Gastric Cancer MGC-803 Cells Research Articles

Bufalin inhibits the growth and epithelial to mesenchymal transition of human gastric cancer cells via modulation of MEK/ERK pathway

This study was designed to evaluate the anti-cancer effects of bufalin against the human gastric cancer cells and unveil the underlying mechanism. The results showed that bufalin inhibited the proliferation and colony formation of the MGC-803 gastric cancer cells and exhibited an IC50 of 10 μM. These antiproliferative effects were found to be due to the induction of G2/M cell cycle arrest. The G2/M cell cycle arrest was also concomitant with inhibition of cdc2, cdc25 and cyclin B1. Furthermore, bufalin suppressed the epithelial-to-mesenchymal transition, migration, and invasion of the MGC-803 gastric cancer cells. The Western blot analysis revealed that bufalin exerted its effects via deactivation of EK/ERK signaling pathway. Taken together, these results suggest the potential of bufalin as the lead molecule for the development of chemotherapy for gastric cancer.

Влияние биринапанта на экспрессию маркерных протеинов, коррелирующее с ингибированием пролиферации и инвазии клеток MGC-803 рака желудка

Влияние биринапанта на экспрессию маркерных протеинов, коррелирующее с ингибированием пролиферации и инвазии клеток MGC-803 рака желудка

GPER1 Silencing Suppresses the Proliferation, Migration, and Invasion of Gastric Cancer Cells by Inhibiting PI3K/AKT-Mediated EMT.

G protein coupled estrogen receptor (GPER1) is a membrane estrogen receptor, belonging to the seven-transmembrane G protein-coupled receptors family, and has important biological functions in cancer. However, the functional role of GPER1 in gastric cancer (GC) remain incompletely understood. In the present study, we employed gene set enrichment analysis and discovered that GPER1 expression was concomitant with EMT process and was positively correlated with activation of the PI3K/AKT pathway in GC. Knockdown of GPER1 with siRNA suppressed the proliferation, migration, and invasion of AGS and MGC-803 GC cells. Knockdown of GPER1 also downregulated the mesenchymal markers N-cadherin and vimentin, upregulated E-cadherin, an epithelial marker, and suppressed expression of the Snail, Slug and Twist1 transcription factors, indicating that knockdown of GPER1 inhibited EMT. Moreover, 740Y-P, a PI3K activator, reversed the effects of GPER1 knockdown on EMT processes. Overexpression of GPER1 with plasmid can further prove these findings. In summary, these data demonstrate that GPER1 inhibition suppresses the proliferation, migration, and invasion of gastric cancer cells by inhibiting PI3K/AKT-mediated EMT. Our study elucidated the function of GPER1 in gastric cancer, and we identified PI3K/AKT-mediated EMT as a novel mechanism by which GPER1 contributes to proliferation, migration, and invasion of gastric cancer. These data suggest that combining inhibition of GPER1 and PI3K may be a potential therapeutic approach to inhibit gastric cancer metastasis.

Gramine-based structure optimization to enhance anti-gastric cancer activity

Gramine is a natural indole alkaloid with a wide range of biological activities, but its anti-gastric cancer activity is poor. Herein, a pharmacophore fusion strategy was adopted to design and synthesize a new series of indole-azole hybrids on the structural basis of gramine. Based on our previous studies, different nitrogen-containing five-membered heterocyclic rings and terminal alkyne group were introduced into the indole-based scaffold to investigate their effect on improving the anti-gastric cancer activity of gramine derivatives. Structure-activity relationship (SAR) studies highlighted the role played by terminal alkyne in enhancing the inhibitory effect, and compound 16h displayed the best antiproliferative activity against gastric cancer MGC803 cells with IC50 value of 3.74 μM. Further investigations displayed compound 16h could induce mitochondria-mediated apoptosis, and caused cell cycle arrest at G2/M phase. Besides, compound 16h could inhibit the metastasis ability of MGC803 cells. Our studies may provide a new strategy for structural optimization of gramine to enhance anti-gastric cancer activity, and provide a potential candidate for the treatment of gastric cancer.

LncRNA FAM230B Promotes Gastric Cancer Growth and Metastasis by Regulating the miR-27a-5p/TOP2A Axis.

