scholarly journals Cannabidiol Effectively Promoted Cell Death in Bladder Cancer and the Improved Intravesical Adhesion Drugs Delivery Strategy Could Be Better Used for Treatment

Pharmaceutics ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1415
Author(s):  
Shanshan Chen ◽  
Changping Deng ◽  
Wenyun Zheng ◽  
Shihui Li ◽  
Yuping Liu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Molecular Mechanisms ◽  
Bladder Wall ◽  
Plga Nanoparticles ◽  
Akt Pathway ◽  
Adhesion System ◽  
Tumorigenic Activity ◽  
And Migration ◽  
Cell Transcriptome ◽  
Induced Apoptosis

Cannabidiol (CBD), a primary bioactive phytocannabinoid extracted from hemp, is reported to possess potent anti-tumorigenic activity in multiple cancers. However, the effects of CBD on bladder cancer (BC) and the underlying molecular mechanisms are rarely reported. Here, several experiments proved that CBD promoted BC cells (T24, 5637, and UM-UC-3) death. For example, T24 cells were treated with 12 µM CBD for 48 h, flow cytometry analysis demonstrated that early and late apoptotic cells were accounted for by 49.91%, indicating CBD enhanced cell apoptosis ability. To deeper explore molecular mechanisms, the CBD-treated T24 cell transcriptome libraries were established. KEGG analysis implied that the significantly changed genes were enriched in the PI3K/Akt pathway. qRT-PCR and Western blot assays verified that CBD regulated BC cells growth and migration and induced apoptosis by inactivating the PI3K/Akt pathway. Meanwhile, the developed chitosan to wrap CBD-loaded PLGA nanoparticles can significantly enhance the adhesion of the material to the mouse bladder wall, and the binding efficiency of mucin to chitosan-PLGA nanoparticles reached 97.04% ± 1.90%. In summary, this work demonstrates that CBD may become a novel reliable anticancer drug and the developed intravesical adhesion system is expected to turn into a potential means of BC chemotherapy drug delivery.

scholarly journals EGCG inhibited bladder cancer T24 and 5637 cell proliferation and migration via PI3K/AKT pathway

Oncotarget ◽  
2018 ◽  
Vol 9 (15) ◽  
pp. 12261-12272 ◽  
Author(s):  
Ke-Wang Luo ◽  
Wing-Yin Lung ◽  
Chun-Xie ◽  
Xin-Le Luo ◽  
Wei-Ren Huang
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Akt Pathway ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

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 MiR-454-3p and miR-374b-5p suppress migration and invasion of bladder cancer cells through targetting ZEB2

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Suogang Wang ◽  
Geng Zhang ◽  
Wanxiang Zheng ◽  
Qin Xue ◽  
Di Wei ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Pcr Analysis ◽  
Inhibitory Effects ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Invasion And Migration ◽  
And Migration

Bladder cancer (BCa) threatens human health due to the high occurrence and mortality. Nowadays, more and more researchers focussed on the molecular mechanisms and biological functions of miRNAs in human cancers. The present study aims to study the biological role of miR-454-3p and miR-374b-5p in BCa. The expression levels of miR-454-3p and miR-374b-5p were detected in BCa tissues and cell lines by qRT-PCR analysis. Kaplan–Meier analysis revealed that the expression levels of miR-454-3p and miR-374b-5p were positively correlated with the overall survival (OS) rate of BCa patients. Gain-of-function assays were conducted to demonstrate the inhibitory effects of miR-454-3p and miR-374b-5p on the invasion, migration, and epithelial–mesenchymal transition (EMT) of BCa cells. Mechanically, ZEB2 was found to be a target of both miR-454-3p and miR-374b-5p. Rescue assays revealed that ZEB2 reversed the inhibitory effects of miR-454-3p and miR-374b-5p on the invasion and migration of BCa cell lines. In summary, miR-454-3p and miR-374b-5p negatively regulated invasion and migration of BCa cell lines via targetting ZEB2.

scholarly journals miRNA-103 promotes chondrocyte apoptosis by down-regulation of Sphingosine kinase-1 and ameliorates PI3K/AKT pathway in osteoarthritis

2019 ◽  
Vol 39 (10) ◽  
Author(s):  
Fang Li ◽  
Jianhua Yao ◽  
Qingqing Hao ◽  
Zheping Duan
Keyword(s):  
Cell Proliferation ◽  
Molecular Mechanisms ◽  
Sphingosine Kinase ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Chondrocyte Apoptosis ◽  
Sphingosine Kinase 1 ◽  
Down Regulation ◽  
Induced Apoptosis

