Up-regulation of LRP16 mRNA by 17beta-estradiol through activation of estrogen receptor alpha (ERalpha), but not ERbeta, and promotion of human breast cancer MCF-7 cell proliferation: a preliminary report.

Han, Wei; Ym, Mu; Lü, Xin; Zhou, Xu; Xj, Li; Yu, Li; Song, Ho-Young; M, Li; Jm, Lu; Zhao, Yanbin; Cy, Pan

doi:10.1677/erc.0.0100217

Cited by 37 publications

(76 citation statements)

References 29 publications

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“…As seen in Fig. 1A, the mRNA expression level of LRP16 was upregulated by E 2 (10 K8 M/l) in BG-1 cells as it was in MCF-7 and Ishikawa cells (Han et al 2003). However, in SKOV3 cells, LRP16 expression was not upregulated by E 2 treatment; conversely, it was downregulated by E 2 in a does-dependent fashion (Fig.…”

Section: Lrp16 Expression Is Upregulated By E 2 In Bg-1 Cells But Ismentioning

confidence: 64%

“…The pcDNA3.1-LRP16 expression vector containing human LRP16 full-length cDNA was previously constructed (Han et al 2003). Mammalian expression plasmid for ERa (pS5G-hERa) was provided by Prof. Hajime Nawata at Kyushu University, and the reporter 3!ERE-TATA-Luc was provided by Prof. Donald P McDonnell at Duke University Medical Center (Norris et al 1998).…”

Section: Plasmidsmentioning

confidence: 99%

“…Previous reports from our laboratory demonstrated that overexpression of LRP16 promotes proliferation of estrogen sensitive MCF-7 breast cancer cells (Han et al 2003). To investigate the effect of LRP16 on SKOV3 cell growth, we stably transfected pcDNA3.1-LRP16 or pcDNA3.1 empty vector into SKOV3 cells and performed cell proliferation assays.…”

Section: Lrp16 Does Not Significantly Modulate the Growth Responsivenmentioning

confidence: 99%

“…LRP16 was previously identified as an estrogen-responsive target gene. Estrogen-induced upregulation of LRP16 expression is mediated by ERa, but not by ERb (Han et al 2003). In cell culture, it has been shown that the expression level of LRP16 is strongly dependent on the estrogen actions in ERa-positive breast and endometrial cancer cell lines .…”

Section: Introductionmentioning

confidence: 99%

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Differential induction of LRP16 by liganded and unliganded estrogen receptor α in SKOV3 ovarian carcinoma cells

Tian

Wu²,

Zhao³

et al. 2009

Journal of Endocrinology

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Previously, we investigated the induction effect of LRP16 expression by estrogen (17b-estradiol, E 2 ) and established a feed-forward mechanism that activated estrogen receptor a (ERa) transactivation in estrogen-dependent epithelial cancer cells. LRP16 is required for ERa signaling transduction by functioning as an ERa coactivator. In this study, we demonstrated that LRP16 expression was upregulated in E 2 -responsive BG-1 ovarian cancer cells, but was downregulated in estrogen-resistant SKOV3 ovarian cancer cells. Pure estrogen antagonist ICI 182 780 did not affect LRP16 expression in SKOV3 cell. The unliganded ERa upregulated LRP16 expression and enhanced LRP16 promoter activity in SKOV3 cells; however, this induction was blocked by estrogen stimulation. Results from chromatin immunoprecipitation experiment revealed a strong recruitment of the unliganded ERa at LRP16 promoter in the absence of estrogen; however, ERa was largely released from the DNA upon E 2 stimulation. Modulation in LRP16 expression level did not significantly change the proliferation rate of SKOV3 cells and the growth responsiveness of cells to E 2 . Knockdown of LRP16 by RNA interference in SKOV3 cells markedly attenuated estrogen response elementdependent ERa reporter gene activity and E 2 -induced c-Myc expression. Our study suggests a novel mechanism of estrogen resistance of ovarian cancer by which estrogenrepressed signaling pathway antagonizes estrogen-activated signaling transduction.

