scholarly journals The Anti-Proliferative and Anti-Invasive Effect of Leaf Extracts of Blueberry Plants Treated with Methyl Jasmonate on Human Gastric Cancer In Vitro Is Related to Their Antioxidant Properties

Antioxidants ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 45 ◽  
Author(s):  
Alejandra Ribera-Fonseca ◽  
Danae Jiménez ◽  
Pamela Leal ◽  
Ismael Riquelme ◽  
Juan Carlos Roa ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cell ◽  
Leaf Extract ◽  
Antioxidant Properties ◽  
Human Gastric Cancer ◽  
Leaf Extracts ◽  
And Migration ◽  
Related Proteins

Gastric cancer is the third main cause of cancerous tumors in humans in Chile. It is well-accepted that a diet rich in antioxidant plants could help in fighting cancer. Blueberry is a fruit crop with a high content of antioxidants. Methyl jasmonate (MeJA) is a phytohormone involved in plant defenses under stress conditions. The exogenous application of MeJA can improve the antioxidant properties in plants. We studied in vitro and in vivo anticancer action on human gastric cancer (cell line AGS) and the antioxidant properties of extracts from blueberry plants untreated and treated with MeJA. The results demonstrated that leaf extracts displayed a higher inhibition of cancer cell viability as well as greater antioxidant properties compared to fruit extracts. Besides, MeJA applications to plants improved the antioxidant properties of leaf extracts (mainly anthocyanins), increasing their inhibition levels on cell viability and migration. It is noteworthy that leaf extract from MeJA-treated plants significantly decreased cancer cell migration and expression of gastric cancer-related proteins, mainly related to the mitogen-activating protein kinase (MAPK) pathway. Interestingly, in all cases the anticancer and antioxidant properties of leaf extracts were strongly related. Despite highlighted outcomes, in vivo results did not indicate significant differences in Helicobacter pylori colonization nor inflammation levels in Mongolian gerbils unfed and fed with blueberry leaf extract. Our findings demonstrated that MeJA increased antioxidant compounds, mainly anthocyanins, and decreased the viability and migration capacity of AGS cells. In addition, leaf extracts from MeJA-treated plants were also able to decrease the expression of gastric cancer-related proteins. Our outcomes also revealed that the anthocyanin-rich fraction of blueberry leaf extracts showed higher in vitro antiproliferative and anti-invasive effects than the crude leaf extracts. However, it is still uncertain whether the leaf extracts rich in anthocyanins of blueberry plants are capable of exerting a chemopreventive or chemoprotective effect against gastric cancer on an in vivo model.

scholarly journals miR-26a/b Inhibit Tumor Growth and Angiogenesis by Targeting the HGF-VEGF Axis in Gastric Carcinoma

2017 ◽  
Vol 42 (4) ◽  
pp. 1670-1683 ◽  
Author(s):  
Yiran Si ◽  
Haiyang Zhang ◽  
Tao Ning ◽  
Ming Bai ◽  
Yi Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Luciferase Assay ◽  
Human Gastric Cancer ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Background/Aims: Abnormal expression of HGF is found in various cancers and correlates with tumor proliferation, metastasis and angiogenesis. However, the regulatory mechanism of the HGF-VEGF axis remains unclear. Methods: The expression characteristic of HGF in human gastric cancer tissues was shown by an immunohistochemistry assay, and the expression levels of target protein were detected by Western blot. The relative levels of miR-26a/b and target mRNA were examined by qRT-PCR. We used bioinformatics tools to search for miRNAs that can potentially target HGF. A luciferase assay was used to confirm direct targeting. Furthermore, the functions of miR-26a/b and HGF were evaluated by cell proliferation and migration assays in vitro and by the mouse xenograft tumor model in vivo. Results: We found that the HGF protein was clearly increased while miR-26a/b were dramatically down-regulated in gastric cancer. miR-26a/b directly bind to the 3’-UTR of HGF mRNA at specific targeting sites. We demonstrated that the repression of the HGF-VEGF pathway by miR-26a/b overexpression suppressed gastric cancer cell proliferation and migration. Furthermore, miR-26a/b also showed an anti-tumor effect in the xenograft mouse model by suppressing tumor growth and angiogenesis. Conclusions: miR-26a/b could suppress tumor tumorigenesis and angiogenesis by targeting the HGF-VEGF axis and could serve as a potential treatment modality for targeted therapy in the clinical treatment of gastric cancer.