Long non-coding RNAs serve as key components of competing endogenous RNA (ceRNA) networks that underlie tumorigenesis. We investigated the pathogenic roles of lncRNA FAM230B and its molecular mechanism in gastric cancer (GC). The levels of FAM230B expression in five gastric cancer cell lines and in human gastric mucosal cells were compared by quantitative RT-PCR. To analyze the function of FAM230B in GC, we overexpressed FAM230B in AGS cells, silenced FAM230B in MGC-803 cells, and tested the effect of FAM230B on tumor growth in nude mice. The interaction between miR-27a-5p and FAM230B was predicted by a bioinformatics analysis and then verified with a dual-luciferase reporter assay. We also further investigated the role and mechanism of FAM230B by forcing overexpression of miR-27a-5p in MGC-803 gastric cancer cells. We found that FAM230B was highly expressed in gastric cancer cell lines and mainly located in the cytoplasm. FAM230B overexpression promoted the proliferation, migration, and invasion of AGS cells and repressed their apoptosis; it also facilitated tumor growth in vivo. In contrast, FAM230B knockdown suppressed the proliferation, migration, and invasion of MGC0803 cells, but enhanced their apoptosis and inhibited tumor growth in vivo. MiR-27a-5p expression was suppressed by FAM230B overexpression in AGS cells. MiR-27a-5p inhibited the proliferation, migration, and invasion of gastric cancer cells, and promoted the apoptosis of gastric cancer cells by reducing TOP2A (topoisomerase 2 alpha) expression. Our study showed that lncRNA FAM230B might function to promote GC. FAM230B functioned as a ceRNA by sponging miR-27a-5p and enhancing TOP2A expression.

Abstract 5914: URI participates in cisplatin-induced DNA damage repair of gastric cancer cells via the ATM/CHK2 pathway

Abstract Gastric cancer is the most common gastrointestinal malignant tumor and also the second leading cause of cancer-related mortality worldwide. Given its high rate of non- symptoms at early stage, gastric cancer is usually diagnosed at middle or advanced stage with metastasis. Therefore, chemotherapy, including Cisplatin, becomes a main treatment option, in addition to surgery. However, it is not uncommon for patients to develop cisplatin resistance which limits its clinical applications. URI, a prefoldin family member and also an oncoprotein, has been shown to promote multiple cancer development, including gastric cancer. The aim of this study was to investigate how URI may participate in the DNA damage repair of gastric cancer cells induced by Cisplatin and its possible mechanism via the ATM/CHK2 pathway. URI knockdown cell lines from gastric cancer cells MGC-803 and SGC-7901 were established and treated with different concentrations of Cisplatin. Cell viability, proliferation and apoptosis were analyzed by CCK-8, EDU assay, and flow cytometry respectively. DNA injury marker H2AX were examined by qRT-PCR and Western blot analysis. Comet assay was used to detect the DNA damage. The results showed that URI knockdown reduces cell viability and proliferation, as well as the Cisplatin-induced apoptosis of gastric cancer cells. Cisplatin dose responsively induced DNA damage in gastric cancer cells and URI knockdown enhanced this damage as indicated by comet assay and increased γH2AX expression. We have also detected increased levels of P-ATM and P-CHK2 in gastric cancer cells treated with Cisplatin, while URI knockdown decreased the P-ATM and P-CHK2 expression after the cells were treated with cisplatin for 12 hours. Taken together, our results support that URI reduces DNA damage and promotes DNA repair of gastric cancer cells induced by cisplatin and therefore, enhances its resistance possibly via the ATM/CHK2 pathway Citation Format: Huiqin Bian, Yaojuan Lu, Yu Gu, Xiaojing Zhang, Lichun Sun, Junxia Gu, Qiping Zheng. URI participates in cisplatin-induced DNA damage repair of gastric cancer cells via the ATM/CHK2 pathway [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 5914.

ANP reduced Hedgehog signaling-mediated activation of matrix metalloproteinase-9 in gastric cancer cell line MGC-803.

