title: In vivo growth regulation by cytokine in breast cancer cells showing an estradiol-inhibitive response in vitro.
abstract: The rates of the stimulative, insensitive, and inhibitive responses to 10(-2) nM E2 in sixty clinical breast cancer cases were 24.2%, 45.2%, and 30.6%, respectively. We then examined the expression of mRNAs of such cytokines as TNF-alpha, TGF-alpha, EGF, and TGF-beta, in cancer tissue specimens from these three different groups. In MCF-7 showing an E2-stimulative response, the expression of mRNAs of both TNF-alpha and TGF-alpha were suppressed by 10(-2) nM E2, but these same expressions in KSE-1 showing an E2 stimulative response were enhanced by E2. The mRNA expression of TGF-beta in these two cell lines was suppressed by 10(-2) nM E2, but that of EGF was enhanced. In clinical cases showing an E2-inhibitive response, the mRNA expression ratio of TNF-alpha/TGF-beta was above 2.5, but under 2.5 in E2-uninhibitive response cases. The mRNA expression ratio of TGF-alpha/TGF-beta was over 1.8 in the E2-inhibitive responsive cases, but under 1.8 in the E2-uninhibitive response cases. The mRNA expression ratio of EGF/TGF-beta did not show any regular tendency in three groups showing a different E2-response in vitro. Based on in vitro results and mRNA expression in clinical cases, the cytokine expression for E2-inhibitive cancer cells differed from those of E2-stimulative and -insensitive cells. Therefore, E2-inhibitive cancer cells are thus considered to possibly possess a characteristic growth regulation which is different from that for E2-uninhibitive cancer cells.
authors.affiliation: Clinical Research Institute, National Kyushu Cancer Center, Fukuoka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Matsuoka
authors.forename: S
authors.initials: S
authors.lastname: Tomisaki
authors.forename: S
authors.initials: S
authors.lastname: Ohno
authors.forename: K
authors.initials: K
authors.lastname: Ikejiri
authors.forename: M
authors.initials: M
authors.lastname: Saku
authors.forename: C
authors.initials: C
authors.lastname: Shirasaka
authors.forename: H
authors.initials: H
authors.lastname: Ueo
authors.forename: K
authors.initials: K
authors.lastname: Sugimachi
mesh_terms: D001943:Breast Neoplasms / Q000473:pathology*; D002455:Cell Division / Q000187:drug effects; D016207:Cytokines / Q000235:genetics*; D004815:Epidermal Growth Factor / Q000235:genetics; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D011960:Receptors, Estrogen / Q000378:metabolism; D016211:Transforming Growth Factor alpha / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000235:genetics; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D016207:Cytokines; D011960:Receptors, Estrogen; D016211:Transforming Growth Factor alpha; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D004958:Estradiol; D004815:Epidermal Growth Factor