scholarly journals Myrrh induces the apoptosis and inhibits the proliferation and migration of gastric cancer cells through down-regulating cyclooxygenase-2 expression

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Mengxue Sun ◽  
Jie Hua ◽  
Gaoshuang Liu ◽  
Peiyun Huang ◽  
Ningsheng Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cellular Proliferation ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cox 2 ◽  
And Migration ◽  
Proliferation And Migration

Abstract Objective: The present study is designed to evaluate the anti-tumor effects of myrrh on human gastric cancer both in vitro and in vivo. Methods: The gastric cancer cell proliferation was determined by MTT assay. Apoptosis was measured by flow cytometry and Hoechst 33342 staining. Wound healing was performed to evaluate the effects of myrrh on the migration. COX-2, PCNA, Bcl-2, and Bax expressions were detected by Western blot analysis. A xenograft nude mice model of human gastric cancer was established to evaluate the anti-cancer effect of myrrh in vivo. Results: Myrrh significantly inhibited cellular proliferation, migration, and induced apoptosis in vitro as well as inhibited tumor growth in vivo. In addition, myrrh inhibited the expression of PCNA, COX-2, and Bcl-2 as well as increased Bax expression in gastric cancer cells. Conclusion: Myrrh may inhibit the proliferation and migration of gastric cancer cells, as well as induced their apoptosis by down-regulating the expression of COX-2.

Acacetin inhibits invasion, migration and TGF-β1-induced EMT of gastric cancer cells through the PI3K/Akt/Snail pathway

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Guangtao Zhang ◽  
Zhaoyan Li ◽  
Jiahuan Dong ◽  
Weili Zhou ◽  
Zhanxia Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Peritoneal Metastasis ◽  
Western Blots ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
Related Proteins ◽  
Tgf Β1

Abstract Background Epithelial-to-mesenchymal transition (EMT) is a pivotal cellular phenomenon involved in tumour metastasis and progression. In gastric cancer (GC), EMT is the main reason for recurrence and metastasis in postoperative patients. Acacetin exhibits various biological activities. However, the inhibitory effect of acacetin on EMT in GC is still unknown. Herein, we explored the possible mechanism of acacetin on EMT in GC in vitro and in vivo. Methods In vitro, MKN45 and MGC803 cells were treated with acacetin, after which cell viability was detected by CCK-8 assays, cell migration and invasion were detected by using Transwell and wound healing assays, and protein expression was analysed by western blots and immunofluorescence staining. In vivo, a peritoneal metastasis model of MKN45 GC cells was used to investigate the effects of acacetin. Results Acacetin inhibited the proliferation, invasion and migration of MKN45 and MGC803 human GC cells by regulating the expression of EMT-related proteins. In TGF-β1-induced EMT models, acacetin reversed the morphological changes from epithelial to mesenchymal cells, and invasion and migration were limited by regulating EMT. In addition, acacetin suppressed the activation of PI3K/Akt signalling and decreased the phosphorylation levels of TGF-β1-treated GC cells. The in vivo experiments demonstrated that acacetin delayed the development of peritoneal metastasis of GC in nude mice. Liver metastasis was restricted by altering the expression of EMT-related proteins. Conclusion Our study showed that the invasion, metastasis and TGF-β1-induced EMT of GC are inhibited by acacetin, and the mechanism may involve the suppression of the PI3K/Akt/Snail signalling pathway. Therefore, acacetin is a potential therapeutic reagent for the treatment of GC patients with recurrence and metastasis.

scholarly journals Silencing of EphA2 inhibits invasion of human gastric cancer SGC-7901 cells in vitro and in vivo

Neoplasma ◽  
2012 ◽  
Vol 59 (01) ◽  
pp. 105-113 ◽  
Author(s):  
W. Yuan ◽  
Z. Chen ◽  
Z. Chen ◽  
S. Wu ◽  
J. Guo ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Human Gastric Cancer

scholarly journals Evaluation of Antioxidant Properties ofPhaulopsis fascisepalaC.B.Cl. (Acanthaceae)

