iridoids has been researched along with Stomach-Neoplasms* in 9 studies
1 review(s) available for iridoids and Stomach-Neoplasms
1 trial(s) available for iridoids and Stomach-Neoplasms
8 other study(ies) available for iridoids and Stomach-Neoplasms
Article | Year |
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Impact of Amarogentin on Gastric Carcinoma Cell Multiplication, Apoptosis and Migration via circKIF4A/miR-152-3p.
The active ingredients extracted from natural plants have anti-GC actions and can slow down gastric carcinoma (GC) progression. To investigate the impact of Amarogentin (AG) on GC cell multiplication, apoptosis and migration and the possible mechanisms.. qRT-PCR quantification of circKIF4A and miR-152-3p in GC tissues and normal counterparts as well as HGC-27 (human GC cell strain) and GES-1 (human gastric mucosal epithelial cell strain) was performed. HGC-27 cells were intervened by AG of various concentrations. si-NC, si-circKIF4A were further transfected into HGC-27 cells. Besides, pcDNA and pcDNA-circKIF4A were transfected into HGC-27 cells, after which 60 mmol/L AG was added for intervention. Cell multiplication, clone formation, as well as apoptosis and migration measurements were made by MTT, plate clone formation, flow cytometry and Transwell assays, respectively; Double luciferase reporter assay was performed for targeting relationship identification between circKIF4A and miR-152-3p; Western blots were carried out to measure Bax and Bcl-2 protein levels.. circKIF4A increased (P <0.05) and miR-152-3p decreased (P <0.05) in GC tissues and cell strains. Concentration-dependently, AG intervention contributed to enhanced cell multiplication inhibitory rate, apoptosis rate, miR-152-3p expression and Bax protein level (P <0.05), together with declined number of cell clones formed, migrating cells, circKIF4A expression and Bcl-2 protein level (P <0.05). After transfection of si-circKIF4A, cell multiplication inhibition rate, apoptosis rate and Bax protein level enhanced (P <0.05), while cell clones formed and migrating cells as well as Bcl-2 protein level reduced (P <0.05). miR-152-3p can be controlled by circKIF4A; pcDNA-circKIF4A transfection antagonized AG's effects on HGC-27 cell multiplication, clone formation, apoptosis and migration.. AG can decrease GC multiplication, clone formation and migration and induce apoptosis via modulating circKIF4A/miR-152-3p expression. Topics: Apoptosis; bcl-2-Associated X Protein; Carcinoma; Cell Line, Tumor; Cell Movement; Cell Proliferation; Gene Expression Regulation, Neoplastic; Humans; Iridoids; MicroRNAs; Proto-Oncogene Proteins c-bcl-2; Stomach Neoplasms | 2022 |
Genipin induces mitochondrial dysfunction and apoptosis via downregulation of Stat3/mcl-1 pathway in gastric cancer.
Genipin is a compound derived from gardenia fruit extract. Although Genipin has anti-tumor effects in various cancers, its effect and mechanism in gastric cancer remain unclear. Here, we investigated the relationship between the anticancer effect of Genipin and signal transducer and activator of transcription (Stat3)/myeloid cell leukemia-1 (Mcl-1) in human gastric cancers.. MTT assays were performed to determine the cell viability of gastric cancer and gastric epithelial cell lines (AGS, MKN45, SNU638, MKN74, HFE-145). A TUNEL assay and Western blotting were carried out to investigate apoptosis. Stat3 activity was measured by proteome profiler phospho kinase array, immunofluorescence and immunoblotting. Mitochondria function was monitored with an XF24 analyzer and by flow cytometry, confocal microscopy using fluorescent probes for general mitochondrial membrane potential (MMP).. Genipin induced apoptosis in gastric cancer cells, including AGS and MKN45 cells. Genipin also reduced Mcl-1 mRNA and protein levels. Furthermore, we found that phosphorylation of Stat3 is regulated by Genipin. Additionally, the protein level of phospho Janus kinase 2 (JAK2) was decreased by Genipin treatment, indicating that the Stat3/JAK2/Mcl-1 pathway is suppressed by Genipin treatment in gastric cancer cells. Mcl-1 is closely related to mitochondrial function. These findings suggest that Genipin contributes to the collapse of mitochondrial functions like MMP.. Genipin induced apoptosis by suppressing the Stat3/Mcl-1 pathway and led to mitochondrial dysfunction. Our results reveal a novel mechanism for the anti-cancer effect of Genipin in gastric cancer. Topics: Apoptosis; Cell Line, Tumor; Cell Proliferation; Cell Survival; Down-Regulation; Gene Knockdown Techniques; Humans; Iridoids; Janus Kinase 2; Membrane Potential, Mitochondrial; Mitochondria; Myeloid Cell Leukemia Sequence 1 Protein; Phosphorylation; Signal Transduction; STAT3 Transcription Factor; Stomach Neoplasms; Transfection | 2019 |
Geniposide suppresses growth, migration and invasion of MKN45 cells by down-regulation of lncRNA HULC.
