scholarly journals Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Hua Zhang ◽  
Pingling Lin ◽  
Lei Fu ◽  
Zhijun Li ◽  
Yan Ding
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Experimental Conditions ◽  
Cell Progression ◽  
Related Proteins ◽  
Dose Dependent

Background. Propofol is an anesthetic commonly used clinically and has been found to have antitumor activity in various cancers. The purpose of this study was to investigate the role of propofol in hepatoblastoma (HB). Methods. CCK-8 and transwell were used to measure cell proliferation, migration, and invasion in HB cells. Cell apoptosis rate was measured by FCM. The expression of CCL18 in HB tissues and cells was detected by RT-qPCR. Western blotting was used to explore the protein expression of CCK18- and PI3K/AKT-related proteins. Results. The expression of CCL18 in HB tissues and cells was overexpressed compared with control groups. CCL18 knockdown was found to notably block cell proliferation and progression, while enhancing cell apoptosis in HuH-6 and HepT1 cells. Furthermore, propofol suppressed the proliferation of HB cells in a dose-dependent manner. According to the results, we chose 5 μg/mL of propofol-treated cells for 48 hours as the subsequent experimental conditions. We found that propofol (5 μg/mL, 48 h) significantly blocked cell migration and invasion, but induced cell apoptosis in HuH-6 and HepT1 cells. In addition, CCK18 overexpression facilitated cell progression in HB cells, while propofol dramatically suppressed the effect of CCK18. Besides that, propofol suppressed the PI3K/AKT pathway. Conclusion. Propofol suppressed the development of HB cells by inhibiting CCK18 expression and the PI3K/AKT pathway. Therefore, we infer that propofol plays a role in the treatment of HB.

Plantamajoside Inhibits Hepatic Carcinoma Cell Proliferation, Migration, Invasion and Induces Apoptosis Through Regulating Phosphatidylinositol-3-Kinase/ Protein Kinase B Pathway

2020 ◽  
Vol 10 (5) ◽  
pp. 662-668
Author(s):  
Yiqun Zhou ◽  
Yong Tan ◽  
Zheng Shi ◽  
Renshou Chen
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Biological Activities ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Hepatic Carcinoma ◽  
Plantago Asiatica ◽  
Related Proteins ◽  
Hcc Cells

Background: Plantamajoside (PMS) is the main active compound of Plantago asiatica . It is a traditional Chinese medicine and has been reported to have various biological activities. However, the function of PMS on hepatic carcinoma cells (HCC) and the potential mechanism of action still remains unevaluated. Here, we investigated the effect of PMS on HCC cells and the potential molecular mechanism. Methods: Firstly, HCC cells were treated with different dose of PMS (0, 20, 80 and 160 g/ml). Then, cell viability was determined by MTT assay. Furthermore, we investigated the cell apoptosis, migration and invasion by flow cytometry assay and Transwell assay. In addition, PI3K/AKT related proteins p-AKT and AKT were determined via Western blotting assay. Results: Our results showed that PMS dose-dependently reduced HCC cell viability. PMS also induced HCC cell apoptosis, up-regulated the expression of Bax and down-regulated expression of Bcl-2. In addition, the Bcl-2/Bax ratio was also decreased. The migration and invasion of HCC cells were also consistently suppressed by PMS treatment in a dose-dependent manner. Subsequently, the results indicated that PMS down-regulated the expression of p-AKT, suggesting the inhibition of the PI3K/AKT pathway in HCC progression. Conclusion: The results indicated that PMS could inhibit HCC progression through regulating cell viability, apoptosis, migration, invasion and PI3K/AKT pathway. Thus, PMS might be a hopeful pharmacological agent for the treatment of hepatic carcinoma.

FOXD3 inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma through regulation of the PI3K–Akt pathway

2020 ◽  
Vol 98 (6) ◽  
pp. 653-660 ◽  
Author(s):  
Xiaoxing Xie ◽  
Gaoyun Xiong ◽  
Wenjun Chen ◽  
Hongdan Fu ◽  
Mingqian Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Cell Apoptosis ◽  
Inhibitory Effect ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Inhibitory Effects ◽  
Protein Levels ◽  
Flow Cytometric ◽  
Phosphoinositide 3 Kinase