2009 ◽  
Vol 6 (2) ◽  
pp. 227-231 ◽  
Author(s):  
S. A. Adesegun ◽  
A. Fajana ◽  
C. I. Orabueze ◽  
H. A. B. Coker
Keyword(s):  
Ascorbic Acid ◽  
Leaf Extract ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Reducing Power ◽  
Total Phenolic ◽  
Chelating Ability

The antioxidant activities of crude extract ofPhaulopsis fascisepalaleaf were evaluated and compared with α-tocopherol and BHT as synthetic antioxidants and ascorbic acid as natural-based antioxidant.In vitro, we studied its antioxidative activities, radical-scavenging effects, Fe2+-chelating ability and reducing power. The total phenolic content was determined and expressed in gallic acid equivalent. The extract showed variable activities in all of thesein vitrotests. The antioxidant effect ofP. fascisepalawas strongly dose dependent, increased with increasing leaf extract dose and then leveled off with further increase in extract dose. Compared to other antioxidants used in the study, α-Tocopherol, ascorbic acid and BHT,P. fascisepalaleaf extract showed less scavenging effect on α,α,-diphenyl-β-picrylhydrazyl (DPPH) radical and less reducing power on Fe3+/ferricyanide complex but better Fe2+-chelating ability. These results revealed thein vitroantioxidant activity ofP.fascisepala.Further investigations are necessary to verify these activitiesin vivo.

scholarly journals CDK10 Regulates Gastric Cancer Metastasis By Inhibiting lncRNA-C5ORF42-5 Via Phosphorylation Level of AKT/ERK

2021 ◽  
Author(s):  
Zi-Jian Deng ◽  
Dong-Wen Chen ◽  
Xi-Jie Chen ◽  
Jia-Ming Fang ◽  
Liang Xv ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
High Throughput ◽  
Cancer Metastasis ◽  
High Throughput Sequencing ◽  
Gastric Cancer Cells ◽  
Related Proteins

Abstract Background: Gastric cancer is the fourth most common malignant disease. Both CDK10 and long noncoding RNAs (lncRNAs) have been found to exert biological functions in multiple cancers. However, it is still unclear whether CDK10 represses tumor progression in gastric cancer by reducing potential targeting lncRNAs.Methods: The functions of CDK10 and lncRNA-C5ORF42-5 in proliferation, invasion and migration were assessed by MTS assays, colony formation assays, cell cycle and apoptosis assays, Transwell assays, wound healing assays and animal experiments. We used high-throughput sequencing to confirm the existence of lncRNA-C5ORF42-5 and quantitative real-time PCR was used to evaluate lncRNA expression. Then, with RNA-seq sequencing as well as GO function and KEGG enrichment analysis, we identified the signaling pathways in which lncRNA-C5ORF42-5 was involved in gastric cancer. Finally, western blotting was used to identify the genes regulated by lncRNA-C5ORF42-5.Results: Our results showed that CDK10 is expressed at relatively low levels in gastric cancer cell lines and inhibits the progression of gastric cancer cells both in vitro and in vivo. Next, based on high-throughput sequencing, we identified a novel lncRNA, lncRNA-C5ORF42-5, in the stable CDK10-overexpressing cell line compared with the CDK-knockdown cell line and their controls. Additionally, we confirmed that lncRNA-C5ORF42-5 acts as an oncogene to promote metastasis in gastric cancer in vitro and in vivo. We then ascertained that lncRNA-C5ORF42-5 is a major contributor to the function of CDK10 in gastric cancer metastasis by upregulating lncRNA-C5ORF42-5 to reverse the effects of CDK10 overexpression. Finally, we explored the mechanism by which lncRNA-C5ORF42-5 overexpression affects gastric cancer cells to elucidate whether lncRNA-C5ORF42-5 may increase the activity of the SMAD pathway of BMP signaling and promote the expression of EMT-related proteins, such as E-cadherin. Additionally, overexpression of lncRNA-C5ORF42-5 affected the phosphorylation levels of AKT and ERK.Conclusion: Our findings suggest that CDK10 overexpression represses gastric cancer tumor progression by reducing lncRNA-C5ORF42-5 and hindering activation of the related proteins in metastatic signaling pathways, which provides new insight into developing effective therapeutic strategies in the treatment of metastatic gastric cancer.

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