ライフサイエンスコーパス: HOSE cell

1 HOSE cell proliferation was not affected by treatment wi

2 2-12) and two malignant (OVCA 429, OVCA 432) HOSE cell lines.

3 gen IV and laminin secreted and deposited by HOSE cells in culture.

4 all normal human ovarian surface epithelial (HOSE) cell cultures but not in ovarian cancer cell lines

5 zed normal human ovarian surface epithelial (HOSE) cell lines and 315 genes whose expression was affe

6 umorigenic human ovarian surface epithelial (HOSE) cell lines and three OCa (OVCA) cell lines were su

7 n 4 normal human ovarian surface epithelial (HOSE) cell lines, 13 ovarian cancer cell lines, paraffin

8 zed normal human ovarian surface epithelial (HOSE) cell lines.

9 the normal human ovarian surface epithelial (HOSE) cells and demonstrated that it is expressed at hig

10 generated human ovarian surface epithelial (HOSE) cells constitutively expressing wild-type claudin-

11 arrest of human ovarian surface epithelial (HOSE) cells via induction of the cyclin-dependent kinase

12 , cultured human ovarian surface epithelial (HOSE) cells were examined for their abilities to produce

13 stablished human ovarian surface epithelial (HOSE) cells which abundantly express the protein.

14 ow that in human ovarian surface epithelial (HOSE) cells, overexpression of BRCA1-IRIS triggers expre

15 action in human ovarian surface epithelial (HOSE) cells, the tissue of origin of >90% of ovarian can

16 ic, normal human ovarian surface epithelial (HOSE) cells.

17 malignant human ovarian surface epithelial (HOSE) cells.

18 rom normal human ovarian surface epithelial (HOSE) cells.

19 oproteinase (MMP)-9 activities secreted from HOSE cells.

20 -fold enhancement), followed by immortalized HOSE cell lines (4-5-fold enhancement) and by OCa cell l

21 proliferation and migration of immortalized HOSE cell lines.

22 mpared with primary cultures or immortalized HOSE cell lines.

23 All but 18 of the genes affected by FSH in HOSE cell lines were different from those altered in OVC

24 inhibition in OVCA cell cultures, but not in HOSE cell cultures, while forced expression of ATF-3 sup

25 on of the BRCA1-IRIS-AKT-survivin cascade in HOSE cells, whereas under similar conditions cisplatin f

26 Expression of these claudins in HOSE cells increased cell invasion and motility as measu

27 Forced expression of CYP1A1wt or CYP1A1v in HOSE cells resulted in nuclear localization of the enzym

28 , rap-2, and SKIIP were upregulated by E2 in HOSE cells but downregulated by estrogen in OVCA cells,

29 ss of ERalpha, PR, and AR mRNA expression in HOSE cells may be responsible for neoplastic transformat

30 enhanced levels of FasL mRNA and protein in HOSE cells, but lowered their levels in OVCA cells.

31 n expression also increased cell survival in HOSE cells but did not significantly affect cell prolife

32 nd protein were higher in OVCA cells than in HOSE cells.

33 ay act to oppose oncogenic transformation in HOSE cells.

34 MMP-2, the other major HOSE cell-secreted gelatinase, is constitutively produce

35 les played by ERbeta in normal and malignant HOSE cells remain elusive.

36 ose observed in immortalized, nontumorigenic HOSE cells and in OCa cell lines.

37 In normal HOSE cell cultures/lines, 5alpha-dihydrotestosterone was

38 y an indispensable role in regulating normal HOSE cell functions.

39 A along with AR and PR transcripts in normal HOSE cells and disruption of ERalpha mRNA expression as

40 In general, primary cultures of normal HOSE cells exhibited the greatest hormone-stimulated gro

41 it is expressed at high levels in the normal HOSE cells but at much lower levels in ovarian carcinoma

42 ceptor (AR) mRNA in four primary cultures of HOSE cells obtained from postmenopausal women to those f

43 tably absent in all subcellular fractions of HOSE cells.

44 veal that (1) E2 exerts different actions on HOSE cells than on OVCA cells by affecting two distinct

45 ent biological actions on OVCA cells than on HOSE cells, by differential regulation of a set of putat

46 x steroids in primary cultures of human OSE (HOSE) cells with those observed in immortalized, nontumo

47 Among the HOSE cell lines, FSH increased expression of 57% of the

48 DOC-2 from a cDNA library generated from the HOSE cells was carried out using the 3' and 5' RACE appr

49 ole in growth and and differentiation of the HOSE cells and support the hypothesis that SPARC functio

50 downregulated in OVCA cell lines compared to HOSE cell lines, and (2) whose expression was restored i

51 nderexpressed in OVCA cell lines compared to HOSE cell lines, while the opposite was true for rap-2 a

52 f these genes in OVCA cells when compared to HOSE cells and their upregulation following P4 treatment

53 an cancer cells and tumor tissue relative to HOSE cells.

54 in the cytoplasmic compartment of untreated HOSE cells and translocated to the nucleus after P4 trea