Gastric cancer is the most common malignant tumor. Most patients suffering from gastric cancer die of metastasis. The role of Atrial natriuretic peptide (ANP) in inhibiting and eliminating kinds of cancer cells has been reported. Aberrant activation of Hedgehog (Hh) signaling pathway contributes to initiation and progression of various malignancies. We have previously reported that the inhibitor of Hh, cyclopamine, reduces the metastatic activity of MGC-803 via inhibiting the expression of matrix metalloproteinases (MMP)-9. It remains to be further demonstrated that ANP has the suppressive effects on invasion and metastasis in gastric cancer via Hh-mediated MMP-9 production. Transwell, western blot, qRT-PCR were used after application of ANP on MGC-803 gastric cancer cells to determine the levels of cell migration and invasion, protein levels of MMP-9 and Hh, as well as mRNAs of MMP-9 and Hh, respectively. It was demonstrated that the migration and invasion were significantly lower, MMP-9 and Hh as well as their mRNAs were lower as well, in ANP-treated MGC-803 gastric cancer cells than those in control. The expression of MMP-9 induced by aberrant activation of Hh in MGC-803 was inhibited by ANP, which may contribute to the inhibition of cell migration and invasion. These results suggested the potential of ANP to be used in gastric cancer therapy as an inhibitor targetting Hh signaling pathway to inhibit the proliferation as well as invasion and metastasis of gastric cancer.

Cyclin-Dependent Kinase 1 (CDK1) is Co-Expressed with CDCA5: Their Functions in Gastric Cancer Cell Line MGC-803.

BackgroundGastric cancer (GC) is a worldwide malignancy and the molecular mechanism of the GC carcinogenesis has not been fully elucidated. Our previous study suggested CDCA5 played a role in GC development via regulating cell proliferation, migration, and apoptosis in GC cells.Material/MethodsHere, we first carried out bioinformatics analysis and found cyclin-dependent kinase 1 (CDK1) was possibly associated with CDCA5 using STRING. Then, the expression levels of CDK1 and CDCA5 in cancer tissues were estimated through Oncomine and The Cancer Genome Atlas (TCGA) database. After that, functional experiments were exerted to detect the association of CDK1 and CDCA5. Finally, cell proliferation assay, colon formation assay, cell scratch assay, transwell migration and invasion assays were applied to explore the roles of CDK1 and CDCA5 in GC cells MGC-803.ResultsCDK1 and CDCA5 were both upregulated and co-expressed in GC tissues. The expression of CDK1 and CDCA5 in MGC-803 was positively related. CDK1 or CDCA5 inhibition can suppress the proliferation, colon formation, migration, and invasion abilities of GC cells.ConclusionsCo-expression of CDK1 and CDCA5 might confer cell proliferation, migration, and invasion abilities in GC cells, and this can provide some clues for further therapies of gastric tumors.

Kang-Ai Injection Inhibits Gastric Cancer Cells Proliferation through IL-6/STAT3 Pathway.

To explore the mechanisms underlying the proliferative inhibition of Chinese herbal medicine Kang-Ai injection (KAI) in gastric cancer cells. Gastric cancer cell lines MGC803 and BGC823 were treated by 0, 0.3%, 1%, 3% and 10% KAI for 24, 48 and 72 h, respectively. The cell proliferation was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. The apoptosis and cell cycle were evaluated by flow cytometry. Interleukin (IL)-6 mRNA and protein expression levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immune sorbent assay (ELISA), respectively. The protein expression levels of cyclin A, cyclin E, cyclin B1, cyclin D1, p21, retinoblastoma (RB), protein kinase B (AKT), extracellular regulated protein kinases (ERK), signal transducer and activator of transcription (STAT) 1 and STAT3 were detected by Western blot. KAI inhibited the proliferation of MGC803 and BGC823 gastric cancer cells in dose- and time-dependent manner. After treated with KAI for 48 h, the proportion of G1 phase was increased, expression level of cyclin D1 and phosphorylation-RB were down-regulated, whereas the expression of p21 was up-regulated (all P<0.01). Furthermore, 48-h treatment with KAI decreased the phosphorylation level of STAT3, inhibited the mRNA and protein expressions of IL-6 (all P<0.01). IL-6 at dose of 10 ng/mL significantly attenuated the proliferative effect of both 3% and 10% KAI, and recovered KAI-inhibited STAT3 phosphorylation and cyclin D1 expression level (all P<0.01). KAI exerted an anti-proliferative function by inhibiting IL-6/STAT3 signaling pathway followed by the induction of G1 phase arrest in gastric cancer cells.

Resistance to FGFR1-targeted therapy leads to autophagy via TAK1/AMPK activation in gastric cancer.