FOXD3 has been found previously to positively regulate miR-26b, a tumor inhibitor of nasopharyngeal carcinoma (NPC). However, FOXD3’s precise function and associated mechanism of action in NPC have not yet been investigated. In this study, the expression of FOXD3 mRNA and protein was evaluated using RT-qPCR, western blotting, and immunohistochemistry. Protein levels involved in the phosphoinositide 3-kinase – protein kinase B (PI3K–Akt) pathway were assessed by western blot, and cell proliferation was determined by MTT and colony forming assays. Additionally, cell apoptosis was assessed by flow cytometric assay. Finally, the migration and invasion capabilities of the NPC cells were determined using wound healing and Transwell assays. We found that FOXD3 levels were relatively low in NPC tissue and cells, while an increase caused the inhibition of the PI3K–Akt pathway. Functional experiments found that overexpression of FOXD3 suppressed cell proliferation, migration, and invasion and enhanced cell apoptosis in NPC C6661 cells. IGF-1, an activator of the PI3K–Akt pathway, reversed the inhibitory effect of FOXD3. Furthermore, we found upregulation of the PI3K–Akt pathway and upregulation of the inhibitory effects of FOXD3 on C6661 cellular activities. In conclusion, FOXD3 negatively affected the PI3K–Akt pathway to restrain the processes involved in C6661 cell pathology. These findings further exposed the function and downstream axis of FOXD3 in NPC and displayed a promising new target for NPC therapy.

scholarly journals Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Shihua Ding ◽  
Shaohui Tang ◽  
Min Wang ◽  
Donghai Wu ◽  
Haijian Guo
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Sw620 Cells ◽  
Role Of It

Background and Aims. Acyl-CoA synthetase 5 (ACS5) has been reported to be associated with the development of various cancers, but the role of it in colorectal cancer (CRC) is not well understood. The present study aimed to explore the potential role of ACS5 in the development and progression of CRC. Methods. ACS5 expression in CRC tissues and CRC cell lines was examined, and its clinical significance was analyzed. The role of ACS5 in cell proliferation, apoptosis, and invasion was examined in vitro. Results. We found that ACS5 expression was upregulated in CRC cells and CRC tissues and that high ACS5 expression was more frequent in CRC patients with excess muscular layer and with poor tumor differentiation. Furthermore, knockdown of ACS5 in HT29 and SW480 cells significantly dampened cell proliferation, induced cell apoptosis, and reduced cell migration and invasion. In contrast, the ectopic overexpression of ACS5 in LOVO and SW620 cells remarkably promoted cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion. Enhanced cell growth and invasion ability mediated by the gain of ACS5 expression were associated with downregulation of caspase-3 and E-cadherin and upregulation of survivin and CD44. Conclusions. Our data demonstrate that ACS5 can promote the growth and invasion of CRC cells and provide a potential target for CRC gene therapy.

scholarly journals MicroRNA-19b-3p promotes cell proliferation and osteogenic differentiation of BMSCs by interacting with lncRNA H19

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Gan Xiaoling ◽  
Liu Shuaibin ◽  
Liang Kailu
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Postmenopausal Osteoporosis ◽  
Critical Role ◽  
Dependent Manner ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
17Β Estradiol ◽  
Dose Dependent

Abstract Background To investigated the role of miR-19b-3p in regulating bone marrow mesenchymal stem cell (BMSC) proliferation and osteoblast differentiation. Methods The expression of miR-19b-3p and lncRNA H19 were measured in postmenopausal osteoporosis patients and BMP-22 induced BMSCs using qRT-PCR. MiR-19b-3p mimic or inhibitor was transfected into BMP-2 induced BMSCs. Cell proliferation was measured by BrdU method. Protein expression of RUNX2 and COL1A1 were measured by western blot. PcDNA3.1-lncRNA H19 with or without miR-19b-3p mimic was transfected into BMP-2 induced BMSCs. Results The expression of miR-19b-3p was significantly up-regulated in postmenopausal osteoporosis patients and BMP-2 induced BMSCs. MiR-19b-3p overexpression dramatically elevated, while miR-19b-3p inhibition decreased cell proliferation of BMSCs. Additionally, protein expression levels of RUNX2 and COL1A1, as well as ALP activity were significantly promoted by miR-19b-3p mimic transfection and inhibited by miR-19b-3p inhibitor transfection. LncRNA H19 was obviously down-regulated in postmenopausal osteoporosis patients. H19 overexpression significantly decreased cell proliferation and differentiation by down-regulating miR-19b-3p. Moreover, the expression of miR-19b-3p was inhibited, while H19 elvated in 17β-estradiol (E2) treated BMSCs in a dose-dependent manner. Conclusion These data were the first to reveal the critical role of H19/miR-19b-3p in postmenopausal osteoporosis, and provided a new therapeutic target for OP.

scholarly journals Glucocorticoids induce the expression of the uteroglobin gene in rabbit foetal lung explants cultured in vitro

1985 ◽  
Vol 225 (1) ◽  
pp. 255-258 ◽  
Author(s):  
M S López de Haro ◽  
A Nieto
Keyword(s):  
Cell Proliferation ◽  
Developmental Regulation ◽  
Dependent Manner ◽  
Total Proteins ◽  
Foetal Lung ◽  
Dose Dependent

