PubMed · 9174338
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J C De Mey. 1997. A sitting position without pressure points.. https://doi.org/10.1097/00000539-199706000-00057
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This study focused on the effects of repetitive pulsed magnetic stimulation (RPMS) on normal and malignant cells of humans. We used three human cell lines, HBL-100 (human normal breast epithelium), MCF-7 (human breast cancer), and HeLa (human cervical cancer). Cell proliferation at 37 degrees C and 40 degrees C and the expression of heat shock protein (HSP) 70 at 37 degrees C, 40 degrees C, and 42 degrees C, before and after the exposure to RPMS, was investigated. Cell proliferation showed no effects of exposure to RPMS in both normal and malignant cells; however, HSP70 expression was increased by RPMS exposure under thermal stress at 40 degrees C and 42 degrees C in HBL-100 and HeLa. We concluded that RPMS exposure potentiates the effect of thermal stress on both normal and malignant cells, and malignant cells derived from different organs respond differently to RPMS exposure.
Osteopontin (OPN) has been associated with enhanced malignancy in breast cancer, but its functional role in this disease is poorly understood. To study the effect of OPN on cellular invasiveness, basal OPN expression was first assessed in members of a progression series of human mammary epithelial cell lines (21PT: immortalized, non-tumorigenic; 21NT: weakly tumorigenic; 21MT-1: tumorigenic, weakly metastatic; MDA-MB-435 cells: tumorigenic, highly metastatic). The two lines which expressed lowest basal levels of OPN (21PT, 21NT) were then examined for up-regulation of invasive behavior in response to exogenous or transfected (endogenous) OPN. Both 21PT and 21NT showed increased invasiveness through Matrigel when human recombinant (hr)OPN was added to the lower chamber of transwells. Both also showed a cell migration response to hrOPN. Populations of 21PT and 21NT cells stably transfected with an OPN-expression vector showed higher levels of cell invasiness than control vector transfectants. Examination of transfectants for mRNA of a number of secreted proteases showed that only urokinase-type plasminogen activator (uPA) expression was closely associated with OPN expression and cellular invasiveness. Treatment of the parental 21PT and 21NT cells with exogenous hrOPN resulted in increased uPA mRNA expression and increased urokinase activity of the conditioned media. Both increased cell migration and induction of uPA expression are thus potential mechanisms of increased invasiness of breast epithelial cells in response to OPN.
Estrogen-induced growth stimulation has not previously been demonstrated in estrogen receptor (ER) cDNA transfected human cell lines in contrast to breast cancer cell lines expressing endogenous ER. On the contrary, estrogen usually inhibits cell growth of ER transfected cell lines. Growth inhibition by estrogen has also been demonstrated in our cell line, F9, which is an ER transfected subline of HMT-3522 breast epithelial cells derived from fibrocystic disease and propagated in chemically defined medium. By omitting EGF in the medium, we have demonstrated not only an increased transcriptional activity of the ER but also--after an adaptation period--estrogen-dependent growth of the cells, and we have succeeded in establishing a new subline, S3B, that requires 17beta-estradiol (E2) for growth. This is the first example of a nonmalignant, human breast epithelial cell line which is dependent on estrogen for continued growth. The S3B cells express functional ER as measured by transcriptional activity. ER-E2 induced transcription was not inhibited by EGF as in F9 cells. We propose that a growth-stimulatory response of breast epithelial cells in vitro to E2 is dependent on an inactive or down-regulated EGF receptor signaling pathway and it is possible that the effect of estrogen on normal breast epithelium in vivo also is modulated by the EGFR.