scholarly journals miR‑20b promotes cellular proliferation and migration by directly regulating phosphatase and tensin homolog in prostate cancer

2017 ◽  
Author(s):  
Ju Guo ◽  
Zewen Xiao ◽  
Xingwei Yu ◽  
Runfu Cao
Keyword(s):  
Prostate Cancer ◽  
Cellular Proliferation ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals BMI1 promotes cardiac fibrosis in ischemia-induced heart failure via the PTEN-PI3K/Akt-mTOR signaling pathway

2019 ◽  
Vol 316 (1) ◽  
pp. H61-H69 ◽  
Author(s):  
Wenbo Yang ◽  
Zhijun Wu ◽  
Ke Yang ◽  
Yanxin Han ◽  
Yanjia Chen ◽  
...  
Keyword(s):  
Cardiac Fibrosis ◽  
Mammalian Target Of Rapamycin ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatase And Tensin Homolog ◽  
B Lymphoma ◽  
Tensin Homolog ◽  
And Migration ◽  
Proliferation And Migration

Cardiac fibrosis has been known to play an important role in the etiology of heart failure after myocardial infarction (MI). B lymphoma Mo-MLV insertion region 1 homolog (BMI1), a transcriptional repressor, is important for fibrogenesis in the kidneys. However, the effect of BMI1 on ischemia-induced cardiac fibrosis remains unclear. BMI1 was strongly expressed in the infarct region 1 wk post-MI in mice and was detected by Western blot and histological analyses. Lentivirus-mediated overexpression of BMI1 significantly promoted cardiac fibrosis, worsened cardiac function 4 wk after the intervention in vivo, and enhanced the proliferation and migration capabilities of fibroblasts in vitro , whereas downregulation of BMI1 decreased cardiac fibrosis and prevented cardiac dysfunction in mice 4 wk post-MI in vivo. Furthermore, upregulated BMI1 inhibited phosphatase and tensin homolog (PTEN) expression, enhanced phosphatidylinositol 3-kinase (PI3K) expression, and increased the phosphorylation level of Akt and mammalian target of rapamycin (mTOR) in mice 4 wk after lentiviral infection, which was in accordance with the changes seen in their infarcted myocardial tissues. At the same time, the effects of BMI1 on cardiac fibroblasts were reversed in vitro when these cells were exposed to NVP-BEZ235, a dual-kinase (PI3K/mTOR) inhibitor. In conclusion, BMI1 is associated with cardiac fibrosis and dysfunction after MI by regulating cardiac fibroblast proliferation and migration, and these effects could be partially explained by the regulation of the PTEN-PI3K/Akt-mTOR pathway. NEW & NOTEWORTHY Ischemia-induced B lymphoma Mo-MLV insertion region 1 homolog (BMI1) significantly promoted cardiac fibrosis and worsened cardiac function in vivo, whereas downregulation of BMI1 decreased cardiac fibrosis and prevented cardiac dysfunction in myocardial infarcted mice. BMI1 also enhanced proliferation and migration capabilities of fibroblasts in vitro; these effects were reversed by NVP-BEZ235. Effects of BMI1 on cardiac fibrosis could be partially explained by regulation of the phosphatase and tensin homolog-phosphatidylinositol 3-kinase/Akt-mammalian target of rapamycin pathway.

LINC00893 inhibits papillary thyroid cancer by suppressing AKT pathway via stabilizing PTEN

2020 ◽  
pp. 1-10
Author(s):  
Shujing Li ◽  
Yanyan Zhang ◽  
Jian Dong ◽  
Ruihuan Li ◽  
Bo Yu ◽  
...  
Keyword(s):  
Akt Pathway ◽  
Phosphatase And Tensin Homolog ◽  
Fused In Sarcoma ◽  
Tensin Homolog ◽  
Phosphorylated Akt ◽  
Pten Mrna ◽  
Non Coding Rnas ◽  
And Migration ◽  
Fus Protein ◽  
Proliferation And Migration

Long non-coding RNAs (lncRNAs) are important to the occurrence and advancement of human cancers. We found through GEPIA that LINC00893 was lowly expressed in thyroid carcinoma (THCA) tissues, whereas the specific functions of LINC00893 has never been reported in PTC. In the current study, we confirmed that LINC00893 was expressed at a low level in PTC cells. Through gain-of-function assays, we determined that LINC00893 overexpression abrogated proliferation and migration abilities of PTC cells. Through signal transduction reporter array we found that LINC00893 potentially modulated the signals of phosphatase and tensin homolog (PTEN)/AKT pathway. In addition, overexpression of LINC00893 increased the expression of PTEN but reduced the levels of phosphorylated AKT in PTC. Additionally, mechanism assays unveiled that LINC00893 stabilized PTEN mRNA via recruiting Fused in sarcoma (FUS) protein. Finally, rescue assays demonstrated that LINC00893 hampered the proliferation and migration of PTC cells via PTEN/AKT pathway. Together, our study first clarified that LINC00893 functions as a tumor suppressor in PTC by blocking AKT pathway through PTEN upregulation.