Fibroblast growth factor receptor 1 (FGFR1) is frequently dysregulated in various tumors. FGFR inhibitors have shown promising therapeutic value in several preclinical models. However, tumors resistant to FGFR inhibitors have emerged, compromising therapeutic outcomes by demonstrating markedly aggressive metastatic progression; however, the underlying signaling mechanism of resistance remains unknown. We established FGFR inhibitor-resistant cell models using two gastric cancer (GC) cell lines, MGC-803 and BGC-823. RNA-seq was performed to determine the continuous cellular transcriptome changes between parental and resistant cells. We explored the mechanism of resistance to FGFR inhibitor, using a subcutaneous tumor model and GC patient-derived tumor organotypic culture. We observed that FGFR1 was highly expressed in GC and FGFR1 inhibitor-resistant cell lines, demonstrating elevated levels of autophagic activity. These resistant cells were characterized by epithelial-mesenchymal transition (EMT) required to facilitate metastatic outgrowth. In drug-resistant cells, the FGFR1 inhibitor regulated GC cell autophagy via AMPK/mTOR signal activation, which could be blocked using either pharmacological inhibitors or essential gene knockdown. Furthermore, TGF-β-activated kinase 1 (TAK1) amplification and metabolic restrictions led to AMPK pathway activation and autophagy. In vitro and in vivo results demonstrated that the FGFR inhibitor AZD4547 and TAK1 inhibitor NG25 synergistically inhibited proliferation and autophagy in AZD4547-resistant cell lines and patient-derived GC organotypic cultures. We elucidated the molecular mechanisms underlying primary resistance to FGFR1 inhibitors in GC, and revealed that the inhibition of FGFR1 and TAK1 signaling could present a potential novel therapeutic strategy for FGFR1 inhibitor-resistant GC patients.

Porous Cu(II)-organic framework for solvent-free cyanosilylation and anti-gastric cancer activity by inducing cell apoptosis

A novel metal–organic framework (MOF) containing Cu(II) ions with the chemical formula of {[Cu(L)2(H2O)2](DMF)3}n (1) was successfully prepared by solvothermal reaction method using metal Cu2+ ions as nodes and bifunctional ligand 3-(1H-tetrazol-5-yl)pyridine as organic linker. The activated MOF 1 (1a) could be utilized as catalyst for solvent-free heterogeneous catalytic cyanosilylation reaction because of its open Cu(II) metal positions, and its large amount of nitrogen atoms could be applied as Lewis basic positions. Thus, its catalytic mechanism was also investigated in detail. The specific mechanism was discussed, and its inhibition of the viability of MGC-803 gastric cancer cells was assessed. First, cell counting kit-8 assay was performed to determine the anti-cancer effect of compound 1a against the viability of MGC-803 cells. Then, Annexin V-fluorescein isothiocyanate/propidium iodide method was implemented to determine the percentage of apoptotic MGC-803 cells. Finally, the accumulation of reactive oxygen species in MGC-803 cells treated with the compound was determined via dichloro-dihydro-fluorescein diacetate assay.

Aspeterreurone A, a Cytotoxic Dihydrobenzofuran-Phenyl Acrylate Hybrid from the Deep-Sea-Derived Fungus Aspergillus terreus CC-S06-18.

A new dihydrobenzofuran-phenyl acrylate hybrid, aspeterreurone A (1), was obtained from the culture of the deep-sea-derived fungus Aspergillus terreus CC-S06-18. The relative configuration of 1 was elucidated by HSQMBC NMR, calculated NMR chemical shifts coupled with a statistical procedure (DP4+), and the absolute configuration was established by ECD calculations. 1 exhibited cytotoxicities against the gastric cancer cell lines HGC27, MGC803, BGC823, and AGS, with minimal effects on normal gastric epithelial cell line GES-1. Further studies showed that 1 inhibited cell cycle progression and induced apoptosis of gastric cancer MGC803 cells in a concentration-dependent manner. Western blot analysis indicated that 1 inhibited the phosphorylation of STAT3, which might contribute to its cytotoxic activity.

