scholarly journals Bioactivity and Apoptotic Efficacy of the Purified Terpenoid Extract from the Moss Brachythecium Buchananii (Hook.) A. Jaeger against MG 63 Cells

2020 ◽  
pp. 287-294
Author(s):  
Geetha Mohandas Greeshma ◽  
Gopal Sarayu Manoj ◽  
Kumaraswamy Murugan
Keyword(s):  
Cell Lines ◽  
Biological Effects ◽  
Mg63 Cell ◽  
Migration And Invasion ◽  
Antioxidant Enzyme System ◽  
Apoptotic Protein ◽  
Human Osteosarcoma Cells ◽  
Mg63 Cells ◽  
Caspase Cascade ◽  
Induced Apoptosis

Bryophytes are primitive non vascular plants. A little is explored regarding the medicinal effects of bryophytes on carcinoma. This study investigated the biological effects of purified terpenoids from Brachythecium buchananii on selected cell lines such as HeLa, MDAMB-231 and MG63 human osteosarcoma cells and also elucidating the regu­latory signaling pathways underlying the effects of terpenoids towards caspase cascade and the antioxidant enzyme system. The cell lines were treated with various concentrations of purified terpenoid extracts interms of evaluating viability (MTT assay). Interestingly, MG63 cell lines showed poor viability as compared to other ongo cells and was subjected to further molecular evaluations. Migration and invasion assay results using wound-healing and transwell assays, respectively reveal the pro-antimetastatic potential of the purified terpenoids from the moss. The flow cytometry study substantiated terpenoid induced apoptosis in MG63 cells. Cell cycle analysis revealed the significant increase in the number of cells arrested at the S growth phase. Terpenoid extract also displayed DNA fragmentation in the cells. Western blot analysis revealed the down regulation of the anti‑apoptotic proteins Bcl‑2, pro‑caspase 3 and over expression of the pro‑apoptotic protein Bax. In addition, the caspase cascade profile of the terpenoid extract substantiated their efficacy in tumour inhibition. Thus, the overall results confirmed the biological features of terpenoid induced apoptosis in the MG63 cells.

11-O-Galloyl Bergenin from Corylopsis coreanas Leaves Induces Autophagy and Apoptosis in Human Osteosarcoma

2021 ◽  
Vol 49 (08) ◽  
pp. 2017-2031
Author(s):  
Kyung-Ran Park ◽  
Yoon-Ju Kwon ◽  
Myounglae Cho ◽  
Il Keun Kwon ◽  
Jin Tae Hong ◽  
...  
Keyword(s):  
Annexin V ◽  
Mg63 Cell ◽  
Underlying Mechanism ◽  
Mapk Signaling ◽  
Migration And Invasion ◽  
Boyden Chamber ◽  
Antitumor Effects ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Induced Apoptosis

Osteosarcoma is the most common malignant bone-forming tumor, wherein most patients with high grade osteosarcomas are treated with chemotherapy. Despite this, survival for metastatic or relapsed osteosarcoma patients has remained at an overall 5-year survival rate of 20%. In particular, the extracts of Corylopsis coreana (Korean winter hazel), a cultivated woody plant in South Korea, have shown beneficial anti-inflammatory, anti-oxidative, anti-osteoclastic, and antihyperuricemic properties. Therefore, this study aimed to demonstrate the antitumor activities and underlying mechanism of 11-O-Galloyl bergenin (OGAL) isolated from Corylopsis coreanas leaves in human osteosarcoma cells. Herein, we found that OGAL inhibited MG63 cell proliferation and induced cellular apoptosis as evidenced by cleaved-PARP, cleaved-caspase 3, TUNEL-positive cells, and Annexin V-positive cells. Specifically, OGAL-induced apoptosis was accompanied by p53 and p21 upregulation, BAX expression, and decreased Bcl-2 and cdk2. Moreover, OGAL induced autophagy via AKT inactivation, LC3II upregulation, and MG63 cell autophagosome formation. OGAL-induced autophagy was also accompanied by increased p38 phosphorylation, whereas JNK and ERK1/2 activities were found to be unaffected upon examining the MAPK signaling pathway. Furthermore, wound healing and Boyden chamber assays showed that OGAL suppressed MG63 cell migration and invasion. Given these findings, this study provided evidence that OGAL has antitumor effects by apoptosis and autophagy enhancement through increased p53, AKT, and p38 signaling, suggesting that OGAL may be a potential therapeutic strategy for osteosarcoma treatment.