Gastric cancer (GC) is a serious disease with high incidence rate and high mortality. Geniposide (GEN) exhibits multiple biological properties including anti-tumor function. However, effect of GEN on GC is not well studied. Hence, the effects of GEN on GC were investigated in our study. HULC expression in GC tissue and GC cell lines (MKN45, SGC-7901, MKN28, AGS) was detected by qRT-PCR. Cell viability, colony formation, migration, invasion and cell apoptosis were examined by CCK-8 assay, survival fraction assay, modified two-chamber migration assay, Millicell Hanging Cell Culture and flow cytometry analysis, respectively. The expression of matrix metalloproteinase (MMP)-2/9 and vimentin was detected by qRT-PCR and western blot, respectively. The expression of PI3K/AKT and JNK was measured by western blot. The expression of HULC was up-regulated both in GC tissue and cell lines (P < .05, P < .01 or P < .001). GEN negatively regulated the expression of HULC in MKN45 cells (P < .05 or P < .01). GEN decreased cell viability (P < .05), colony formation (P < .01), migration (P < .05) and invasion (P < .05) while HULC overexpression led to the opposite results in GEN-treated cells. The expression of phosphatidylinositol 3' -kinase (PI3K)/ protein kinase B (AKT) and c-Jun N-terminal kinase (JNK) was down-regulated by GEN (all P < .05) while reversed by HULC overexpression. HULC was up-regulated in GC. GEN inhibited MNK45 cell viability, colony formation, migration and invasion while induced cell apoptosis by down-regulation of HULC in MKN45 cells. GEN inactivated PI3K/AKT and JNK signal pathways through down-regulation of HULC. Topics: Adult; Apoptosis; Cell Movement; Cell Proliferation; Down-Regulation; Female; Humans; Iridoids; Male; Middle Aged; RNA, Long Noncoding; Signal Transduction; Stomach Neoplasms | 2018 |
Impact of high-dose oleuropein on cisplatin-induced oxidative stress, genotoxicity and pathological changes in rat stomach and lung.
The current systemic treatments of the various solid tumors involve Cisplatin (CIS)-based chemotherapy. Due to its cytotoxicity, this approach is limited. Moreover, the safety of CIS is only discussed especially in breast and stomach cancers. Therefore, we, for the first time, explored the restorative efficacy of oleuropein (OLE), in stomach and lung injuries induced by CIS. Sprague-Dawley rats were divided into eight groups: control CIS, OLE and CIS + OLE. Single dose of (7 mg/kg) CIS was administered intraperitoneally to CIS and CIS + OLE groups. After 24 h, 50, 100 and 200 mg/kg OLE was given for three consecutive days to OLE and CIS + OLE groups. The 8-OH-dG, total oxidative/antioxidant status (TOS/TAS) and malondialdehyde (MDA) levels were evaluated and histopathological analyses were performed on the studied tissues. The results indicated that CIS significantly increased 8-OH-dG, MDA and TOS levels and caused severe tissue damages. However, high dose of OLE induced a significant decrease in the 8-OH-dG, MDA levels, an increase in TAS levels and it restores CIS-induced tissue damages. We hope that the results of this study will provide an impetus for future studies on novel therapeutic strategies including the protective use of oleuropein in gastric and lung cancers due to chemotherapy. Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Antioxidants; Cisplatin; Deoxyguanosine; DNA Damage; Iridoid Glucosides; Iridoids; Lung Neoplasms; Male; Malondialdehyde; Molecular Structure; Oxidative Stress; Rats; Rats, Sprague-Dawley; Stomach Neoplasms | 2017 |
Chemopreventive Properties of Genipin on AGS Cell Line via Induction of JNK/Nrf2/ARE Signaling Pathway.
Roles of dietary phytochemicals in cancer chemoprevention via induction of nuclear factor-erythroid-2-related factor 2 (Nrf2)-mediated antioxidant enzymes have been well established in a number of studies. In this study, FACS analysis was used to reveal that the intracellular reactive oxygen species level decreased at 0-25 μM of genipin treatment. Furthermore, immunofluorescence analysis and Western blotting were used to demonstrate that genipin treatment resulted in the upregulation and nuclear translocation of Nrf2, as well as upregulation of gastrointestinal glutathione peroxidase. Finally, we found that C-Jun-NH2-kinase (JNK) was also dose-dependently activated, where depleting JNK by using a biochemical inhibitor indicated that JNK was upstream of Nrf2. Interestingly, the antioxidant effects were limited to the treatment in the lower dosage of genipin, where higher dosage of genipin treatment resulted in the increased reactive oxygen species level and cytotoxicity. Thus, this study demonstrates for the first time that lower dosage of genipin results in the induction of JNK/Nrf2/ARE signaling pathway and protection from cell death. Topics: Adenocarcinoma; Anticarcinogenic Agents; Cell Line, Tumor; Humans; Iridoids; JNK Mitogen-Activated Protein Kinases; MAP Kinase Signaling System; NF-E2-Related Factor 2; Oxidative Stress; Reactive Oxygen Species; Response Elements; Stomach Neoplasms | 2016 |
Genipin as a novel chemical activator of EBV lytic cycle.
Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus that causes acute infection and establishes life-long latency. EBV causes several human cancers, including Burkitt's lymphoma, nasopharyngeal and gastric carcinoma. Antiviral agents can be categorized as virucides, antiviral chemotherapeutic agents, and immunomodulators. Most antiviral agents affect actively replicating viruses, but not their latent forms. Novel antiviral agents must be active on both the replicating and the latent forms of the virus. Gardenia jasminoides is an evergreen flowering plant belonging to the Rubiaceae family and is most commonly found growing wild in Vietnam, Southern China, Taiwan, Japan, Myanmar, and India. Genipin is an aglycone derived from an iridoid glycoside called geniposide, which is present in large quantities in the fruit of G. jasminoides. In this study, genipin was evaluated for its role as an antitumor and antiviral agent that produces inhibitory effects against EBV and EBV associated gastric carcinoma (EBVaGC). In SNU719 cells, one of EBVaGCs, genipin caused significant cytotoxicity (70 μM), induced methylation on EBV C promoter and tumor suppressor gene BCL7A, arrested cell-cycle progress (S phases), upregulated EBV latent/lytic genes in a dose-dependent manner, stimulated EBV progeny production, activated EBV F promoter for EBV lytic activation, and suppressed EBV infection. These results indicated that genipin could be a promising candidate for antiviral and antitumor agents against EBV and EBVaGC. Topics: Antineoplastic Agents; Antiviral Agents; Apoptosis; Cell Cycle; Cell Line, Tumor; DNA Methylation; Gene Expression Regulation, Viral; HEK293 Cells; Herpesvirus 4, Human; Humans; Iridoids; Microfilament Proteins; Oncogene Proteins; Promoter Regions, Genetic; S Phase; Stomach Neoplasms; Viral Proteins; Virus Latency; Virus Replication | 2015 |
Induction of apoptosis by genipin inhibits cell proliferation in AGS human gastric cancer cells via Egr1/p21 signaling pathway.
Natural compounds are becoming important candidates in cancer therapy due to their cytotoxic effects on cancer cells by inducing various types of programmed cell deaths. In this study, we investigated whether genipin induces programmed cell deaths and mediates in Egr1/p21 signaling pathways in gastric cancer cells. Effects of genipin in AGS cancer cell lines were observed via evaluation of cell viability, ROS generation, cell cycle arrest, and protein and RNA levels of p21, Egr1, as well as apoptotic marker genes. The cell viability of AGS cells reduced by genipin treatment via induction of the caspase 3-dependent apoptosis. Cell cycle arrest was observed at the G2/M phase along with induction of p21 and p21-dependent cyclins. As an upstream mediator of p21, the transcription factor early growth response-1 (Egr1) upregulated p21 through nuclear translocation and binding to the p21 promoter site. Silencing Egr1 expression inhibited the expression of p21 and downstream molecules involved in apoptosis. We demonstrated that genipin treatment in AGS human gastric cancer cell line induces apoptosis via p53-independent Egr1/p21 signaling pathway in a dose-dependent manner. Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Cell Survival; Cyclin-Dependent Kinase Inhibitor p21; Dose-Response Relationship, Drug; Drug Screening Assays, Antitumor; Humans; Iridoids; Molecular Structure; Repressor Proteins; Signal Transduction; Stomach Neoplasms; Structure-Activity Relationship | 2015 |
Gardenia jasminoides Ellis ethanol extract and its constituents reduce the risks of gastritis and reverse gastric lesions in rats.
In this study we investigated the effects of Gardenia jasminoides Ellis (GJE) extract and its constituents, such as ursolic acid and genipin, on gastritis in rats and the growth of human gastric cancer cells. The GJE extract, ursolic acid and genipin showed the acid-neutralizing capacities, the antioxidant activities, and the inhibitory effects on the growth of Helicobacter pylori (H. pylori), which are almost equivalent to positive control compounds. In addition, the GJE extract and ursolic acid had cytotoxic activity against AGS and SUN638 gastric cancer cells. The genipin and ursolic acid inhibited significant HCl/ethanol-induced gastric lesions. Taken together, GJE extract and its constituents might have antigastritic activities, associated with the antioxidant activities, acid-neutralizing capacities, and anti-H. pylori action. Also, we could suggest that genipin and ursolic acid may be useful for the treatment and/or protection of gastritis. Topics: Animals; Anti-Ulcer Agents; Antineoplastic Agents, Phytogenic; Antioxidants; Cell Line, Tumor; Ethanol; Free Radical Scavengers; Gardenia; Gastritis; Helicobacter Infections; Helicobacter pylori; Indicators and Reagents; Iridoid Glycosides; Iridoids; Lipid Peroxidation; Male; Plant Extracts; Rats; Rats, Sprague-Dawley; Solvents; Stomach Neoplasms; Stomach Ulcer; Triterpenes; Ursolic Acid | 2009 |