RETRACTED ARTICLE: Synthesis, Crystal Structure, and Anti-Gastric Cancer Activity of a Heterometallic Coordination Polymer Based on Flexible 6,6-Dithiodinicotinic Acid

A new bimetallic coordination polymer [In2Na(H2O)2(ddca)3](NO3)·4H2O (1, H2ddca = 6,6′-dithiodinicotinic acid) is produced via a hydrothermal reaction of In(NO3)3, H2ddca with NaOH as the pH modulator. Various characterization methods, such as thermogravimetric analysis (TGA), elemental analysis (EA), single crystal and powder X-ray diffraction measurements, are used. Furthermore, a process of sonochemistry with oleic acid at 453 K is used to produce nanoparticles of 1 (nano-1). In terms of the biological function of the synthesized complex, the real-time reverse transcription-polymerase chain reaction is carried out to explore the relative mRNA expression of miR-181 in MGC-803, BGC-823, and SGC-7901 gastric cancer cell lines, and the western blot is used to explore the protein expression of apoptotic protein Bcl-2.

Antitumor activity of a novel Aurora A/B kinases inhibitor TY-011 against gastric cancer by inducing DNA damage.

TY-011, a novel Aurora A/B kinases inhibitor, was found in our previous study to exhibit prominent inhibitory effects on growth of gastric cancer, both in vitro and in vivo. To clarify the mechanisms of TY-011 in inhibiting proliferation of gastric cancer cells, the effects of TY-011 on mitosis, cell cycle, apoptosis and cellular DNA were checked in the present study. Our results showed that TY-011 treatment induced aberrant mitosis, G2/M phase arrest and apoptosis. Importantly, TY-011 induced evident DNA damage in MGC-803 and MKN-45 human gastric cancer cells, which was further characterized as DNA double-strand break. Furthermore, cells treated with TY-011 appeared to generate multiple spindle fibers emanating from several spindle poles, leading to poly-merotelic kinetochore. These results suggested that TY-011 induced abnormal microtubule-kinetochores attachment and thus DNA damage, apoptosis and finally inhibition of cell proliferation of human gastric cancer cells.

RETRACTED ARTICLE: Crystal Structures and Anti-Gastric Cancer Activities of Two Cd(II)-Based Coordination Polymers Constructed from Different Donor Ligands

Two new Cd(II)-containing coordination polymers, namely [Cd(H2O)2(L1)2](NO3)2(1, L1 = 1,3-bis-(imidazol-1-yl)-5-methyl-benzene) and [Cd2(L2)(H2O)6](DMF)3(2, H4L2 = 5,5′-(p-xylylenediamino)-1,1′,3,3′-(benzene-tetra-carboxylic acid), are successfully prepared under the solvothermal conditions using different donor ligands. Complex 1 is a 2D layered structure whose network could be considered as a sql uninodal topological network, while complex 2 reveals a 3D supramolecular structure via H bond interactions between the adjacent 2D layers. Furthermore, the anticancer activity of the two complexes is studied via the CCK-8 assay against the MGC-803 gastric cancer cell lines, which reveals that compound 1 exhibits a significantly stronger activity than compound 2.

Activation of SREBP-1c alters lipogenesis and promotes tumor growth and metastasis in gastric cancer

PurposeAggressively growing tumors are characterized by significant variations in metabolites, including lipids, and can involve the elevated synthesis ofde novo fatty acids. MethodsUltra-performance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS)-based metabolomics and lipidomics were performed to compare human gastric cancer tissues and adjacent normal tissues from clinical patients. A series of cellular and molecular biological methods were applied to validate the lipidomics results. ResultsPalmitic acid (PA) was found to be significantly downregulated in gastric cancer tissues, and it was found that a high concentration of PA specifically inhibited cell proliferation and impaired cell invasiveness and migrationin vitro in AGS, SGC-7901, and MGC-803 gastric cancer cell lines. Moreover, sterol regulatory element-binding protein 1 (SREBP-1c) was activated in human gastric cancer tissues, and it promoted the expression of a series of genes associated with the synthesis of fatty acids, such as SCD1 and FASN. SREBP-1c knockdown rescued the migration and invasion defects in AGS and SGC-7901 gastric cancer cells. ConclusionTaken together, our findings confirmed the variation in fatty acid synthesis in gastric cancer and identified SREBP-1c as a promising target for gastric cancer treatment.

BRD9 controls the oxytocin signaling pathway in gastric cancer via CANA2D4, CALML6, GNAO1, and KCNJ5.