scholarly journals TUFT1 promotes osteosarcoma cell proliferation and predicts poor prognosis in osteosarcoma patients

2018 ◽  
Vol 13 (1) ◽  
pp. 396-403 ◽  
Author(s):  
Yao-Ping Yu ◽  
Jian-Guo He ◽  
Ping Li ◽  
Ning-Hui Qiu ◽  
Li-Jun Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Mg63 Cell ◽  
Mapk Signaling ◽  
Gene Expression Omnibus ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Mg63 Cells

AbstractObjectiveThis study is aimed at exploring the role of TUFT1 in osteosarcomas.MethodsWe investigated the expression of TUFT1 in osteosarcoma cell lines and explored the correlation between TUFT1 expression and prognosis in osteosarcoma patients based on the expression data downloaded from Gene Expression Omnibus (GEO) website. The effects of TUFT1 on osteosarcoma cell proliferation, migration and invasion were investigated by silencing TUFT1 in osteosarcoma MG63 cell line. Finally, western blot was performed to determine the expression changes of MAPK signaling pathway related proteins after silencing TUFT1.ResultsWe found that the expression of TUFT1 was significantly up-regulated in osteosarcoma cell lines compared with the normal control. Using Kaplan-Meier analysis, we identified that high TUFT1 expression was positively correlated with poor prognosis in osteosarcoma patients. Furthermore, knockdown of TUFT1 remarkably inhibited MG63 cell proliferation, migration and invasion. Using western blot analysis, we found that the phosphorylation levels of MEK and ERK were reduced obviously in MG63 cells after silencing TUFT1 (p<0.01).ConclusionsOur results demonstrated that TUFT1 plays a promoting role in MG63 cell proliferation and metastasis and has the potential to be a predictor as well as a therapeutic target for osteosarcoma patients.

scholarly journals Sevoflurane represses the migration and invasion of gastric cancer cells by regulating forkhead box protein 3

2021 ◽  
Vol 49 (4) ◽  
pp. 030006052110059
Author(s):  
Fangfang Yong ◽  
Hemei Wang ◽  
Chao Li ◽  
Huiqun Jia
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Control Group ◽  
Gastric Cancer Cells ◽  
Cell Migration And Invasion ◽  
Forkhead Box ◽  
Induced Apoptosis

Objective Previous studies suggested that sevoflurane exerts anti-proliferative, anti-migratory, and anti-invasive effects on cancer cells. To determine the role of sevoflurane on gastric cancer (GC) progression, we evaluated its effects on the proliferation, migration, and invasion of SGC7901, AGS, and MGC803 GC cells. Methods GC cells were exposed to different concentrations of sevoflurane (1.7, 3.4, or 5.1% v/v). Cell viability, migration, and invasion were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. Immunohistochemical staining and immunoblotting were performed to analyze forkhead box protein 3 (FOXP3) protein expression in tissue specimens and cell lines, respectively. Results FOXP3 was downregulated in human GC specimens and cell lines. Functionally, FOXP3 overexpression significantly inhibited the proliferation, migration, and invasion of GC cells and accelerated their apoptosis. Moreover, sevoflurane significantly blocked GC cell migration and invasion compared with the findings in the control group. However, FOXP3 silencing neutralized sevoflurane-induced apoptosis and the inhibition of GC cell migration and invasion. Sevoflurane-induced apoptosis and the suppression of migration and invasion might be associated with FOXP3 overactivation in GC cells. Conclusions Sevoflurane activated FOXP3 and prevented GC progression via inhibiting cell migration and invasion in vitro.

scholarly journals Rhotekin 2 silencing inhibits proliferation and induces apoptosis in human osteosarcoma cells

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Xiong Wang ◽  
Lei Zhang ◽  
Wenji Wang ◽  
Yuchen Wang ◽  
Ye Chen ◽  
...  
Keyword(s):  
Cell Lines ◽  
Phase Cell ◽  
Osteosarcoma Cell ◽  
Cyclin Dependent Kinase ◽  
Potential Therapeutic Target ◽  
Human Osteosarcoma ◽  
Cycle Arrest ◽  
Human Osteosarcoma Cells ◽  
Human Osteosarcoma Cell ◽  
Induced Apoptosis

