17β-Estradiol regulates cell proliferation, colony formation, migration, invasion and promotes apoptosis by upregulating miR-9 and thus degrades MALAT-1 in osteosarcoma cell MG-63 in an estrogen receptor-independent manner

2015 ◽  
Vol 457 (4) ◽  
pp. 500-506 ◽  
Author(s):  
Dengfeng Fang ◽  
Hui Yang ◽  
Jing Lin ◽  
Yi Teng ◽  
Yingying Jiang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Colony Formation ◽  
Osteosarcoma Cell ◽  
Independent Manner ◽  
17Β Estradiol

scholarly journals Palmitoylation-dependent Estrogen Receptor α Membrane Localization: Regulation by 17β-Estradiol

2005 ◽  
Vol 16 (1) ◽  
pp. 231-237 ◽  
Author(s):  
Filippo Acconcia ◽  
Paolo Ascenzi ◽  
Alessio Bocedi ◽  
Enzo Spisni ◽  
Vittorio Tomasi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Plasma Membrane ◽  
Estrogen Receptor Α ◽  
Membrane Localization ◽  
Target Cells ◽  
Dependent Manner ◽  
Caveolin 1 ◽  
17Β Estradiol

A fraction of the nuclear estrogen receptor α (ERα) is localized to the plasma membrane region of 17β-estradiol (E2) target cells. We previously reported that ERα is a palmitoylated protein. To gain insight into the molecular mechanism of ERα residence at the plasma membrane, we tested both the role of palmitoylation and the impact of E2 stimulation on ERα membrane localization. The cancer cell lines expressing transfected or endogenous human ERα (HeLa and HepG2, respectively) or the ERα nonpalmitoylable Cys447Ala mutant transfected in HeLa cells were used as experimental models. We found that palmitoylation of ERα enacts ERα association with the plasma membrane, interaction with the membrane protein caveolin-1, and nongenomic activities, including activation of signaling pathways and cell proliferation (i.e., ERK and AKT activation, cyclin D1 promoter activity, DNA synthesis). Moreover, E2 reduces both ERα palmitoylation and its interaction with caveolin-1, in a time- and dose-dependent manner. These data point to the physiological role of ERα palmitoylation in the receptor localization to the cell membrane and in the regulation of the E2-induced cell proliferation.

Estrogen receptor α L429 and A430 regulate 17β-estradiol-induced cell proliferation via CREB1

2015 ◽  
Vol 27 (12) ◽  
pp. 2380-2388 ◽  
Author(s):  
Valeria Pesiri ◽  
Pierangela Totta ◽  
Marco Segatto ◽  
Fabrizio Bianchi ◽  
Valentina Pallottini ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
17Β Estradiol

RNF38 inhibits osteosarcoma cell proliferation by binding to CRY1

2021 ◽  
pp. 1-7
Author(s):  
Jian Zhou ◽  
Zhen-yu Tang ◽  
Xiao-liang Sun
Keyword(s):  
Cell Proliferation ◽  
Western Blotting ◽  
Colony Formation ◽  
Akt Pathway ◽  
Osteosarcoma Cell ◽  
Mrna Levels ◽  
Osteosarcoma Cells ◽  
Protein Levels ◽  
Qrt Pcr

The PI3K/AKT pathway plays an important role in the development of osteosarcoma. RNF38 interferes with activation of the AKT pathway. Cryptochrome1 (CRY1) inhibits osteosarcoma proliferation through the AKT pathway. We aimed to clarify whether RNF38 affects the proliferation of osteosarcoma cells by regulating the PI3K/AKT pathway through its interaction with CRY1. The mRNA levels of RNF38 were determined using qRT-PCR. Protein levels of RNF38, p-p70S6, p70S6, +p-AKT, AKT, p-mTOR, mTOR, and CRY1 were detected by western blotting. The proliferation of osteosarcoma cells was detected using CCK-8 and colony formation assays. The interaction between CRY1 and RNF38 was detected by co-immunoprecipitation and GST pull-down assays. RNF38 expression was higher in Saos-2 and U20S cells than in hFOB cells. Overexpression of RNF38 promoted the proliferation of osteosarcoma cells, the number of colonies, and p-AKT and p-mTOR levels, suggesting that overexpression of RNF38 activated the PI3K/AKT pathway. In addition, RNF38 directly binds to the N-terminal of CRY1. The simultaneous knockdown of RNF38 and CRY1 restored the level of p-AKT, which was reduced by RNF38 knockdown alone. RNF38 affects the proliferation of osteosarcoma cells by regulating the PI3K/AKT pathway through its interaction with CRY1.