BackgroundFirst-line chemotherapeutic agents lead to remarkable activation treatment in cancers, but the side effects of these drugs also damage healthy cells. In some cases, drug resistance to chemotherapeutic agents is induced in cancer cells. The molecular mechanisms underlying such a side effect have been studied in a range of cancer types, yet little is known about how the adverse effects of chemotherapeutic drugs can be diminished by targeting bromodomain-containing protein 9 (BRD9) in gastric cancers.MethodsWe used two gastric cancer cell lines (MGC-803 and AGS) for comparison. We applied molecular and cellular techniques to measure cell survival and mRNA expression, investigated clinical data in the consensus of The Cancer Genome Atlas, and utilized high-throughput sequencing in MGC-803 cells and AGS cells for global gene expression analysis in inhibiting BRD9 conditions.ResultsOur studies showed that cancer cells with BRD9 overexpression, MGC-803 cells, were more sensitive to BRD9 inhibitors (i.e., BI9564 or BI7273) than AGS cells. The mechanism of BRD9 was related to the regulation of calcium voltage-gated channel auxiliary subunit alpha2 delta 4 (CANA2D4), calmodulin-like 6 (CALML6), guanine nucleotide binding protein (G protein), alpha activating activity polypeptide O (GNAO1) and Potassium Inwardly Rectifying Channel Subfamily J, Member 5 (KCNJ5) oncogenes in the oxytocin signaling pathway. BRD9 inhibitors could enhance the sensitivity of gastric cancer MGC-803 cells to adriamycin and cisplatin, so we may reduce the dosage of chemotherapeutic agents in curing gastric cancers with BRD9 over expression by combining BI9564 or BI7273 with adriamycin or cisplatin.ConclusionsOur study elucidated the feasibility and effectiveness of inhibiting BRD9 to reduce the adverse effects of first-line chemotherapeutic agents in treating gastric cancer with BRD9 overexpression. This study provides a scientific theoretical basis for a chemotherapy regimen in gastric cancer with BRD9 overexpression.

MiR-129-5p inhibits proliferation of gastric cancer cells through targeted inhibition on HMGB1 expression.

The aim of this study was to investigate the effects of micro ribonucleic acid (miR)-129-5p on the proliferation and apoptosis of gastric cancer cells via targeted repression on the expression of high mobility group protein B1 (HMGB1). Expression levels of miR-129-5p and HMGB1 in gastric cancer tissues (n=25) and adjacent normal tissues were measured via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The regulatory effect of miR-129-5p on the proliferation of gastric cancer MGC-803 and SGC7901 cells was determined through Cell Counting Kit-8 (CCK-8) assay. Flow cytometry was employed to analyze the apoptosis rate of gastric cancer cells. To further discover the mechanism of miR-129-5p in regulating malignant behaviors of gastric cancer cells, the miRDB database was employed to predict the binding targets of miR-129-5p. Finally, binding sites of HMGB1 3'-untranslated region (3'-UTR) to miR-129-5p were discovered. Subsequently, HMGB1 wild-type or mutant 3'-UTR Luciferase reporter vectors were constructed, and transfected to MGC-803 and SGC7901 cells together with miR-129-5p or negative control miRNA. Next, Western blotting was adopted to measure the protein expression level of HMGB1 in MGC-803 and SGC7901 cells transfected with miR-129-5p or negative control miRNA, so as to investigate whether miR-129-5p affected HMGB1 protein expression. Additionally, to determine whether HMGB1 mediated the regulatory effect of miR-129-5p on the proliferation of gastric cancer cells, MGC-803 and SGC7901 cells were transfected with pcDNA-HMGB1 or pcDNA-vector, respectively. The expression level of HMGB1 was measured via RT-qPCR, and cell proliferation was determined by CCK-8 assay. The expression level of miR-129-5p in gastric cancer tissues was significantly lower than that in adjacent normal tissues (p<0.001). Meanwhile, the level of miR-129-5p was overtly lower in gastric cancer MGC-803 and SGC7901 cell lines than that in normal gastric mucosal epithelial GES-1 cells (p<0.001). These results indicated that miR-129-5p was lowly expressed in gastric cancer tissues and cell lines. Subsequent results demonstrated that the expression of HMGB1 increased remarkably in gastric cancer tissues compared with normal adjacent tissues (p<0.05). The proliferation ability of MGC-803 (p<0.001) and SGC7901 (p<0.01) cells with over-expressed miR-129-5p was remarkably weakened. Overexpression of miR-129-5p distinctly promoted the apoptosis rate of gastric cancer MGC-803 (p<0.01) and SGC7901 (p<0.001) cells. Moreover, miR-129-5p up-regulation significantly reduced the Luciferase activity of wild-type HMGB1 (p<0.001). However, no significant effect was observed on that of mutant HMGB1. The results suggested that overexpression of miR-129-5p significantly down-regulated the level of HMGB1 in gastric cancer cells. In addition, the messenger RNA (mRNA) level of HMGB1 in cells transfected with miR-129-5p also decreased significantly (p<0.001). HMGB1 overexpression overtly reversed the inhibitory effect of miR-129-5p on the proliferation of gastric cancer cells (p<0.05). All these results demonstrated that the miR-129-5p/HMGB1 axis played a key role in regulating the growth of gastric cancer cells. MiR-129-5p suppresses the progression of gastric cancer through targeted inhibition on the expression of HMGB1.

