scholarly journals Protective effects of ginsenoside Rb1 on H2O2-induced oxidative injury in human endothelial cell line (EA.hy926) via miR-210

2019 ◽  
Vol 33 ◽  
pp. 205873841986602 ◽  
Author(s):  
Fubao Jia ◽  
Lei Mou ◽  
Hanming Ge
Keyword(s):  
Oxidative Injury ◽  
Nuclear Factor Κb ◽  
Migration And Invasion ◽  
Protective Effects ◽  
Ginsenoside Rb1 ◽  
Interacting Protein ◽  
Positive Effects ◽  
Adenovirus E1b ◽  
And Migration ◽  
Induced Apoptosis

Ginsenoside Rb1 (Rb1) possesses a cardioprotective effect via mediating microRNAs (miRs), while it is unexplored whether miR-210 is regulated by Rb1 in response to oxidative stress. Human endothelial EA.hy926 cells were stimulated with H2O2 before Rb1 treatment. After transfection, cell viability, apoptosis, migration, and invasion assays were conducted. Western blot was applied to quantify protein. BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3) and miR-210 were analyzed with quantitative reverse transcription polymerase chain reaction. Dual luciferase activity assay was performed. Rb1 elevated viability, migration, and invasion of H2O2-treated cells. H2O2-induced apoptosis was moderated by Rb1. miR-210 was augmented in H2O2-treated cells after Rb1 stimulation. miR-210 inhibitor abolished the positive effects of Rb1. BNIP3 was negatively modulated by miR-210 and implicated in modulating viability, apoptosis, and migration and invasion. In addition, BNIP3 modulated phosphorylation of regulators. Rb1 repressed oxidative injury via elevating miR-210. miR-210 negatively mediated BNIP3, which participated in oxidative damage via regulating mammalian targets of rapamycin (mTOR) and nuclear factor-κB (NF-κB).

scholarly journals Bnip3 and AIF cooperate to induce apoptosis and cavitation during epithelial morphogenesis

2012 ◽  
Vol 198 (1) ◽  
pp. 103-114 ◽  
Author(s):  
Yanmei Qi ◽  
Xiaoxiang Tian ◽  
Jie Liu ◽  
Yaling Han ◽  
Alan M. Graham ◽  
...  
Keyword(s):  
Protein A ◽  
Hypoxia Inducible Factor ◽  
Embryonic Stem ◽  
Embryoid Bodies ◽  
Epithelial Morphogenesis ◽  
Dependent Manner ◽  
Interacting Protein ◽  
The Core ◽  
Adenovirus E1b ◽  
Induced Apoptosis

Apoptosis is an essential step in cavitation during embryonic epithelial morphogenesis, but its mechanisms are largely unknown. In this paper, we used embryonic stem cell–differentiated embryoid bodies (EBs) as a model and found that Bnip3 (Bcl-2/adenovirus E1B 19-kD interacting protein), a BH3-only proapoptotic protein, was highly up-regulated during cavitation in a hypoxia-dependent manner. Short hairpin RNA silencing of Bnip3 inhibited apoptosis of the core cells and delayed cavitation. We show that the Bnip3 up-regulation was mediated mainly by hypoxia-inducible factor (HIF)–2. Ablation of HIF-2α or HIF-1β, the common β subunit of HIF-1 and -2, suppressed Bnip3 up-regulation and inhibited apoptosis and cavitation. We further show that apoptosis-inducing factor (AIF) cooperated with Bnip3 to promote lumen clearance. Bnip3 silencing in AIF-null EBs nearly blocked apoptosis and cavitation. Moreover, AIF also regulated Bnip3 expression through mitochondrial production of reactive oxygen species and consequent HIF-2α stabilization. These results uncover a mechanism of cavitation through hypoxia-induced apoptosis of the core cells mediated by HIFs, Bnip3, and AIF.

scholarly journals Gold Nanoparticles Suppressed Proliferation, Migration, and Invasion in Papillary Thyroid Carcinoma Cells via Downregulation of CCT3