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Section: Lrp16 Expression Is Upregulated By E 2 In Bg-1 Cells But Ismentioning

confidence: 64%

Section: Plasmidsmentioning

confidence: 99%

Section: Lrp16 Does Not Significantly Modulate the Growth Responsivenmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Differential induction of LRP16 by liganded and unliganded estrogen receptor α in SKOV3 ovarian carcinoma cells

Tian

Wu²,

Zhao³

et al. 2009

Journal of Endocrinology

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“…(5,44) Overexpression of LRP16 significantly stimulated MCF-7 cell proliferation by promoting G1 ⁄ S transition. (4) Suppression of the endogenous LRP16 in ERa-positive MCF-7 cells not only inhibits cell growth but also significantly attenuates the cellular estrogen-responsive proliferation ability and sensitizes tumor cells to radiation.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathological significance and prognostic value of leukemia‐related protein 16 expression in invasive ductal breast carcinoma

Zhao¹,

Lu²,

Han³

2010

Cancer Science

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To explore the expression of leukemia-related protein 16 (LRP16) in invasive ductal breast carcinoma and analyze its correlation with clinicopathological feature and prognosis, immunohistochemistry was performed on 100 cases of invasive ductal breast carcinoma. Medical records were reviewed and clinicopathological analysis was performed. Leukemia-related protein 16 expression was detected in 33 of 100 cases (33%) of the invasive ductal breast carcinoma. Expression of LRP16 in carcinoma was obviously higher than that in normal breast tissue. LRP16 protein expression was found in 27.6% (21/76) of carcinoma at stage I and II, and 50.0% (12/24) of carcinoma at stage III and IV. LRP16 expression was found correlative with metastasis in the axillary lymph node (P = 0.001), stage (P = 0.042), estrogen receptor (ER) expression (P = 0.001), fragile histidine triad (FHIT) expression (P = 0.015) and CD133 expression (P = 0.038), but not with grade (P = 0.543), tumor size (P = 0.263), age (P = 0.840), menopause (P = 0.701) and HER-2 gene amplification (P = 0.463). The difference of the mean disease free survival (DFS) time between cancer patients with LRP16 expression (43.7 months) and those without (77.7 months) was statistically significant (Log rank = 9.989, P = 0.002). The difference of the mean overall survival (OS) time between cancer patients with LRP16 expression (50.0 months) and those without (120.0 months) was statistically significant (Log rank = 9.977, P = 0.002). Our finding suggests that expression of LRP16 protein is correlated with the stage, metastasis, prognosis and expression of ER, progesterone receptor, Ki-67, CD133 and FHIT in invasive ductal breast carcinoma. (Cancer Sci 2010; 101: 2262-2268 B reast cancer has become the second most frequent cause of death in women, threatening females all over the world. In China, the incidence of breast cancer increases very rapidly and breast cancer has become the most common female malignant tumor. In spite of advances in diagnosis and treatment, almost one-fourth of women with this neoplasm will die. The major causes of treatment failure and ⁄ or death for breast cancer patients are tumor recurrence and metastasis. The use of adjuvant and palliative therapies in patients with breast carcinoma rely primarily on prognostic factors, such as tumor grade and size, axillary nodal status, distant metastasis and candidate biomarkers, such as hormone receptor (nuclear estrogen receptor [nER] and progesterone receptor [PR]) expression, and c-erbB2 ⁄ HER-2 ⁄ neu amplification ⁄ overexpression. Furthermore, expression of hormone receptors and overexpression of cerbB2 help in guiding therapeutic strategies and predict response to chemotherapy, endocrine therapy and specific immunotherapy with the antibody, trastuzumab. Therefore, such biomarkers in breast neoplasms provide information regarding the outcome of patients. A study in search of additional biomarkers is necessary for patients with breast cancer.Leukemia-related protein 16 (LRP16), which was originally recognized a...

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Macro domains as metabolite sensors on chromatin

Posavec

Timinszky

Buschbeck

2013

Cell. Mol. Life Sci.

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How metabolism and epigenetics are molecularly linked and regulate each other is poorly understood. In this review, we will discuss the role of direct metabolite-binding to chromatin components and modifiers as a possible regulatory mechanism. We will focus on globular macro domains, which are evolutionarily highly conserved protein folds that can recognize NAD(+)-derived metabolites. Macro domains are found in histone variants, histone modifiers, and a chromatin remodeler among other proteins. Here we summarize the macro domain-containing chromatin proteins and the enzymes that generate relevant metabolites. Focusing on the histone variant macroH2A, we further discuss possible implications of metabolite binding for chromatin function.

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Up-regulation of LRP16 mRNA by 17beta-estradiol through activation of estrogen receptor alpha (ERalpha), but not ERbeta, and promotion of human breast cancer MCF-7 cell proliferation: a preliminary report.

Cited by 37 publications

References 29 publications

Differential induction of LRP16 by liganded and unliganded estrogen receptor α in SKOV3 ovarian carcinoma cells

Differential induction of LRP16 by liganded and unliganded estrogen receptor α in SKOV3 ovarian carcinoma cells

Clinicopathological significance and prognostic value of leukemia‐related protein 16 expression in invasive ductal breast carcinoma

Macro domains as metabolite sensors on chromatin

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