Autocrine Proliferative Effects of hGH Are Maintained in Primary Cultures of Human Mammary Carcinoma Cells

Chiésa, Jean; Ferrer, Catherine; Arnould, Cécile; Vouyovitch, Cécile M.; Diaz, Jean‐Jacques; Gonzalez, S.; Marès, P.; Morel, Gérard; Wu, Zhengsheng; Zhu, Tao; Lobie, Peter E.; Mertani, Hichem C.

doi:10.1210/jc.2011-0473

Cited by 14 publications

(9 citation statements)

References 36 publications

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“…Evidence from experimental models is emerging that functional antagonism of hGH or hPRL is indicated to inhibit progression of tumors such as meningioma, breast, colorectal, endometrial and prostate carcinoma [ 4 , 52 – 57 ]. Previous studies have demonstrated that B2036, a hGH antagonist, decreased oncogenicity of endometrial carcinoma cells [ 4 ] and decreased proliferation of primary human mammary carcinoma cells in vitro [ 58 ]. Furthermore, Pegvisomant, the pegylated form of B2036 with FDA approval for the treatment of acromegaly, produced shrinkage of mammary carcinoma xenografts associated with reduced proliferation and increased apoptosis [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

Human growth hormone and human prolactin function as autocrine/paracrine promoters of progression of hepatocellular carcinoma

Kong

Yuan

et al. 2016

Oncotarget

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The death rates of hepatocellular carcinoma (HCC) are extremely high due to the paucity of therapeutic options. Animal models and anecdotal clinical evidence indicate a potential role of hGH and hPRL in HCC. However, the prognostic relevance and the functional role of tumor expression of these hormones in human HCC are not defined. Herein, we analyzed the mRNA and protein expression of hGH and hPRL in histopathological samples of non-neoplastic liver and HCC by in situ hybridization, PCR and immunohistochemistry techniques. Increased mRNA and protein expression of both hormones was observed in HCC compared with non-neoplastic liver tissues. hGH expression was significantly associated with tumor size and tumor grade. No significant association was observed between the expression of hPRL and any histopathological features. Amplification of both hGH and hPRL genes in HCC was observed when compared to non-neoplastic tissue. Expression of both hGH and hPRL was associated with worse relapse-free and overall survival in HCC patients. In vitro and in vivo functional assays performed with HCC cell lines demonstrated that autocrine expression of hGH or hPRL in HCC cells increased STAT3 activation, oncogenicity and tumor growth while functional antagonism with hGH-G120R significantly reduced these parameters. Hence, tumor expression of hGH/hPRL is associated with a worse survival outcome for patients with HCC and hGH/hPRL function as autocrine/paracrine promoters of HCC progression.

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Section: Discussionmentioning

confidence: 99%

Human growth hormone and human prolactin function as autocrine/paracrine promoters of progression of hepatocellular carcinoma

Kong

Yuan

et al. 2016

Oncotarget

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“…Cells were rinsed three times with PBS and incubated in serum-free medium for 24 hours, and afterwards 100 ng/ml doxycycline in DMEM (CDox cells) or the equal volume of DMEM (-Dox cells) were added as described. 48 The MTT assay was executed as recommended by the manufacture (Life Technologies, France) shortly after doxycycline administration ("0" timepoint) and also 24 and 48 hours later. Absorbance was read at 540 nm with a Thermo Scientific Multiskan EX ELISA reader (Thermo Fisher Scientific, USA).…”

Section: Mtt Assaymentioning

confidence: 99%

Involvement of the specific nucleolar protein SURF6 in regulation of proliferation and ribosome biogenesis in mouse NIH/3T3 fibroblasts