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Fangzhou Liu ◽  
Dawei Ma ◽  
Wei Chen ◽  
Xinyuan Chen ◽  
Yichun Qian ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Molecular Mechanisms ◽  
Target Therapy ◽  
Migration And Invasion ◽  
Control Group ◽  
Papillary Thyroid ◽  
And Migration ◽  
Induced Apoptosis

Emerging evidences have demonstrated that gold nanoparticles (AuNPs) have been used for cancer treatment. The aim of this study was to investigate the effects and molecular mechanisms of AuNPs on papillary thyroid carcinoma (PTC) cells (BCPAP and TPC-1). Characterizations of AuNPs were detected by UV-Vis spectra, transmission electron microscopy (TEM), and dynamic light scattering (DLS). Cell proliferation and apoptosis, migration, and invasion of PTC cells were evaluated by MTT, flow cytometry, wound healing, and transwell assays, respectively. Furthermore, qRT-PCR and western blot assays were performed to assess the protein expressions related to apoptosis and migration including caspase-3, caspase-9, Bax, Bcl-2, MMP-2, and MMP-9. The study revealed that AuNPs significantly suppressed cell viability, migration, and invasion and remarkably induced apoptosis of BCPAP and TPC-1 cells compared with the control group. Moreover, AuNPs negatively regulated the expression of CCT3 and silencing of CCT3 obviously promoted the proliferation, migration, and invasion inhibition and apoptosis induction of PTC cells combined with AuNPs. Collectively, these results highlighted the potential application of AuNPs in PTC target therapy.

scholarly journals MicroRNA-30e targets BNIP3L to protect against aldosterone-induced podocyte apoptosis and mitochondrial dysfunction

2017 ◽  
Vol 312 (4) ◽  
pp. F589-F598 ◽  
Author(s):  
Yan Guo ◽  
Xu Deng ◽  
Shuang Chen ◽  
Lingyun Yang ◽  
Jiajia Ni ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Underlying Mechanism ◽  
Protective Role ◽  
Early Event ◽  
Dependent Manner ◽  
Podocyte Injury ◽  
Interacting Protein ◽  
Adenovirus E1b ◽  
Induced Apoptosis

MicroRNAs are essential for the maintenance of podocyte homeostasis. Emerging evidence has demonstrated a protective role of microRNA-30a (miR-30a), a member of the miR-30 family, in podocyte injury. However, the roles of other miR-30 family members in podocyte injury are unclear. The present study was undertaken to investigate the contribution of miR-30e to the pathogenesis of podocyte injury induced by aldosterone (Aldo), as well as the underlying mechanism. After Aldo treatment, miR-30e was reduced in a dose-and time-dependent manner. Notably, overexpression of miR-30e markedly attenuated Aldo-induced apoptosis in podocytes. In agreement with this finding, miR-30e silencing led to significant podocyte apoptosis. Mitochondrial dysfunction (MtD) has been shown to be an early event in Aldo-induced podocyte injury. Here we found that overexpression of miR-30e improved Aldo-induced MtD while miR-30e silencing resulted in MtD. Next, we found that miR-30e could directly target the BCL2/adenovirus E1B-interacting protein 3-like (BNIP3L) gene. Aldo markedly enhanced BNIP3L expression in podocytes, and silencing of BNIP3L largely abolished Aldo-induced MtD and cell apoptosis. On the contrary, overexpression of BNIP3L induced MtD and apoptosis in podocytes. Together, these findings demonstrate that miR-30e protects mitochondria and podocytes from Aldo challenge by targeting BNIP3L.

scholarly journals Heptapeptide Isolated from Isochrysiszhanjiangensis Exhibited Anti-Photoaging Potential via MAPK/AP-1/MMP Pathway and Anti-Apoptosis in UVB-Irradiated HaCaT Cells

