scholarly journals Role of MicroRNA-214–Targeting Phosphatase and Tensin Homolog in Advanced Glycation End Product-Induced Apoptosis Delay in Monocytes

2011 ◽  
Vol 186 (4) ◽  
pp. 2552-2560 ◽  
Author(s):  
Li-Min Li ◽  
Dong-Xia Hou ◽  
Ya-Lan Guo ◽  
Jun-Wei Yang ◽  
Yuan Liu ◽  
...  
Keyword(s):  
Advanced Glycation ◽  
Phosphatase And Tensin Homolog ◽  
Advanced Glycation End Product ◽  
Tensin Homolog ◽  
Induced Apoptosis

scholarly journals Answer to Controversy: miR-10a Replacement Approaches Do Not Offer Protection against Chemotherapy-Induced Gonadotoxicity in Mouse Model

2019 ◽  
Vol 20 (19) ◽  
pp. 4958 ◽  
Author(s):  
Chrysanthi Alexandri ◽  
Christina-Anna Stratopoulou ◽  
Isabelle Demeestere
Keyword(s):  
Fertility Preservation ◽  
Ovarian Function ◽  
Chemotherapeutic Agents ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Newborn Mouse ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
Phosphoinositide 3 Kinase ◽  
Induced Apoptosis

It is well known that chemotherapeutic agents may lead to premature ovarian failure and infertility. Therefore, fertility preservation is highly recommended for female cancer survivors. Despite the currently available techniques, new, non-invasive methods need to be developed to protect the ovarian follicles during oncological treatments. MicroRNAs can be effective tools in this field, as they alter their expression during chemotherapy exposure, and hence they can be useful to minimize the off-target toxicity. Previously, we identified several miRNAs with an important role in newborn mouse ovaries exposed to chemotherapy; among them, the miR-10a was one of the most downregulated miRNAs. Given the controversial role of miR-10a in the ovarian function, we decided to investigate its implication in chemotherapy-induced gonadotoxicity. The downregulated levels of miR-10a were restored by a liposome system conjugated with a mimic miR-10a, and the overexpressed miR-10a prevented the upregulation of the targeted gene, phosphatase and tensin homolog (Pten). The apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) Assay and Bax expression quantification, while histological studies were also performed to evaluate the follicle count and development. Our results showed that the miR-10a replacement could not protect the ovaries from chemotherapy-induced apoptosis, whereas the targeting of Pten may affect the follicle activation via the phosphoinositide 3-kinase (PI3K)/PTEN/protein kinase B (AKT) pathway. Consequently, the application of miR-10a in fertility preservation is not recommended, and the role of miR-10a needs to be further elucidated.

scholarly journals The role of microRNA-572 in the proliferation and chemotherapeutic treatment of prostate cancer

2021 ◽  
Vol 49 (5) ◽  
pp. 030006052110143
Author(s):  
Mingcui Zang ◽  
Xun Guo ◽  
Manqiu Chen
Keyword(s):  
Prostate Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Prostate Tumorigenesis ◽  
Expression Levels ◽  
Matrigel Invasion ◽  
Tensin Homolog ◽  
Docetaxel Treatment ◽  
Induced Apoptosis

Objective MicroRNAs (miRNAs) regulate prostate tumorigenesis and progression by involving different molecular pathways. In this study, we examined the role of miR-572 in prostate cancer (PCa). Methods The proliferation rates of LNCaP and PC-3 PCa cells were studied using MTT assays. Transwell migration and Matrigel invasion assays were performed to evaluate cell migration and invasion, respectively. Protein expression levels were examined using western blotting. Docetaxel-induced apoptosis was evaluated by Caspase-Glo3/7 assays. The putative miR-572 binding site in the phosphatase and tensin homolog (PTEN) 3ʹ untranslated region (3ʹ UTR) was assessed with dual-luciferase reporter assays. Additionally, miR-572 expression levels in human PCa tissues were examined by qRT-PCR assays. Results Upregulation of miR-572 promoted proliferation, migration, and invasion of PCa cells. Overexpression of miR-572 decreased sensitivity of PCa cells to docetaxel treatment by reducing docetaxel-induced apoptosis. MiR-572 can regulate migration and invasion in PCa cells. Furthermore, miR-572 could regulate expression of PTEN and p-AKT in PCa cells by directly binding to the PTEN 3ʹ UTR. MiR-572 expression levels were increased in human PCa tissues and associated with PCa stage. Conclusions miR-572 displayed essential roles in PCa tumor growth and its expression level may be used to predict docetaxel treatment in these tumors.

scholarly journals Cellular homeostasis, implantation window and unexplained infertility: role of phosphatase and tensin homolog deleted on chromosome 10

2019 ◽  
Vol 8 (7) ◽  
pp. 2754
Author(s):  
Annu Makker ◽  
Madhu Mati Goel ◽  
Kumari Manu ◽  
Renu Makker
Keyword(s):  
Cell Proliferation ◽  
Unexplained Infertility ◽  
Endometrial Cell ◽  
Chromosome 10 ◽  
Cellular Homeostasis ◽  
Phosphatase And Tensin Homolog ◽  
Implantation Window ◽  
Tensin Homolog ◽  
Proliferation And Apoptosis