scholarly journals MicroRNA-222 promotes the proliferation and migration of cervical cancer cells

2014 ◽  
Vol 37 (3) ◽  
pp. 131 ◽  
Author(s):  
Yi Sun ◽  
Bo Zhang ◽  
Jiajing Cheng ◽  
Yi Wu ◽  
Fing Xing ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Phosphatase And Tensin Homolog ◽  
Migration Assay ◽  
Tensin Homolog ◽  
Siha Cells ◽  
Non Coding Rna ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Purpose: This study aimed to investigate the role of small non-coding RNA-222 (microRNA-222; miR-222) in the development of cervical cancer (CC). Methods: Normal and CC specimens were obtained from 18 patients. HeLa and SiHa cells were grown in Dulbecco’s modified Eagle’s medium. RT–PCR, Western blot, migration assay, flow cytometry and immunofluorescence microscopy were used for analyses. Results: When compared with normal cervical tissues, miR-222 was upregulated in human CC, and the extent of up-regulation was associated with the extent and depth of CC invasion. Expression of miR-222 was inversely related to the expression of phosphatase and tensin homolog (PTEN) and p27. The reduced the expression of PTEN and p27 by miR-222 in HeLa cells and SiHa cells was associated with increased proliferation and migration of CC cells. The expression of proteins (E-cadherin and paxillin) related to the proliferation and migration was also elevated. Conclusion: MiR-222 plays an important role in the tumorigenesis of CC, possibly by specifically down-regulating p27Kip1 and PTEN. Our findings suggest that miR-222 may serve as a new therapeutic target in CC.

scholarly journals Beyond the Limits of Oxygen: Effects of Hypoxia in a Hormone-Independent Prostate Cancer Cell Line

ISRN Oncology ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
A. C. Mamede ◽  
A. M. Abrantes ◽  
L. Pedrosa ◽  
J. E. Casalta-Lopes ◽  
A. S. Pires ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Line ◽  
Cellular Proliferation ◽  
Cancer Cell Line ◽  
Prostate Cancer Cell Line ◽  
Antiproliferative Effect ◽  
Key Factor ◽  
Long Time ◽  
And Migration ◽  
Proliferation And Migration

Prostate cancer (PCa) has a high incidence worldwide. One of the major causes of PCa resistance is intratumoral hypoxia. In solid tumors, hypoxia is strongly associated with malignant progression and resistance to therapy, which is an indicator of poor prognosis. The antiproliferative effect and induced death caused by doxorubicin, epirubicin, cisplatin, and flutamide in a hormone-independent PCa cell line will be evaluated. The hypoxia effect on drug resistance to these drugs, as well as cell proliferation and migration, will be also analyzed. All drugs induced an antiproliferative effect and also cell death in the cell line under study. Hypoxia made the cells more resistant to all drugs. Moreover, our results reveal that long time cell exposure to hypoxia decreases cellular proliferation and migration. Hypoxia can influence cellular resistance, proliferation, and migration. This study shows that hypoxia may be a key factor in the regulation of PCa.

scholarly journals AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO

Life ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1208
Author(s):  
Yali Lu ◽  
Xuechao Wan ◽  
Wenhua Huang ◽  
Lu Zhang ◽  
Jun Luo ◽  
...  
Keyword(s):  
Transcriptional Activity ◽  
Target Genes ◽  
Cellular Proliferation ◽  
Mechanisms Of Action ◽  
Adenocarcinoma Cell Line ◽  
Specific Mechanism ◽  
Rna Immunoprecipitation ◽  
Non Coding Rnas ◽  
And Migration ◽  
Proliferation And Migration

The androgen receptor (AR) and its related signaling pathways play an important role in the development of prostate cancer (PCa). Long non-coding RNAs (lncRNAs) are involved in the regulation of tumorigenesis and development, but their specific mechanism of action remains unclear. This study examines the function and mechanisms of action of lncRNA AC016745.3 in the development of PCa. It shows that dihydrotestosterone (DHT) results in the AR-dependent suppression of AC016745.3 expression in the LNCaP androgen-sensitive human prostate adenocarcinoma cell line. In addition, overexpression of AC016745.3 inhibits the proliferation and migration of PCa cells, and suppresses the expression of AR target genes. This research also demonstrates that the protein NONO interacts with AR and functions as an AR co-activator, promoting AR transcriptional activity. Furthermore, using RNA immunoprecipitation (RIP)-PCR experiments, the study demonstrates that both NONO and AR can bind AC016745.3. Moreover, cell phenotypic experiments reveal that NONO can promote cellular proliferation and migration, and that AC016745.3 can partially antagonize the pro-oncogenic functions of NONO in PCa cells. In summary, the results indicate that AC016745.3 can bind NONO, suppressing its ability to promote AR-dependent transcriptional activity. Furthermore, DHT-dependent suppression of AC016745.3 expression can enhance NONO’s promotion effect on AR.

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