Marine Drugs ◽  
2021 ◽  
Vol 19 (11) ◽  
pp. 626
Author(s):  
Zhaowan Zheng ◽  
Zhenbang Xiao ◽  
Yuan-Lin He ◽  
Yanfei Tang ◽  
Lefan Li ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Animal Health ◽  
Caspase 8 ◽  
Hacat Cells ◽  
Oxygen Species ◽  
Protective Effects ◽  
Protein Sources ◽  
Positive Effects ◽  
Endogenous Antioxidants ◽  
Induced Apoptosis

Marine microalgae can be used as sustainable protein sources in many fields with positive effects on human and animal health. DAPTMGY is a heptapeptide isolated from Isochrysis zhanjiangensis which is a microalga. In this study, we evaluated its anti-photoaging properties and mechanism of action in human immortalized keratinocytes cells (HaCaT). The results showed that DAPTMGY scavenged reactive oxygen species (ROS) and increase the level of endogenous antioxidants. In addition, through the exploration of its mechanism, it was determined that DAPIMGY exerted anti-photoaging effects. Specifically, the heptapeptide inhibits UVB-induced apoptosis through down-regulation of p53, caspase-8, caspase-3 and Bax and up-regulation of Bcl-2. Thus, DAPTMGY, isolated from I. zhanjiangensis, exhibits protective effects against UVB-induced damage.

scholarly journals LncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataract via miR-34a/SMAD2 axis

2021 ◽  
Author(s):  
Chao Wang ◽  
Ruiling Zhao ◽  
Suhong Zhang
Keyword(s):  
Cell Proliferation ◽  
Target Gene ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Diabetic Cataract ◽  
Lncrna Xist ◽  
Non Coding Rnas ◽  
And Migration ◽  
Induced Apoptosis ◽  
Proliferation And Migration

AbstractEmerging evidence has manifested that long non-coding RNAs (lncRNAs) played critical roles in diabetes. The present research aimed to investigate the role and mechanism of XIST on proliferation, migration and apoptosis in diabetic cataract (DC). In the present study, lens epithelial cells (SRA01/04) were treated by high glucose (HG). The levels of XIST, miR-34a and SMAD2 were examined by RT-qPCR. MTT, transwell, wound healing and TUNEL assays were employed to examine cell proliferation, invasion, migration and apoptosis. The interaction between miR-34a and XIST or SMAD2 was verified by luciferase reporter assay. It was found that XIST expression was increased and miR-34a level was decreased in DC tissues and HG-induced SRA01/04 cells. XIST knockdown or miR-34a addition attenuated cell proliferation and migration, and induced apoptosis in SRA01/04 cells under HG. XIST targeted miR-34a and regulated DC progression via miR-34a. SMAD2 was a target gene of miR-34a and was positively modulated by XIST. SMAD2 addition accelerated cell proliferation, migration and inhibited the apoptosis in HG-stimulated SRA01/04 cells, which were abrogated by XIST depletion. In conclusion, XIST facilitated the proliferation, migration and invasion, and inhibited the apoptosis via miR-34a/SMAD2 axis in DC.

scholarly journals Artesunate inhibits cell proliferation, migration, and invasion of thyroid cancer by regulating the PI3K/AKT/FKHR pathway

2021 ◽  
Author(s):  
Zhiwei Xu ◽  
Xiaojian Liu ◽  
Daoping Zhuang
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Molecular Mechanism ◽  
Western Blotting ◽  
Inhibitory Effect ◽  
Migration And Invasion ◽  
And Migration ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells

This study characterized the effects of artesunate on thyroid cancer and partially identified its related molecular mechanism. We determined the effect of artesunate on the proliferation of thyroid cancer cells using the MTT assay, cell colony formation experiments, and western blotting, and used flow cytometry to detect the apoptosis of cancer cells. Using a wound-healing assay, Transwell chamber experiments, and western blotting, we determined the effect of artesunate on cancer cell migration. By co-cultivating artesunate with the PI3K agonist, 740Y-P, we also partially identified the molecular mechanism. Artesunate significantly inhibited the growth, proliferation, migration, and invasion of thyroid cancer cells, and promoted the apoptosis of cancer cells. Using co-cultivation with a PI3K agonist, we found that the inhibitory effect of artesunate on cancer cells was mainly due to suppressing the PI3K/AKT/FKHR signaling pathway. By inhibiting the PI3K/AKT/FKHR signaling pathway, artesunate induced apoptosis of thyroid cancer cells and inhibited their proliferation and migration.