Background: Balance between endometrial cell proliferation and apoptosis is crucial for successful embryo implantation. PTEN (phosphatase and tensin homolog deleted on chromosome 10), a pro-apoptotic factor, is proposed to be one of the signaling proteins through which estrogen and progesterone act to affect cellular homeostasis. Although reports in literature have suggested role of PTEN in regulating endometrial cell proliferation and apoptosis during window of implantation, its involvement in women with unexplained infertility is not clear. In the present study, we examined expression, cellular distribution and activation status of PTEN, cell proliferation, and apoptosis in midsecretory endometrium from women with unexplained infertility as compared to fertile controls.Methods: Endometrial biopsies from infertile (n=11) and fertile women (n=22) were used for immunohistochemical evaluation of PTEN, phospho-PTEN and Ki67. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling assay was performed for detection of apoptotic cells.Results: Biopsies from infertile women as compared to fertile controls demonstrated statistically significant: i) decrease in nuclear PTEN (P < 0.001), increase in nuclear phospho-PTEN (P < 0.05), increase in nuclear and cytoplasmic phospho-PTEN/PTEN ratio (P < 0.001 and P < 0.05 respectively) in endometrial stroma, ii) increase in cytoplasmic phospho-PTEN (P < 0.001) and phospho-PTEN/PTEN ratio (P < 0.05) in glandular epithelium (GE), iii) increase in Ki67 labeling in GE (P < 0.01) and stroma (P < 0.05) and, iv) decrease in (P < 0.001) apoptosis.Conclusions: Altered PTEN expression and associated modulation in cellular homeostasis during the implantation window might contribute to mechanism underlying unexplained infertility.

scholarly journals SP103PROTECTION ROLE OF AUTOPHAGY IN ADVANCED GLYCATION END PRODUCT-INDUCED MESENGIAL CELL INJURY

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii412-iii412
Author(s):  
Chien-Ling Lee ◽  
Tien-Fong Lu ◽  
Chih Kang Chiang ◽  
Shing Hwa Liu
Keyword(s):  
Cell Injury ◽  
Advanced Glycation ◽  
Advanced Glycation End Product

The role of phosphatase and tensin homolog in drug-induced gingival overgrowth

2013 ◽  
Vol 49 (3) ◽  
pp. 307-313 ◽  
Author(s):  
B. O. Cetinkaya ◽  
F. Pamuk ◽  
G. C. Keles ◽  
B. Ayas ◽  
G. K. Ozfidan ◽  
...  
Keyword(s):  
Drug Induced ◽  
Phosphatase And Tensin Homolog ◽  
Gingival Overgrowth ◽  
Tensin Homolog

scholarly journals Succinate Accumulation Is Associated with a Shift of Mitochondrial Respiratory Control and HIF-1α Upregulation in PTEN Negative Prostate Cancer Cells

2018 ◽  
Vol 19 (7) ◽  
pp. 2129 ◽  
Author(s):  
Anja Weber ◽  
Helmut Klocker ◽  
Herbert Oberacher ◽  
Erich Gnaiger ◽  
Hannes Neuwirt ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Mitochondrial Respiration ◽  
Respiratory Control ◽  
Phosphatase And Tensin Homolog ◽  
Permeabilized Cells ◽  
Tensin Homolog ◽  
Viable Cells ◽  
Sodium Dependent

The idea of using metabolic aberrations as targets for diagnosis or therapeutic intervention has recently gained increasing interest. In a previous study, our group discovered intriguing differences in the oxidative mitochondrial respiration capacity of benign and prostate cancer (PCa) cells. In particular, we found that PCa cells had a higher total respiratory activity than benign cells. Moreover, PCa cells showed a substantial shift towards succinate-supported mitochondrial respiration compared to benign cells, indicating a re-programming of respiratory control. This study aimed to investigate the role of succinate and its main plasma membrane transporter NaDC3 (sodium-dependent dicarboxylate transporter member 3) in PCa cells and to determine whether targeting succinate metabolism can be potentially used to inhibit PCa cell growth. Using high-resolution respirometry analysis, we observed that ROUTINE respiration in viable cells and succinate-supported respiration in permeabilized cells was higher in cells lacking the tumor suppressor phosphatase and tensin-homolog deleted on chromosome 10 (PTEN), which is frequently lost in PCa. In addition, loss of PTEN was associated with increased intracellular succinate accumulation and higher expression of NaDC3. However, siRNA-mediated knockdown of NaDC3 only moderately influenced succinate metabolism and did not affect PCa cell growth. By contrast, mersalyl acid—a broad acting inhibitor of dicarboxylic acid carriers—strongly interfered with intracellular succinate levels and resulted in reduced numbers of PCa cells. These findings suggest that blocking NaDC3 alone is insufficient to intervene with altered succinate metabolism associated with PCa. In conclusion, our data provide evidence that loss of PTEN is associated with increased succinate accumulation and enhanced succinate-supported respiration, which cannot be overcome by inhibiting the succinate transporter NaDC3 alone.

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