In 27-day-old rabbit foetal lung explants cultured in vitro, the synthesis of the protein uteroglobin decreased progressively during several days of culture. Addition of glucocorticoids to the medium progressively induced the synthesis of uteroglobin in a dose-dependent manner without affecting the synthesis of total proteins. The glucocorticoid-mediated induction of uteroglobin appears mainly due to increased amounts of uteroglobin mRNA and seems to be independent of simultaneous cell proliferation, suggesting a glucocorticoid-triggered differentiation of pre-existing cells. The results suggest a major role of glucocorticoids in the developmental regulation of the uteroglobin gene in the lung.

scholarly journals LncRNA HAND2-AS1 inhibits proliferation and promotes apoptosis of non-small cell lung cancer cells by inactivating PI3K/Akt pathway

2020 ◽  
Vol 40 (11) ◽  
Author(s):  
Ting Gao ◽  
Xiaoqiang Dai ◽  
Yindi Jiang ◽  
Xiaopeng He ◽  
Shuli Yuan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Akt Pathway ◽  
Healthy Controls ◽  
Small Cell Lung ◽  
Nsclc Patients ◽  
Related Proteins

Abstract Background: Non-small cell lung cancer (NSCLC) is a major subtype of lung cancer and is correlated with high incidence and mortality rate. Functionality of lncRNA HAND2-AS1 is only reported in endometrioid endometrial carcinoma and osteosarcoma. In our study, the role of HAND2-AS1 in NSCLC was investigated. Methods: We first detected the expression of HAND2-AS1 in lung tissues and serum of both NSCLC patients and healthy controls by qRT-PCR. Correlation between HAND2-AS1 expression level and clinical data of NSCLC patients was analyzed by Chi-square test. NSCLC cells, and cell proliferation, cell apoptosis and expression of PI3K/Akt pathway-related proteins were detected by CCK-8 assay, cell apoptosis assay and Western blot, respectively. Results: HAND2-AS1 expression was significantly down-regulated in NSCLC. HAND2-AS1 and tumor size of NSCLC patients were closely associated. Serum HAND2-AS1 can be used to effectively distinguish osteosarcoma patients from healthy controls, and it can also be used to predict prognosis of osteosarcoma patients. HAND2-AS1 overexpression inhibited osteosarcoma cell proliferation, promoted cell apoptosis, and down-regulated phosphorylation of PI3K/Akt pathway-related proteins. PI3K/Akt pathway inhibitor showed no significant effects on HAND2-AS1 expression, but reduced its effects on cell proliferation and apoptosis. Conclusion: We conclude that HAND2-AS1 may suppress the proliferation of NSCLC cells by targeting PI3K/Akt pathway.

Celastrol inhibits the proliferation and induces apoptosis of colorectal cancer cells via downregulating NF-κB/COX-2 signaling pathways

2021 ◽  
Vol 21 ◽  
Author(s):  
Hua Zhang ◽  
Xiaojin Zhao ◽  
Fajun Shang ◽  
Huan Sun ◽  
Xu Zheng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Cycle Arrest ◽  
The World ◽  
Cox 2

Background: Colorectal cancer (CRC) is the third-ranked malignant tumor in the world that contributes to the death of a major population of the world. Celastrol, a bioactive natural product isolated from the medicinal plant Tripterygium wilfordii Hook F, has been proved to be an effective anti-tumor inhibitor for multiple tumors. Objective: To reveal the therapeutic effect and underlying mechanisms of celastrol on CRC cells. Methods: CCK-8 and clonogenic assay were used to analyze the cell proliferation in CRC cells. Flow cytometry analysis was conducted to assess the cell cycle and cell apoptosis. Wound-healing and cell invasion assay were used to evaluate the migrating and invasion capability of CRC cells. The potential antitumor mechanism of celastrol was investigated by qPCR, western blot, and confocal immunofluorescence analyses. Results: Celastrol effectively inhibited CRC cell proliferation by activating caspase-dependent cell apoptosis and facilitating G1 cell cycle arrest in a dose-dependent manner, as well as cell migration and invasion by downregulating the MMP2 and MMP9. Mechanistic protein expression revealed that celastrol suppressed the expression of COX-2 by inhibiting the phosphorylation of NF-κB p65 and subsequently leading to cytoplasmic retention of p65 protein, thereby inhibiting its nuclear translocation and transcription activities. Conclusion: These findings indicate that celastrol is an effective inhibitor for CRC, regulating the NF-κB/COX-2 pathway, leading to the inhibition of cell proliferation characterized by cell cycle arrest and caspase-dependent apoptosis, providing a potential alternative therapeutic agent for CRC patients.

scholarly journals Effects of Jiawei Shaoyao-Gancao Decoction and Its Drug-Containing Serum on Proliferation, Apoptosis, and Ultrastructure of Human Adenomyosis Foci Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Yu-yan Zeng ◽  
Kun-yin Li
Keyword(s):  
Electron Microscopy ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Chromatin Condensation ◽  
Primary Cultures ◽  
Cell Ultrastructure ◽  
Dependent Manner ◽  
Transmission Electron ◽  
Dose Dependent ◽  
Insight Into