Abstract Objectives: The aim of the present study was to determine the effects of miRNA-103 on chondrocyte apoptosis and molecular mechanisms in osteoarthritis (OA) progression. Methods: The cell proliferation, apoptosis, and recovery ability were measured by cell counting kit-8 (CCK-8), flow cytometry, and wound healing assays. The interaction of miRNA-103 and Sphingosine kinase-1 (SPHK1) were determined by using luciferase reporter assay. The expression of mRNA and proteins were measured by qRT-PCR and Western blot. OA rat model was established by surgery stimulation. Results: miRNA-103 expression was significantly increased in the cartilage of OA patients and surgery-induced OA rat models. miRNA-103 transfection into primary rat chondrocytes reduced SPHK1 expression, induced apoptosis, inhibited cell proliferation, and impeded scratch assay wound closure. Moreover, expression of total AKT, and p-AKT were significantly reduced in miRNA-103-overexpressing chondrocytes while SPHK1 up-regulation increased the expression of phosphatidylinsitol-3-kinase (PI3K) and p-AKT, and reversed the proliferation suppression induced by the miRNA-103 mimic. Conclusions: Our studies suggest that miRNA-103 contributes to chondrocyte apoptosis, promoting OA progression by down-regulation of PI3K/AKT pathway through the reduction in SPHK1 activity.

scholarly journals LncRNA MEG3 affects cell proliferation, apoptosis and migration by targeting miR-9-5p/MDK axis and activating PDK/AKT pathway in hepatocellular carcinoma

2020 ◽  
Author(s):  
Dezhi Wu ◽  
Zheng Ma ◽  
Deyu Ma ◽  
Qiquan Li
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Normal Liver ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Normal Liver Cell ◽  
Non Coding Rna ◽  
And Migration

Abstract Background Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) was supposed to be a tumor suppressor in various cancers. However, the role of MEG3 in hepatocellular carcinoma (HCC) and the related molecular mechanisms are not well illustrated. This study aimed to determine the biological function of MEG3 in regulating HCC cell proliferation, apoptosis and migration. Moreover, the interaction among MEG3, microRNA (miR)-9-5p and Midkine (MDK), and the activation of phosphoinositide-dependent kinase (PDK)/AKT pathway in HCC cells were examined. Methods and Results Expression of MEG3 in a series of liver cancer cell lines was detected by RT-qPCR. Luciferase reporter assay, RT-qPCR and western blot were used to determine the interaction among MEG3, miR-9-5p and MDK, and the activation of PDK/AKT pathway. Cell proliferation and apoptosis were evaluated by CCK8, flow cytometry analysis for cell cycle and apoptosis, and Caspase 3/9 activity. Cell migration was determined by wound healing assay and MMP1 expression. We found MEG3 was decreased in HCC cell lines compared with the normal liver cell line. MEG3 suppressed HCC cell proliferation and migration, and induced cell apoptosis. Further, we found MEG3 targets miR-9-5p/MDK axis and modulates PDK/AKT pathway in HCC. Conclusion Our findings demonstrated that lncRNA MEG3 affects HCC cell proliferation, apoptosis and migration through its targeting of miR-9-5p/MDK and regulating of PDK/AKT pathway. This study suggested MEG3/miR-9-5p/MDK axis as the potential therapeutic target in HCC.

scholarly journals PI3K–AKT Pathway Protects Cardiomyocytes Against Hypoxia-Induced Apoptosis by MitoKATP-Mediated Mitochondrial Translocation of pAKT

2018 ◽  
Vol 49 (2) ◽  
pp. 717-727 ◽  
Author(s):  
Hua-Pei Song ◽  
Zhi-Gang Chu ◽  
Dong-Xia Zhang ◽  
Yong-Ming Dang ◽  
Qiong Zhang
Keyword(s):  
Molecular Mechanisms ◽  
Signal Pathway ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Mitochondrial Translocation ◽  
Protein Levels ◽  
Apoptotic Effect ◽  
Cellular Apoptosis ◽  
Intracellular Signal ◽  
Induced Apoptosis

Background/Aims: The phosphatidylinositol-3-kinase -AKT (PI3K-AKT) is an important intracellular signal pathway in regulating cell proliferation, differentiation and apoptosis. In previous studies, we’ve demonstrated that PI3K–AKT pathway protects cardiomyocytes from ischemic and hypoxic apoptosis through mitochondrial function. However, the molecular mechanisms underlying hypoxia-induced cardiomyocyte apoptosis via PI3K-AKT pathway remain ill-defined. Here, we addressed this question. Methods: Cardiomyocytes were exposed to hypoxia, with/without different inhibitors and then protein levels were assessed by Western blotting. Results: We found that the PI3K–AKT pathway was activated in cardiomyocytes that were exposed to hypoxia. Moreover, the phospho-AKT (pAKT) translocated from cytosol to mitochondria via mitochondrial adenosine triphosphate-dependent potassium (mitoKATP), leading to an increase in cytochrome c oxidase (CcO) activity to suppress apoptosis. On the other hand, the mitoKATP specific blocker, 5-hydroxydecanote (5-HD), or suppression of CcO using siRNA, inhibited the pAKT mitochondrial translocation to maintain the CcO activity, resulting in mitochondrial dysfunction and cellular apoptosis induced by hypoxia. Conclusion: These findings suggest that the anti-apoptotic effect of the PI3K-AKT pathway through pAKT translocation to mitochondrial via mitoKATP may be conducted through modification of CcO activity.

