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Source: Molecular and Cellular Endocrinology
Cancer: Cancer

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Total 9 results found since Jan 2013.

Identification of retinoid acid induced 16 as a novel androgen receptor target in prostate cancer cells
ConclusionsWe demonstrate for the first time that RAI16 is a direct target gene of AR. RAI16 may involved in cell growth of prostate cancer cells in response to AR signaling.
Source: Molecular and Cellular Endocrinology - January 31, 2020 Category: Endocrinology Source Type: research

Regulation of NADPH oxidase NOX4 by delta iodolactone (IL- δ) in thyroid cancer cells
Conclusions The antiproliferative and pro-apoptotic effect of IL-δ is mediated by different mechanisms and pathway involving different sources of ROS generation depending on the cellular context. Graphical abstract
Source: Molecular and Cellular Endocrinology - May 27, 2018 Category: Endocrinology Source Type: research

Sensitization of androgen refractory prostate cancer cells to anti-androgens through re-expression of epigenetically repressed androgen receptor – Synergistic action of quercetin and curcumin
Publication date: Available online 28 April 2016 Source:Molecular and Cellular Endocrinology Author(s): Vikas Sharma, Lokesh Kumar, Sujit K. Mohanty, Jagdamba P. Maikhuri, Singh Rajender, Gopal Gupta Epigenetic repression of Androgen Receptor (AR) gene by hypermethylation of its promoter causes resistance in prostate cancer (CaP) to androgen deprivation therapy with anti-androgens. Some dietary phytocompounds like quercetin (Q) and curcumin (C) with reported DNMT-inhibitory activity were tested for their ability to re-express the AR in AR-negative CaP cell lines PC3 and DU145. Combined treatment with Q+C was much m...
Source: Molecular and Cellular Endocrinology - April 28, 2016 Category: Endocrinology Source Type: research

Melatonin enhances arsenic trioxide-induced cell death via sustained upregulation of Redd1 expression in breast cancer cells
Publication date: Available online 27 November 2015 Source:Molecular and Cellular Endocrinology Author(s): Sun-Mi Yun, Sang Hyeok Woo, Sang Taek Oh, Sung-Eun Hong, Tae-Boo Choe, Sang-Kyu Ye, Eun-Kyu Kim, Min Ki Seong, Hyun-A Kim, Woo Chul Noh, Jin Kyung Lee, Hyeon-Ok Jin, Yun-Han Lee, In-Chul Park Melatonin is implicated in various physiological functions, including anticancer activity. However, the mechanism(s) of its anticancer activity is not well understood. In the present study, we investigated the combined effects of melatonin and arsenic trioxide (ATO) on cell death in human breast cancer cells. Mela...
Source: Molecular and Cellular Endocrinology - November 27, 2015 Category: Endocrinology Source Type: research

Estrogen suppresses breast cancer proliferation through GPER / p38 MAPK axis during hypoxia
In conclusion, Estrogen suppresses breast cancer growth by inhibiting G1/S phase transition through GPER/ROS/p38 MAPK/p21 mediated signaling during hypoxic condition.
Source: Molecular and Cellular Endocrinology - November 6, 2015 Category: Endocrinology Source Type: research

MMP2 and MMP9 participate in S1P-induced invasion of follicular ML-1 thyroid cancer cells
In conclusion, MMP2 and MMP9 participate in S1P-evoked follicular ML-1 thyroid cancer cell invasion.
Source: Molecular and Cellular Endocrinology - March 10, 2015 Category: Endocrinology Source Type: research

NF-κB increased expression of 17β-hydroxysteroid dehydrogenase 4 promotes HepG2 proliferation via inactivating estradiol
In this study, HepG2 cells were used to investigate the role of HSD17B4 in the proliferation of liver cancer cells treated with the NF-κB activator, tumor necrosis factor-alpha (TNF-α), with the inhibitor of NF-κB activation, pyrrolidinedithiocarbamate (PDTC), or with a related specific siRNA. We demonstrated that the human HSD17B4 gene is a target for NF-κB activation in inflammation-stimulated HepG2 cells. HSD17B4 is up-regulated via the binding of activated NF-κB to the distal NF-κB-responsive element via TNF-α stimulation, which then promotes cell proliferation by decreasing the levels of E2 and enhancing the ex...
Source: Molecular and Cellular Endocrinology - December 12, 2014 Category: Endocrinology Source Type: research

Involvement of insulin-like growth factor binding protein-3 in peroxisome proliferator-activated receptor gamma-mediated inhibition of breast cancer cell growth
Publication date: 5 January 2015 Source:Molecular and Cellular Endocrinology, Volume 399 Author(s): Cindy K. Pon , Sue M. Firth , Robert C. Baxter We have previously reported that insulin-like growth factor binding protein-3 (IGFBP-3), a protein with dichotomous effects on both cell proliferation and cell survival, interacts with peroxisome proliferator-activated receptor gamma (PPARγ) and inhibits adipogenic PPARγ signaling. We now show that IGFBP-3 and PPARγ interact in breast cancer cells, through amino- and carboxyl-terminal residues of IGFBP-3. IGFBP-3 and the PPARγ ligands, rosiglitazone or 15-deoxy-Δ12,14-pro...
Source: Molecular and Cellular Endocrinology - November 13, 2014 Category: Endocrinology Source Type: research

Involvement of insulin-like growth factor binding protein-3 in peroxisome proliferator activated receptor gamma-mediated inhibition of breast cancer cell growth
Publication date: Available online 31 October 2014 Source:Molecular and Cellular Endocrinology Author(s): Cindy K. Pon , Sue M. Firth , Robert C. Baxter We have previously reported that insulin-like growth factor binding protein-3 (IGFBP-3), a protein with dichotomous effects on both cell proliferation and cell survival, interacts with peroxisome proliferator-activated receptor gamma (PPARγ) and inhibits adipogenic PPARγ signaling. We now show that IGFBP-3 and PPARγ interact in breast cancer cells, through amino- and carboxyl-terminal residues of IGFBP-3. IGFBP-3 and the PPARγ ligands, rosiglitazone or 15-deoxy-Δ12,...
Source: Molecular and Cellular Endocrinology - November 3, 2014 Category: Endocrinology Source Type: research