scholarly journals MicroRNA-1271-5p inhibits the tumorigenesis of ovarian cancer through targeting E2F5 and negatively regulates the mTOR signaling pathway

2020 ◽  
Author(s):  
Qin Li ◽  
Junyu Shi ◽  
Xiaoli Xu
Keyword(s):  
Ovarian Cancer ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
Mtor Signaling ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Direct Target ◽  
The Relationship

Abstract Background: MicroRNA-1271-5p (miR-1271-5p) has been reported to participate in the progression of many human cancers. However, the role of miR-1271-5p still remains unclear in ovarian cancer (OC). Therefore, we explored the effect of miR-1271-5p on the development of OC in present study. Methods: We measured the miR-1271-5p expression via the qRT-PCR assay. Then the function of miR-1271-5p was analyzed through MTT and Transwell assays. The relationship among miR-1271-5p and E2F5 was verified by dual luciferase assay. The protein expression levels were examined through western blot.Results: MiR-1271-5p was downregulated in OC tissues which predicted poor prognosis of OC patients. Moreover, E2F5 was a direct target of miR-1271-5p in OC. And miR-1271-5p suppressed cell proliferation, migration and invasion in OC through targeting E2F5. Furthermore, E2F5 was upregulated in OC tissues which predicted poor prognosis of OC patients. Besides that, miR-1271-5p suppressed EMT and mTOR pathway in OC. Conclusion: MiR-1271-5p inhibited the tumorigenesis of OC through targeting E2F5 and negatively regulated the mTOR signaling pathway.

scholarly journals SPAG5 upregulation predicts poor prognosis in cervical cancer patients and alters sensitivity to taxol treatment via the mTOR signaling pathway

2014 ◽  
Vol 5 (5) ◽  
pp. e1247-e1247 ◽  
Author(s):  
L-J Yuan ◽  
J-D Li ◽  
L Zhang ◽  
J-H Wang ◽  
T Wan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Patients ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
Cell Function ◽  
Disease Free Survival ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway

Abstract Previously, we found that sperm-associated antigen 5 (SPAG5) was upregulated in pelvic lymph node metastasis–positive cervical cancer. The aim of this study is to examine the role of SPAG5 in the proliferation and tumorigenicity of cervical cancer and its clinical significance in tumor progression. In our study, SPAG5 expression in cervical cancer patients was detected using quantitative real-time polymerase chain reaction, western blotting, and immunohistochemistry; cervical cancer cell function with downregulated SPAG5 in vitro was explored using tetrazolium assay, flow cytometry, and colony formation and Transwell assays. SPAG5 was upregulated in tumor tissue compared with paired adjacent noncancerous tissues; SPAG5 upregulation in tumor tissues indicated poor disease-free survival, which was also an independent prognostic indicator for cervical cancer patients. In vitro study demonstrated that SPAG5 downregulation inhibited cell proliferation and growth significantly by G2/M arrest and induction of apoptosis, and hindered cell migration and invasion. Under SPAG5 downregulation, the sensitivity of cervical cancer cells differed according to taxol dose, which correlated with mammalian target of rapamycin (mTOR) signaling pathway activity. In general, SPAG5 upregulation relates to poor prognosis in cervical cancer patients, and SPAG5 is a regulator of mTOR activity during taxol treatment in cervical cancer.

MicroRNA-1271-5p inhibits the tumorigenesis of ovarian cancer through targeting E2F5 and negatively regulates the mTOR signaling pathway

2020 ◽  
Author(s):  
Qin Li ◽  
Junyu Shi ◽  
Xiaoli Xu
Keyword(s):  
Ovarian Cancer ◽  
Western Blot ◽  
Signaling Pathway ◽  
Blot Analysis ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Pcr Assay ◽  
Qrt Pcr ◽  
Worse Prognosis

Abstract Background: MicroRNA-1271-5p (miR-1271-5p) has been reported to participate in the progression of many malignancies. However, the molecular mechanism of miR-1271-5p still remains vague in ovarian cancer (OC). Therefore, we explored the effect of miR-1271-5p in the development of OC in present study.Methods: We measured the miR-1271-5p expression via qRT-PCR assay. Western blot analysis was employed to examine protein expression. Then, the functional mechanism of miR-1271-5p was analyzed by MTT, Transwell and dual luciferase assays.Results: Downregulation of miR-1271-5p was found in OC, which can predict worse prognosis in OC patients. Further, miR-1271-5p directly targets E2F5 in OC. And miR-1271-5p restrained the proliferation, migration and invasion of OC cells via targeting E2F5. Additionally, upregulation of E2F5 was observed in OC, which predicted unfavorable prognosis in OC patients. Besides that, miR-1271-5p suppressed EMT and mTOR pathway in OC.Conclusion: MiR-1271-5p inhibited the tumorigenesis of OC through targeting E2F5 and negatively regulated the mTOR signaling pathway.