RETRACTED ARTICLE: Crystal Structure and Evaluation of the Anti-Gastric Cancer Activity of a New Sr(II)-Based Coordination Polymer

In this study, a new Sr(II)-based coordination polymer containing Sr(II)-carboxyl chains with the formula [Sr3(L)2(H2O)2](H2O)3 is successfully prepared with the use of a non-planar tripodal ligand 3,4-bi××(4-carboxyphenyl)-benzoic acid (H3L) under the hydrothermal conditions. A single crystal X-ray diffraction study reveals that complex 1 has a three-dimensional framework with a 3-nodal (4,6,8)-connected topological net. Furthermore, an ultrasonic treatment method is used to produce the crystalline samples of 1 in the nanoscale (nano 1). The CKK-8 assay is performed to detect the cell proliferation of MGC-803 gastric cancer cells under the treatment with nano 1. Moreover, the cancer cell apoptosis is determined by a flow cytometer and the Western blot after treating with nano 1.

Long non-coding RNA FTX promotes gastric cancer progression by targeting miR-215.

Gastric cancer (GC) is one of the most common malignant tumors in the world, which is seriously harmful to people's health. The increasing number of studies have shown that long non-coding RNA (lncRNA) is related to the occurrence of gastric cancer. In this study, we aimed at investigating the role of lnc FTX in the occurrence of gastric cancer. The expression of FTX in gastric cancer patients and gastric cancer cell lines was detected by RT-qPCR. Univariate Kaplan-Meier method was used to analyze the relationship between FTX expression level, clinicopathological parameters and overall survival rate (OS). After transferring si-FTX and overexpression FTX plasmids into MGC-803 and SGC-7901, the expression of miR-215-3p was detected by RT-qPCR, and the changes of cell proliferation and cell cycle were detected by CCK-8 and flow cytometry. In addition, luciferase activity was used to detect whether miR-215-3p combined with FTX and SIVA1. Finally, Western blot (WB) was used to detect the change of SIVA1 protein expression by miR-215 mimic. We found that the expression of FTX in tumor tissues of 71 GC patients was higher than that in paracancerous tissues, and the prognosis of patients with high FTX was poor. The expression of FTX in gastric cancer cells was higher than that in normal human gastric epithelial cells (GES-1). Transferring overexpression plasmid of FTX into gastric cancer cells (MGC-803 and SGC-7901) promoted cell proliferation and the ratio of cells in G0-G1 phase was decreased. Transferring si-FTX to MGC-803 and SGC-7901 led to opposite results. There was a negative correlation between the expression of mi215-3p and FTX in MGC-803 and SGC-7901 gastric cancer cells, and luciferase results showed that mi215-3p could directly bind to FTX and regulate cell growth and cell cycle changes. In addition, luciferase results showed that mi215-3p could bind directly to SIVA1. What's more, RT-qPCR and WB results showed that mi215 mimic could promote the expression of MGC-803, SGC-7901 SIVA1mRNA and protein. According to these results, this study revealed that the previously neglected FTX-miR2153p-SIVA1 regulatory axis for the regulation of gastric cancer progression, which may be a potential target for the treatment of gastric cancer.