.

摘要: Ectopic production of free beta human chorionic gonadotrophin (hCGβ) by bladder carcinoma is well described and occurs in approximately 35% cases. hCGβ secreting tumours are more aggressive, radioresistant have a greater propensity to metastasize. We proposed that the ectopic was contributing an autocrine fashion radioresistance metastatic potential such tumours. Though we demonstrated addition culture media bladder, cervical endometrial cell lines brought about increase populations this not accompanied significant rate replication. Since population size balance mitosis mortality, inhibiting apoptosis. Here following incubation with recombinant hCGβ, cells refrain from undergoing Quantitation apoptotic bodies carried out immunoassay corrected number as determined MTT assay. In each line, reduced dose-dependently, indicating diminished rate. Furthermore, TGFβ1-induced apoptosis could be dose-dependently inhibited co-incubation hCGβ. propose, therefore, decline may account for previously reported. It also explain aggressive nature hCGβ-secreting poor prognosis associated therein. © 2000 Cancer Research Campaign