scholarly journals PO-027 Effects of exercise-induced miRNAs on mitochondrial autophagy signaling pathway in PI3K/Akt/mTOR

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Chang Meng
Keyword(s):  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Relevant Research ◽  
Research Directions ◽  
Exercise Induced ◽  
The Relationship ◽  
Hypoxic Exercise ◽  
New Discovery

Objective To explain the regulation of mitochondrial autophagy by exercise-induced miRNAs, it provides a new reference for the prevention and treatment of diseases such as inflammation and tumor. Methods Through the literature data method, this paper refers to more than 100 articles and writes this review, which provides relevant research directions for relevant researchers.  Results Exercise promotes the up-regulation of miR-30, miR-223 and miR-210 expression through the PI3K /Akt / mTOR signaling pathway to inhibit its related target proteins, and promote mitochondrial autophagy to affect inflammation, tumor and other diseases. Conclusions In recent years, people's concept of exercise has undergone a slow and fundamental change. In addition to medical factors, the role of exercise factors in the prevention or treatment of various diseases such as inflammation and cancer has gradually strengthened. Mitochondrial autophagy has a significant effect on tumor cells. The successful discovery of PI3K/Akt/mTOR signaling pathway provides more support for the involvement of tumor-like diseases. miRNAs may regulate PI3K/Akt/mTOR signaling in mitochondrial autophagy. Pathways significantly affect tumor-like diseases. Exercise is widely recommended as a means of preventing and treating various diseases such as inflammation and tumor. The induction of normoxic exercise and hypoxic exercise has a significant effect on the regulation of PI3K/Akt/mTOR signaling pathway in mitochondrial autophagy by miRNAs. In the future, studies on the regulation of mitochondrial autophagy by miRNAs can focus on the relationship with exercise. At present, the research on mitochondrial autophagy regulated by exercise-induced miRNAs is still insufficient. As a new discovery, it will receive more and more attention. miRNAs regulate the regulation of PI3K/Akt/mTOR signaling pathway in mitochondrial autophagy, which provides a new idea for solving the treatment problems of inflammation, tumor and other diseases.

scholarly journals MiR-450a-5p strengthens the drug sensitivity of gefitinib in glioma chemotherapy via regulating autophagy by targeting EGFR

Oncogene ◽  
2020 ◽  
Vol 39 (39) ◽  
pp. 6190-6202 ◽  
Author(s):  
Yu Liu ◽  
Liang Yang ◽  
Fan Liao ◽  
Wei Wang ◽  
Zhi-Fei Wang
Keyword(s):  
Signaling Pathway ◽  
Drug Sensitivity ◽  
Kinase Inhibitor ◽  
Glioma Cells ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Glioma Growth

Abstract Glioma reported to be refractory to EGFR tyrosine kinase inhibitor is the most common malignant tumor in central nervous system. Our research showed the low expression of miR-450a-5p and high expression of EGFR in glioma tissues. MiR-450a-5p was also observed to synergize with gefitinib to inhibit the proliferation, migration and invasion and induce the apoptosis and autophagy of glioma cells. Furthermore, miR-450a-5p was demonstrated to target 3′UTR of EGFR, and regulated EGFR-induced PI3K/AKT/mTOR signaling pathway. Moreover, the above effects induced by miR-450a-5p in glioma cells were reversed by WIPI1 silencing. The inhibition role of miR-450a-5p on glioma growth was also confirmed in vivo by subcutaneous and intracranial tumor xenografts. Therefore, we conclude that miR-450a-5p synergizes with gefitinib to inhibit the glioma tumorigenesis through inducing autophagy by regulating the EGFR-induced PI3K/AKT/mTOR signaling pathway, thereby enhancing the drug sensitivity of gefitinib.

scholarly journals Mir-20a-5p Induced WTX Deficiency Promotes Gastric Cancer Progressions Through Regulating PI3K/AKT Signaling Pathway