scholarly journals Lysosomal Function Is Involved in 17β-Estradiol-Induced Estrogen Receptor α Degradation and Cell Proliferation

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e94880 ◽  
Author(s):  
Pierangela Totta ◽  
Valeria Pesiri ◽  
Maria Marino ◽  
Filippo Acconcia
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Lysosomal Function ◽  
17Β Estradiol

scholarly journals miR-27b Targets HOXB8 to Inhibit Malignant Behaviors of Osteosarcoma

2019 ◽  
Vol 18 ◽  
pp. 153303381987079
Author(s):  
Yingyong Wu ◽  
Jinyun Peng
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Lines ◽  
Colony Formation ◽  
Cell Counting ◽  
Osteosarcoma Cell ◽  
Polymerase Chain ◽  
And Migration ◽  
Insight Into

MicroRNAs function as either tumor suppressor or oncogene in human cancers. This study aimed to explore the role of miR-27b in osteosarcoma. Expression of miR-27b or homeobox B8 in osteosarcoma cell lines was analyzed by quantitative real-time polymerase chain reaction and Western blot, respectively. Luciferase activity reporter assay and Western blot were conducted to explore the association between miR-27b and homeobox B8. Cell Counting Kit-8, colony formation assay, and wound-healing assay were performed to investigate the role of miR-27b or homeobox B8 on cell proliferation, colony formation, and cell migration. Expression of miR-27b was significantly reduced, while homeobox B8 was increased in osteosarcoma cell lines. In addition, homeobox B8 was validated as a direct target of homeobox B8. Moreover, miR-27b regulates osteosarcoma cell proliferation, colony formation, and migration through targeting homeobox B8. Taken together, our study provides novel insight into the progression of osteosarcoma, and the miR-27b–homeobox B8 axis identified may be developed as therapeutic targets against hepatocellular carcinoma in the future.

scholarly journals miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

2018 ◽  
Vol 50 (6) ◽  
pp. 2249-2259 ◽  
Author(s):  
Xuesong Wang ◽  
Lei Peng ◽  
Xiaojin Gong ◽  
Xiugong Zhang ◽  
Ruifu Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Colony Formation ◽  
Target Gene ◽  
Suppressor Gene ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Osteosarcoma Cell ◽  
Direct Target Gene ◽  
Dual Luciferase Reporter Assay

Background/Aims: Increasing evidences suggest that dysregulated expression of miRNAs contributes to the progression of various tumors. However, the underlying function of miR-423-5p in osteosarcoma remains unexplored. Methods: The expression of miR-423-5p and STMN1 were determined in osteosarcoma samples and cell lines via quantitative real-time PCR. Colony formation and Cell Counting Kit-8 (CCK-8) assays were performed to measure cell proliferation ability and transwell analysis was used to detect cell invasion, and dual luciferase reporter assay was perform to analysis the interaction between the miR-423-5p and STMN1. Results: The expression levels of miR-423-5p and STMN1 in the osteosarcoma tissues and cell lines were measured by qRT-PCR. Cell viability was determined using the clone formation and CCK-8 assays. A dual-luciferase reporter and Western blot were performed to stdudy the target gene of miR-423-5p. Here, we showed that miR-423-5p expression was downregulated in osteosarcoma tissues and cell lines. However, the expression of stathmin1 (STMN1) was downregulated in osteosarcoma tissues and cell lines. Moreover, STMN1 expression level was negatively correlated with the miR-423-5p expression in the osteosarcoma tissues. We identified STMN1 was a direct target gene of miR-423-5p in osteosarcoma cell. Overexpression of miR-423-5p inhibited osteosarcoma cell proliferation, colony formation and invasion. Furthermore, we demonstrated that STMN1 was involved in miR-423-5p-mediated cell behavior such as cell proliferation, colony formation and invasion in the osteosarcoma cell. Conclusion: Our present study indicated that miR-423-5p acted as a tumor suppressor gene in osteosarcoma partly through inhibiting STMN1 expression.

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