Objective. The present study aimed to investigate the effects of Jiawei Shaoyao-Gancao Decoction (JSGD) and its drug-containing serum (CDS) on the proliferation, apoptosis, and ultrastructure of human adenomyosis foci cells. Methods. Primary cultures of human adenomyosis foci cells were prepared from hard uterine lesions of adenomyosis patients. The cells were treated with JSGD (10 and 20 mg/ml), CDS, and mifepristone (MIF) for 24 or 48 h. Cell proliferation was detected using CCK-8 assay, cell apoptosis was measured by flow cytometry, and the cell ultrastructure was observed by transmission electron microscopy (TEM). Results. JSGD and CDS significantly induced cell apoptosis and inhibited cell proliferation for 24 h or 48 h, in which the effects of JSGD were in a dose-dependent manner. The effect of CDS for 24 h was higher than that of CDS for 48 h. Moreover, JSGD and CDS treatments induced marked apoptosis in adenomyosis foci cells, characterized by nucleus chromatin, condensation, fragmentation, mitochondria and endoplasmic swelling, and autophagy-lysosome. Conclusions. JSGD and CDS can suppress proliferation and induce apoptosis in adenomyosis foci cells, through altering their ultrastructure. The results provided support for JSGD and CDS in the treatment of adenomyosis and gained further insight into the effect of this prescription.

Curcumin Inhibits Pancreatic Cancer Progression via Down-Regulation of miR-21-5p

2020 ◽  
Vol 18 (3) ◽  
pp. 236-240
Author(s):  
Li Junjian ◽  
Xu Qigang ◽  
Tao Chonglin
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
B Cell ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Promote Cell Proliferation ◽  
Pancreatic Cancer Cells

In this study, we investigated the role of curcumin in pancreatic cancer through the regulation of miR-21-5p. We first evaluated the expression of miR-21-5p in pancreatic cancer cells (ASPC-1) treated with different concentrations of curcumin. The results showed that curcumin effectively inhibited the expression of miR-21-5p in ASPC-1 cells in a dose-dependent manner. B cell translocation gene 2 was identified as a target gene of miR-21-5p. MiR-21-5p mimics could promote cell proliferation, migration, and invasion of ASPC-1, as well as decrease the expression of B cell translocation gene 2. Curcumin treatment inhibited cell proliferation, migration and invasion of ASPC-1, as well as increased the expression of B cell translocation gene 2. MiR-21-5p could reverse the inhibitory activities of curcumin on ASPC-1 cell proliferation, migration, and invasion. In conclusion, curcumin is capable of inhibiting the proliferation, migration and invasion of pancreatic cancer cells via down-regulating miR-21-5p-mediated B cell translocation gene 2.

scholarly journals KCNQ1OT1 aggravates cell proliferation and migration in bladder cancer through modulating miR-145-5p/PCBP2 axis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jingyu Wang ◽  
Hao Zhang ◽  
Jie Situ ◽  
Mingzhao Li ◽  
Hua Sun
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Apoptosis ◽  
Critical Role ◽  
Migration And Invasion ◽  
Western Blot Assay ◽  
Non Coding Rnas ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background The large involvement of long non-coding RNAs (LncRNAs) in the biological progression of numerous cancers has been reported. The function of lncRNA KCNQ1OT1 in bladder cancer (BC) remains largely unknown. This study aimed to explore the critical role of KCNQ1OT1 in BC. Materials and methods The qRT-PCR was applied to test the expression of RNAs. Cell proliferation was detected by CCK-8 and colony formation assays. Cell apoptosis was measured by TUNEL and flow cytometry experiments. Wound healing and transwell assays were employed to evaluate cell migration and invasion ability respectively. Western blot assay was used to measure relevant protein expression. Immunofluorescence (IF) staining was used to observe EMT process in BC. Results KCNQ1OT1 was significantly overexpressed in BC tissue and cell lines. KCNQ1OT1 depletion repressed cell proliferation, migration and invasion, whereas encouraged cell apoptosis. KCNQ1OT1 was a negatively/positively correlated with miR-145-5p/PCBP2 in respect with expression. Mechanically, KCNQ1OT1 was sponge of miR-145-5p and up-regulated the expression of PCBP2. MiR-145-5p inhibition and PCBP2 up-regulation could countervail the tumor-inhibitor role of KCNQ1OT1 knockdown in BC. Conclusion KCNQ1OT1 serves as competing endogenous RNA (ceRNA) to up-regulate PCBP2 via sponging miR-145-5p in BC progression.

Sign in / Sign up

Export Citation Format

Share Document