2020 ◽  
Author(s):  
Jian Li ◽  
Danli Ye ◽  
Peng Shen ◽  
Xiaorong Liu ◽  
Peirong Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Signaling Pathway ◽  
Wilms Tumor ◽  
Mtor Signaling ◽  
Luciferase Assay ◽  
Mtor Signaling Pathway ◽  
Pathway Analyses

Abstract Background: The X-linked gene WTX (also called AMER1), has been reported to act as a tumor suppress gene in Wilms tumor. Our previous study reported that WTX expression was significantly reduced in gastric cancer (GC), but the function and mechanism of WTX loss had not been fully elucidated yet. Methods: WTX/miR-20a-5p expression was analyzed in paraffin-embedded archived GC tissues and validated in public databases. KEGG pathway analyses were performed to explore the mechanism of WTX in GC progression. The role of WTX/miR-20a-5p in cell growth, migration, invasion and angiogenesis was investigated in vitro and in vivo. Western blot, immunohistochemistry, RT-PCR, luciferase assay, and Co-immunoprecipitation (Co-IP) were used to detect the regulation of WTX and PI3K/AKT/mTOR signaling by miR-20a-5p.Results: We revealed that WTX served as a tumor suppressor whose loss associated with the aggressive feature of GC by showing hyperproliferation in vitro and high metastasis phenotype in vivo. And WTX expression level was positively correlated with the overall survival of GC patients. Microarray, bioinformatics analysis, and verification experiments showed that WTX loss activated PI3K/AKT/mTOR pathway, and promoted the proliferation and invasion of GC cells. We also discovered that the miR-20a-5P aberrant upregulation was one of the reasons inducing WTX loss in GC which stimulated PI3K phosphorylation to activate PI3K/AKT/mTOR signaling pathway, thus promoted GC progression.Conclusions: This study unveiled the mechanism of GC progression which was, at least partially, caused by miR-20a-5p aberrant upregulation which inhibited WTX expression and thus activate PI3K/AKT/mTOR signaling pathway. It provided a comprehensive understanding of the action of miR-20a-5p/WTX/PI3K/AKT/mTOR signaling pathway in the progression and metastasis of GC.

Role of the PI3K/AKT/mTOR signaling pathway in ovarian cancer: Biological and therapeutic significance

2019 ◽  
Vol 59 ◽  
pp. 147-160 ◽  
Author(s):  
Meran Keshawa Ediriweera ◽  
Kamani Hemamala Tennekoon ◽  
Sameera Ranganath Samarakoon
Keyword(s):  
Ovarian Cancer ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

scholarly journals M2 macrophage-derived exosomal microRNAs inhibit cell migration and invasion in gliomas through PI3K/AKT/mTOR signaling pathway

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jie Yao ◽  
Zefen Wang ◽  
Yong Cheng ◽  
Chao Ma ◽  
Yahua Zhong ◽  
...  
Keyword(s):  
Cell Migration ◽  
Western Blot ◽  
Signaling Pathway ◽  
Target Gene ◽  
Glioma Cells ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
M2 Macrophage ◽  
Mtor Signaling Pathway ◽  
Cell Migration And Invasion

Abstract Background Glioma, the most common primary brain tumor, account Preparing figures for 30 to 40% of all intracranial tumors. Herein, we aimed to study the effects of M2 macrophage-derived exosomal microRNAs (miRNAs) on glioma cells. Methods First, we identified seven differentially expressed miRNAs in infiltrating macrophages and detected the expression of these seven miRNAs in M2 macrophages. We then selected hsa-miR-15a-5p (miR-15a) and hsa-miR-92a-3p (miR-92a) for follow-up studies, and confirmed that miR-15a and miR-92a were under-expressed in M2 macrophage exosomes. Subsequently, we demonstrated that M2 macrophage-derived exosomes promoted migration and invasion of glioma cells, while exosomal miR-15a and miR-92a had the opposite effects on glioma cells. Next, we performed the target gene prediction in four databases and conducted target gene validation by qRT-PCR, western blot and dual luciferase reporter gene assays. Results The results revealed that miR-15a and miR-92a were bound to CCND1 and RAP1B, respectively. Western blot assays demonstrated that interference with the expression of CCND1 or RAP1B reduced the phosphorylation level of AKT and mTOR, indicating that both CCND1 and RAP1B can activate the PI3K/AKT/mTOR signaling pathway. Conclusion Collectively, these findings indicate that M2 macrophage-derived exosomal miR-15a and miR-92a inhibit cell migration and invasion of glioma cells through PI3K/AKT/mTOR signaling pathway.

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