CLINICAL SYMPTOMS, ULTRASOUND AND HISTOPATHOLOGY OF TUMORLIKE LESIONS OF THE BLADDER.

2017 ◽  
pp. 41-46
Author(s):  
Van Mao Nguyen ◽  
Thi Bich Chi Nguyen
Keyword(s):  
Bladder Cancer ◽  
Bladder Tumor ◽  
Clinical Symptoms ◽  
Bladder Wall ◽  
Lower Abdominal Pain ◽  
University Hospital ◽  
Wall Thickening ◽  
Health Examination ◽  
Ultrasound Images ◽  
Key Words Bladder Cancer

Background: Bladder cancer is one of the most frequent type of urinary cancer which has been ever increasing. For the better treatment, the early discovery and definite diagnosis of this disease played an important role. Objective: To describe some clinical symptoms and ultrasound features of tumorlike lesions of the bladder. To diagnose and classify the histopathology of tumorlike lesions of the bladder. Materials, method: cross - sectional study on 64 cases in Hue University Hospital and Hue central hospital from April, 2016 to February, 2017. Results: Hematuria was the most common reason that patients went to hospital (79.7%). Lower abdominal pain and irritation during urination accounting for 9.4% and 6.2% respectively. Only 3 patients with bladder cancer were accidentally discovered through periodic health examination (4.7%). The characteristics of hematuria in bladder tumor was flesh red urine (62.5%) and total hematuria (60.7%). With ultrasonography, the results of 64 patients were divided in 3 groups as follow: bladder tumor, which was the highest rate 87.5%, bladder polyp was 3.1% and focal bladder wall thickening was 9.4%. Of which, the vast majority of these ultrasound images was tumor - like lesions protruding in the lumen of the bladder (75%), the rest was wall thickening lesions (25%). Tumors were different in size, the biggest tumor was 7cm in diameter and the smallest was 0.6cm. Those with the diameter 3cm or bigger accounting for 42.2%, the smaller was 57.8%. Most cases have only one lesion (62.5%) and at lateral wall (46.6%). Histopathologically, cancer was 59/64 case (92.2%): urothelial carcinoma was 98.3 %, squamous cell carcinomawas 1.7% and 5 cases (7.8%) were benign. Most cancerous cases were poorly differentiated, grade II (50.9%) and grade III (32.2%). The stage T1NxMx was 20.3% and worse than T2MxNx was 79.7%. Conclusion: hematuria was the most popular symptom, suggesting bladder cancer. Clinical diagnosing bladder cancer was not high sensitive (61.01%). Ultrasound could detect bladder tumor with high sensitive (89.8%). These patients also needed histopathology classification to diagnose and finally choose the best method for the appropriate treatment. Key words: bladder cancer, histopathology, ultrasound, uroepithelial carcinoma, hematuria

Wnt/beta-catenin and PI3K/Akt/mTOR Signaling Pathways in Glioblastoma: Two Main Targets for Drug Design: A Review

2020 ◽  
Vol 26 (15) ◽  
pp. 1729-1741 ◽  
Author(s):  
Seyed H. Shahcheraghi ◽  
Venant Tchokonte-Nana ◽  
Marzieh Lotfi ◽  
Malihe Lotfi ◽  
Ahmad Ghorbani ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Cellular Proliferation ◽  
Chemotherapy Resistance ◽  
Wnt Signaling Pathway ◽  
Therapeutic Interventions ◽  
Beta Catenin ◽  
Clinical Prognosis ◽  
Invasion And Migration ◽  
And Migration

: Glioblastoma (GBM) is the most common and malignant astrocytic glioma, accounting for about 90% of all brain tumors with poor prognosis. Despite recent advances in understanding molecular mechanisms of oncogenesis and the improved neuroimaging technologies, surgery, and adjuvant treatments, the clinical prognosis of patients with GBM remains persistently unfavorable. The signaling pathways and the regulation of growth factors of glioblastoma cells are very abnormal. The various signaling pathways have been suggested to be involved in cellular proliferation, invasion, and glioma metastasis. The Wnt signaling pathway with its pleiotropic functions in neurogenesis and stem cell proliferation is implicated in various human cancers, including glioma. In addition, the PI3K/Akt/mTOR pathway is closely related to growth, metabolism, survival, angiogenesis, autophagy, and chemotherapy resistance of GBM. Understanding the mechanisms of GBM’s invasion, represented by invasion and migration, is an important tool in designing effective therapeutic interventions. This review will investigate two main signaling pathways in GBM: PI3K/Akt/mTOR and Wnt/beta-catenin signaling pathways.

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