miR-129-5p suppresses proliferation, migration, and induces apoptosis in pancreatic cancer cells by targeting PBX3

2019 ◽  
Vol 51 (10) ◽  
pp. 997-1007 ◽  
Author(s):  
Zhisheng Qiu ◽  
Xiaochun Wang ◽  
Yuping Shi ◽  
Mingxu Da
Keyword(s):  
Pancreatic Cancer ◽  
Therapeutic Strategy ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Pancreatic Cancer Cells ◽  
B Cell Leukemia ◽  
And Migration ◽  
Induced Apoptosis ◽  
Dual Luciferase Reporter Assay ◽  
Proliferation And Migration

Abstract Pancreatic cancer (PC) is the seventh most frequent cause of cancer-related deaths worldwide with a high mortality. MicroRNAs (miRNAs) act as important regulators for the development of PC and participate in the progression of PC. miR-129-5p was reported to regulate the progression of tumors, such as thyroid cancer and gastric cancer. However, the function of miR-129-5p in PC is still unclear. In this study, the down-regulation of miR-129-5p was detected in PC tissues and PC cells. miR-129-5p was overexpressed or knocked down in AsPC-1 and BxPC-3 cells. The results showed that miR-129-5p overexpression suppressed proliferation, migration and invasion, and induced apoptosis of PC cells, whereas miR-129-5p knockdown showed opposite effects. In addition, we found that pre–B-cell leukemia homeobox 3 (PBX3) overexpression promoted proliferation, migration and invasion, but reduced apoptosis of PC cells. PBX3 was identified as a target of miR-129-5p by informatics analysis and dual luciferase reporter assay. Finally, our results indicated that miR-129-5p suppressed cell proliferation and migration by targeting PBX3. This study demonstrated that miR-129-5p could function as a tumor suppressor in the progression and development of PC by targeting PBX3, providing a reliable prognostic factor and a new therapeutic strategy for PC.

scholarly journals cIAP1 promotes proliferation and migration and prevents apoptosis in gallbladder cancer in vitro

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Wei Su ◽  
Xiaojie Jiang ◽  
Mingyuan Chen ◽  
Maotuan Huang ◽  
Nanhong Tang ◽  
...  
Keyword(s):  
Gallbladder Cancer ◽  
Protein C ◽  
Caspase 3 ◽  
Nuclear Factor Κb ◽  
Inhibitory Protein ◽  
Tnf Α ◽  
And Migration ◽  
Induced Apoptosis ◽  
Proliferation And Migration

Abstract Gallbladder cancer (GBC) is a demanding fatal disease with no ideal treatment for inoperable patients. Recent reports have determined TNF-α associated lymphatic metastasis in GBC, while its resistance to TNF-α-killing remains largely unexplored. In this assay, we first found cellular inhibitor of apoptosis (cIAP1) overexpressed in GBC tissues and the roles in promoting the proliferation and migration of GBC in vitro as its homology cIAP2 does. Then how GBC cell survives TNF-α toxicity and TNF-α-induced apoptosis first prevail as follows. The reduction in cIAP1 does not give rise to apoptosis even with the stimulation of TNF-α. Importantly, the loss of cIAP1 enhanced TNF-α/cycloheximide-induced apoptosis in higher activation statuses of Caspase-8, Caspase-3 without the induction of Complex Ⅱ. In response to TNF-α, the reduction in cIAP1 caused the suppression in nuclear factor-κB (NF-κB) pathway and inhibition of transcription of cell death regulator cellular FLICE-like Inhibitory Protein (c-FLIP) instead. To conclude, cIAP1 is an oncological protein abundant in GBC tissues, which enhances proliferation and immigration and blocks TNF-α from apoptosis through NF-κB pathway in vitro.

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