et al. 2017

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The nucleolar proteins which link cell proliferation to ribosome biogenesis are regarded to be potentially oncogenic. Here, in order to examine the involvement of an evolutionary conserved nucleolar protein SURF6/Rrp14 in proliferation and ribosome biogenesis in mammalian cells, we established stably transfected mouse NIH/3T3 fibroblasts capable of conditional overexpression of the protein. Cell proliferation was monitored in real-time, and various cell cycle parameters were quantified based on flow cytometry, Br-dU-labeling and conventional microscopy data. We show that overexpression of SURF6 accelerates cell proliferation and promotes transition through all cell cycle phases. The most prominent SURF6 pro-proliferative effects include a significant reduction of the population doubling time, from 19.8 ± 0.7 to 16.2 ± 0.5 hours (t-test, p < 0.001), and of the length of cell division cycle, from 17.6 ± 0.6 to 14.0 ± 0.4 hours (t-test, p < 0.001). The later was due to the shortening of all cell cycle phases but the length of G1 period was reduced most, from 5.7 ± 0.4 to 3.8 ± 0.3 hours, or by ∼30%, (t-test, p < 0.05). By Northern blots and qRT-PCR, we further showed that the acceleration of cell proliferation was concomitant with an accumulation of rRNA species along both ribosomal subunit maturation pathways. It is evident, therefore, that like the yeast homologue Rrp14, mammalian SURF6 is involved in various steps of rRNA processing during ribosome biogenesis. We concluded that SURF6 is a novel positive regulator of proliferation and G1/S transition in mammals, implicating that SURF6 is a potential oncogenic protein, which can be further studied as a putative target in anti-cancer therapy.

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“… 23 Furthermore, there are studies suggesting the role of GHR (growth hormone receptor) affects mediated signaling pathways in the development of human breast cancer either by autocrine or paracrine mechanisms. 24 , 25 …”

Section: Introductionmentioning

confidence: 99%

Caffeic Acid Versus Caffeic Acid Phenethyl Ester in the Treatment of Breast Cancer MCF-7 Cells: Migration Rate Inhibition

et al. 2018

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Epithelium mammary carcinoma is a cancer with a high death rate among women. One factor having a significant impact on metastasis is cell migration. The aim of this study was to compare migration rate inhibition of caffeic acid (CA) and its phenethyl ester (CAPE) on MCF-7 breast cancer cells. Microscopic evaluation was used to determine the morphology of carcinoma cells, before and after 24-hour treatment with CA and CAPE using a dose of 50 µM. The cytotoxic effect was measured by XTT-NR-SRB assay (tetrazolium hydroxide-neutral red-Sulforhodamine B) for 24-hour and 48-hour periods, using CA and CAPE, with doses of 50 and 100 µM. These doses were used to determine cell migration inhibition using a wound closure assay for 0-hour, 8-hour, 16-hour, and 24-hour periods. Both CA and CAPE treatments displayed cytotoxic activity in a dose- and time-dependent trend. CAPE displayed IC50 values more than twice as low as CA. IC50 values for the XTT assay were as follows: CA was 102.98 µM for 24 hours and 59.12 µM for 48 hours, while CAPE was 56.39 µM for 24 hours and 28.10 µM for 48 hours. For the NR assay: CA was 84.87 µM at 24 hours and 65.05 µM at 48 hours, while CAPE was 69.05 µM at 24 hours and 29.05 µM at 48 hours. For the SRB assay: At 24 hours, CA was 83.47 µM and 53.46 µM at 48 hours, while CAPE was 38.53 µM at 24 hours and 20.15 µM at 48 hours. Both polyphenols induced migration inhibition, resulting in practically halting the wound closure. CAPE produced better results than CA with the same doses and experiment times, though both CA and CAPE displayed cytotoxic activity against MCF-7 cells, as well as inhibited migration.

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Autocrine Proliferative Effects of hGH Are Maintained in Primary Cultures of Human Mammary Carcinoma Cells

Abstract: Primary HMCC proliferate in response to hGH, and the proliferation of hGH-positive HMCC is inhibited by hGH antagonism. Inhibition of hGH in patients with mammary carcinoma may therefore limit tumor growth.

Cited by 14 publications

References 36 publications

Human growth hormone and human prolactin function as autocrine/paracrine promoters of progression of hepatocellular carcinoma

Human growth hormone and human prolactin function as autocrine/paracrine promoters of progression of hepatocellular carcinoma

Involvement of the specific nucleolar protein SURF6 in regulation of proliferation and ribosome biogenesis in mouse NIH/3T3 fibroblasts

Caffeic Acid Versus Caffeic Acid Phenethyl Ester in the Treatment of Breast Cancer MCF-7 Cells: Migration Rate Inhibition

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