Human osteosarcoma is the most frequent primary malignant of bone, and often occurs in adolescents. However, molecular mechanism of this disease remains unclear. In the present study, we found that the level of Rhotekin 2 (RTKN2) was up-regulated in osteosarcoma tissues and cell lines. In addition, silencing of RTKN2 of human osteosarcoma cell lines U2OS, inhibited proliferation, and induced G1 phase cell cycle arrest via reducing the level of the cyclin-dependent kinase 2 (CDK2). Furthermore, RTKN2 knockdown in the U2OS cells induced apoptosis by increasing the level of Bax and decreasing the level of Bcl2. These results suggested that RTKN2 is involved in the progression of human osteosarcoma, and may be a potential therapeutic target.

scholarly journals Antiproliferative Properties of Oleuropein in Human Osteosarcoma Cells

2016 ◽  
Vol 11 (4) ◽  
pp. 1934578X1601100 ◽  
Author(s):  
Jose M. Moran ◽  
Olga Leal-Hernandez ◽  
Maria L. Canal-Macías ◽  
Raul Roncero-Martin ◽  
Rafael Guerrero-Bonmatty ◽  
...  
Keyword(s):  
Cell Lines ◽  
Osteosarcoma Cell ◽  
Dependent Manner ◽  
Osteosarcoma Cells ◽  
Probit Regression ◽  
Cytotoxic Effects ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Mg63 Cells ◽  
Human Osteosarcoma Cell

In this study, we evaluated the antiproliferative activity on two human osteosarcoma cell lines (MG-63 and Saos2) of oleuropein, an olive oil compound traditionally found in the Mediterranean diet. Oleuropein exhibited obvious cytotoxic effects on human osteosarcoma cells in a concentration- and time-dependent manner. Statistical analysis of IC50 by the Probit regression method suggested that oleuropein had similar toxic effects on both cell lines tested (IC50 range from 247.4–475.0 μM for MG63 cells and from 798.7–359.9 μM for Saos2 cells).

JS-K, a GST-Activated Nitric Oxide Generator, Induces Apoptosis and Overcomes In Vitro Drug Resistance in Multiple Myeloma Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1593-1593
Author(s):  
Tanyel Kiziltepe ◽  
Kenji Ishitsuka ◽  
Teru Hideshima ◽  
Noopur Raje ◽  
Norihiko Shiraishi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Multiple Myeloma ◽  
Drug Resistance ◽  
Tumor Cells ◽  
Cell Lines ◽  
Biological Effects ◽  
Treatment Modalities ◽  
Cancer Drug ◽  
Induced Apoptosis

Abstract Multiple myeloma (MM) is currently an incurable hematological malignancy. A major reason for the failure of currently existing therapies is the chemotherapeutic resistance acquired by the MM cells upon treatment. Overexpression of glutathione S-transferases (GST) has been shown as one possible mechanism of anti-cancer drug resistance in a broad spectrum of tumor cells. JS-K (O2-(2,4-Dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate) belongs to a class of pro-drugs which are designed to release nitric oxide (NO) on reaction with GST. JS-K can possibly turn GST overexpression to the tumor’s disadvantage by (1) consuming intracellular GSH and preventing drug inactivation; and (2) by exposing tumor cells to high intracellular concentrations of NO. JS-K has potent in vitro and in vivo anti-leukemic activity. The purpose of the present study is to examine the biological effects of JS-K on human MM cells. We demonstrate that JS-K has significant in vitro cytotoxicity on MM cell lines, with an IC50 of 0.3-2 mM at 48 hours. JS-K also induces cytotoxicity on cell lines that are resistant to conventional chemotherapy (i.e., MM1R, RPMI-Dox40, RPMI-LR5, RPMI-MR20). Importantly, no cytotoxic effects of JS-K were detected on peripheral blood mononuclear cells (PBMNC) obtained from healthy volunteers at these doses. Moreover, JS-K could overcome the survival and growth advantages conferred by interleukin-6 (IL-6) and insulin-like growth factor-1 (IGF-1), or by adherence of MM cells to bone marrow stromal cells (BMSC). JS-K caused a transient G2/M arrest followed by apoptosis, as determined by flow cytometric analysis using PI, Annexin V and Apo2.7 staining. JS-K-induced apoptosis was associated with caspase 8, 7, 9 and 3 activation. Interestingly, Fas was upregulated by JS-K, suggesting the involvement of death receptor pathway in induction of apoptosis. JS-K also triggered Mcl-1 cleavage and Bcl-2 phosphorylation, suggesting the involvement of mitochondrial pathway. In addition, apoptosis inducing factor (AIF), endonuclease G (EndoG) and cytochrome c were released into the cytosol during apoptosis. Taken together, these findings suggest the involvement of both intrinsic and extrinsic apoptotic pathways in JS-K-induced apoptosis in MM cells. In summary, our studies demonstrate that JS-K induces apoptosis and overcomes in vitro drug resistance in MM cells. Therefore, JS-K is a novel compound which carries significant potential to be included in the repertoire of existing treatment modalities for MM. Ongoing studies are delineating the mechanism of action of JS-K to provide the preclinical rationale for combination therapies to overcome drug resistance and improve patient outcome.

Long Non-Coding Sprouty4-Intronic Transcript 1 (SPRY4-IT1) Regulates Cancer Biological Effects and Cisplatin Sensitivity in Cervical Cancer

2019 ◽  
Vol 9 (6) ◽  
pp. 789-796
Author(s):  
Hui Cai ◽  
Hongmei Deng
Keyword(s):  
Cervical Cancer ◽  
Cell Lines ◽  
Cancer Progression ◽  
Biological Effects ◽  
Scratch Test ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Potential Biomarker ◽  
Cisplatin Sensitivity ◽  
And Migration

Background: Emerging evidences have revealed that Long noncoding RNAs (LncRNAs) is crucial for cancer progression. Previous studies have elucidated that patients with higher LncRNA SPRY4IT1 was more advanced. This study aims to investigate the biological effects of LncRNA SPRY4-IT1 and preliminary explore the effects of LncRNA SPRY4-IT1 on cisplatin sensitivity. Materials and methods: Quantitative reverse transcriptase PCR was used to validate the expression of SPRY4IT1. Cell migration and invasion were detected by scratch test and Transwell assay. Cell cytometry was performed for cell apoptosis. The expression of proteins was evaluated by immunoblotting. The drug sensitivity was measured by CCK-8. Results: LncRNA SPRY4-IT1 was significantly expressed in cervical cancer cell lines compared to normal cells. Downregulation of LncRNA SPRY4-IT1 in cervical cancer cells suppress the cell viability, cell invasion and migration and promoted apoptosis. In addition, decreases of LncRNA SPRY4-IT1 enhanced the cisplatin sensitivity in cervical cell lines. Conclusion: LncRNA SPRY4-IT1 is a potential biomarker and therapy target for cervical cancer.

scholarly journals LINC01094/miR-577 axis regulates the progression of ovarian cancer

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Jing Xu ◽  
Ping Zhang ◽  
Huajun Sun ◽  
Yang Liu
Keyword(s):  
Ovarian Cancer ◽  
Cyclin D1 ◽  
Cell Lines ◽  
Cancer Biology ◽  
Biological Effects ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Gene Assay

Abstract Background Long intergenic non-coding RNA 01094 (LINC01094) is probably a novel regulator in cancer biology. This study aimed to probe into the function and mechanism of LINC01094 in ovarian cancer (OC). Methods Quantitative real-time polymerase chain reaction (qRT-PCR) assay was utilized to measure LINC01094 and miR-577 expressions in OC tissues and cell lines. Western blot was used to examine the expressions of epithelial-mesenchymal transition (EMT)-related proteins, β-catenin, c-Myc and cyclin D1. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect the proliferation, migration and invasion of SKOV3 and 3AO cells, respectively. Eventually, dual-luciferase reporter gene assay was employed to detect the regulatory relationship between miR-577 and LINC01094. Results LINC01094 expression was elevated in OC tissues and cell lines. High LINC01094 expression was associated with higher FIGO stage, lymph node metastasis and the shorter overall survival rate in patients with OC. Meanwhile, LINC01094 knockdown inhibited OC cell proliferation, migration, invasion and EMT. In addition, miR-577 was demonstrated to be a direct downstream target of LINC01094 in OC and inhibition of miR-577 reversed the biological effects of LINC01094 knockdown on OC cells. Additionally, LINC01094 / miR-577 axis regulated the expressions of β-catenin, c-Myc and cyclin D1 in OC cells. Conclusion LINC01094 promotes the proliferation, migration, invasion and EMT of OC cells by adsorbing miR-577.

scholarly journals miR-10b Downregulated by DNA Methylation Acts as a Tumor Suppressor in HPV-Positive Cervical Cancer via Targeting Tiam1

2018 ◽  
Vol 51 (4) ◽  
pp. 1763-1777 ◽  
Author(s):  
Miaomei Yu ◽  
Yun Xu ◽  
Lili Pan ◽  
Yuehua Feng ◽  
Kaiming Luo ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Biological Effects ◽  
Migration And Invasion ◽  
Normal Tissues ◽  
Underlying Mechanisms ◽  
Induced Apoptosis ◽  
Methylation Ratio ◽  
Invasion Assays

Background/Aims: microRNAs (miRNAs) are known to act as oncogenes or tumor suppressors in diverse cancers. Although miR-10b is an oncogene implicated in many tumors, its role in cervical cancer (CC) remains largely unclear. Here, we investigated the function and underlying mechanisms of miR-10b in human CC. Methods: Quantitative RT-PCR was used to measure miR-10b expression in CC and normal tissues, and its association with clinicopathologic features was analyzed. Methylation of CpG sites in the miR-10b promoter was analyzed by methylation sequencing. Cell proliferation, apoptosis, migration, and invasion assays were used to elucidate the biological effects of miR-10b and expression of the target gene was assayed with Western blot. Results: miR-10b was downregulated in CC tissues compared with normal tissues, and less miR-10b expression was associated with larger tumors, vascular invasion and HPV-type 16 positivity. miR-10b expression decreased in HeLa (HPV18-positive) and SiHa (HPV16-positive) cells compared with C-33A (HPV-negative), but increased after treatment with 5-Aza-CdR. Methylation ratio of site -797 in the miR-10b promoter in C-33A was lower than that in HeLa and SiHa. Further analysis indicates that site -797 is located within a transcription factor AP-2A (TFAP2A) binding element. Functionally, overexpression of miR-10b in HeLa and SiHa suppressed cell proliferation, migration and invasion, and induced apoptosis and miR-10b downregulation had opposite effects. Mechanistically, T-cell lymphoma invasion and metastasis 1 (Tiam1) was identified as a direct and functional target of miR-10b. Conclusion: miR-10b acts as a tumor suppressor in CC by suppressing oncogenic Tiam1, and its expression may be downregulated through methylation of TFAP2A binding element by HPV.

scholarly journals MicroRNA-103 Promotes Proliferation and Inhibits Apoptosis in Spinal Osteosarcoma Cells by Targeting p57

2018 ◽  
Vol 26 (6) ◽  
pp. 933-940 ◽  
Author(s):  
Xuesong Wang ◽  
Yong Lin ◽  
Lei Peng ◽  
Ruifu Sun ◽  
Xiaojin Gong ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Reporter Assay ◽  
Osteosarcoma Cells ◽  
Binding Effect ◽  
Mg63 Cells

Osteosarcoma is one of the most aggressive malignancies with poor prognosis rates. Many studies have demonstrated that miRNAs were involved in osteosarcoma, but the role of miR-103a in osteosarcoma remains elusive. In this study, we detected the expression levels of miR-103 in osteosarcoma and non-osteosarcoma tissues and cell lines. The binding effect of miR-103 on p57 was detected by luciferase reporter assay. After altering expressions of miR-103 or p57, viability, migration, invasion, and apoptosis of MG63 cells and expressions of proteins related with the JNK/STAT and mTOR pathways were all detected. We found the higher expression of miR-103 in osteosarcoma tissues and cell lines compared with non-osteosarcoma tissues and cell lines. miR-103 overexpression promoted survival, migration, and invasion of MG63 cells. Knockdown of miR-103a inhibited cell survival, migration, and invasion by upregulating the expression of p57, which was a target of miR-103. Moreover, miR-103a overexpression activated the JNK/STAT and mTOR pathways probably through inhibiting p57 expression. In conclusion, miR-103a acted as an oncogene in osteosarcoma, probably through activating the JNK/STAT and mTOR pathways by inhibiting p57 expression.

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