S100P Predicts Prognosis and Drug Resistance in Gastric Cancer

2013 ◽  
Vol 28 (4) ◽  
pp. 387-392 ◽  
Author(s):  
Fulin Ge ◽  
Changzheng Wang ◽  
Weihua Wang ◽  
Benyan Wu
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Cancer Patients ◽  
Ectopic Expression ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Patients ◽  
Cancer Tissues ◽  
Normal Controls

Purpose S100P has been shown to participate in processes of various human malignancies. In this study, we analyzed the tissue expression of S100P in gastric cancer and evaluated its significance. Methods We determined the S100P expression in 156 gastric cancer patients by quantitative RT-PCR. Tumor characteristics and overall survival (OS) for each patient were examined. In vitro experiments were conducted to examine whether ectopic expression of S100P modifies the proliferation and drug resistance of gastric cancer cells. Results Higher expression of S100P occurred in human gastric cancer tissues in comparison with normal controls. Highly expressed S100P in gastric cancer was correlated with TNM stage and prognosis. The 5-year survival rate was significantly lower in patients with high levels of S100P expression than in patients with low levels of expression. Ectopic expression of S100P was associated with an increase in tumor cell proliferation and drug resistance. Conclusion The expression of S100P in human gastric cancer tissues was upregulated in comparison with normal controls. By establishing an association between S100P expression and shortened OS, increase in proliferation and drug resistance, this study indicates that S100P may be a useful prognostic marker for gastric cancer patients.

scholarly journals NUDT21 Promotes Tumor Growth and Metastasis Through Modulating SGPP2 in Human Gastric Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Yong Zhu ◽  
Rumeng Zhang ◽  
Ying Zhang ◽  
Xiao Cheng ◽  
Lin Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Tumor Metastasis ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Patients ◽  
Cancer Tissues

Gastric cancer is one of the major malignancies with poor survival outcome. In this study, we reported that NUDT21 promoted cell proliferation, colony formation, cell migration and invasion in gastric cancer cells. The expression levels of NUDT21 were found to be much higher in human gastric cancer tissues compared with normal gastric tissues. NUDT21 expression was positively correlated with tumor size, lymph node metastasis and clinical stage in gastric cancer patients. High level of NUDT21 was associated with poor overall survival (OS) rates in gastric cancer patients. The expression levels of NUDT21 were also much higher in gastric cancer tissues from patients with tumor metastasis compared with those of patients without tumor metastasis. Moreover, forced expression of NUDT21 in gastric cancer cells promoted tumor growth and cell proliferation in xenograft nude mice, and depletion of NUDT21 in gastric cancer cells restrained lung metastasis in vivo. Through high throughput RNA-sequencing, SGPP2 was identified to be positively regulated by NUDT21 and mediated the tumor promoting role of NUDT21 in gastric cancer cells. Therefore, NUDT21 played an oncogenic role in human gastric cancer cells. NUDT21 could be considered as a novel potential target for gastric cancer therapy.

scholarly journals miR-149 Suppresses the Proliferation and Metastasis of Human Gastric Cancer Cells by Targeting FOXC1

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Dan Li ◽  
Yunqing Zhang ◽  
Yulong Li ◽  
Xiaofei Wang ◽  
Fenghui Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Western Blotting ◽  
Luciferase Assay ◽  
Biological Behavior ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Promising Target ◽  
And Migration ◽  
Gastric Cancer Patients ◽  
Cancer Tissues

Purpose. Gastric cancer is one of the most common cancers in the world. miRNAs play an important role in regulating gene expression by binding with 3 ′ -UTR of the target gene. The aim of this study was to investigate the function of miRNA-149 and FOXC1 in gastric cancer. Patients and Methods. qRT-PCR was used to detect the expression of miRNA-149 and FOXC1 in gastric cancer tissues and cells. Human gastric cancer cell lines AGS and MKN28 were cultured and transfected with miR-149 overexpression plasmid and its control or FOXC1 siRNA and its control. The MTT, colony formation, flow cytometry, wound healing, transwell, and western blotting were performed to examine the function of miRNA-149 and FOXC1 in the development of gastric cancer. What is more, dual-luciferase assay and western blotting were used to demonstrated the relationship between miRNA-149 and FOXC1. Results. miRNA-149 was underexpressed in gastric cancer tissues and cells, while overexpression of miRNA-149 promoted cell apoptosis, retarded cell cycle, and inhibited proliferation and migration in AGS and MKN28 cells. In addition, we showed that miRNA-149 targeted FOXC1. What is more, FOXC1 was highly expressed in gastric cancer tissues and cells; the silencing of FOXC1 inhibited the biological function of AGS and MKN28 cells. Conclusion. miRNA-149 inhibits the biological behavior of gastric cancer by targeting FOXC1, providing a promising target in the treatment of human gastric cancer.

scholarly journals Potent and specific MTH1 inhibitors targeting gastric cancer

2019 ◽  
Vol 10 (6) ◽  
Author(s):  
Wenjuan Zhou ◽  
Liying Ma ◽  
Jing Yang ◽  
Hui Qiao ◽  
Lingyu Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Malignant Tumors ◽  
Inhibitory Effect ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Dntp Pool ◽  
Cancer Tissues

Abstract Human mutT homolog 1(MTH1), the oxidized dNTP pool sanitizer enzyme, has been reported to be highly expressed in various malignant tumors. However, the oncogenic role of MTH1 in gastric cancer remains to be determined. In the current study, we found that MTH1 was overexpressed in human gastric cancer tissues and cells. Using an in vitro MTH1 inhibitor screening system, the compounds available in our laboratory were screened and the small molecules containing 5-cyano-6-phenylpyrimidine structure were firstly found to show potently and specifically inhibitory effect on MTH1, especially compound MI-743 with IC50 = 91.44 ± 1.45 nM. Both molecular docking and target engagement experiments proved that MI-743 can directly bind to MTH1. Moreover, MI-743 could not only inhibit cell proliferation in up to 16 cancer cell lines, especially gastric cancer cells HGC-27 and MGC-803, but also significantly induce MTH1-related 8-oxo-dG accumulation and DNA damage. Furthermore, the growth of xenograft tumours derived by injection of MGC-803 cells in nude mice was also significantly inhibited by MI-743 treatment. Importantly, MTH1 knockdown by siRNA in those two gastric cancer cells exhibited the similar findings. Our findings indicate that MTH1 is highly expressed in human gastric cancer tissues and cell lines. Small molecule MI-743 with 5-cyano-6-phenylpyrimidine structure may serve as a novel lead compound targeting the overexpressed MTH1 for gastric cancer treatment.

Regulation of miR-596 on the Apoptosis of Gastric Cancer Cells through Its Targeting Inhibition of BCL-2

2020 ◽  
Author(s):  
Jianmiao WANG ◽  
Jing YANG ◽  
Ji QIU ◽  
Taoyan SONG
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Mechanism Of Action ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Gastric Cancer Patients ◽  
Cancer Tissues ◽  
The Relationship

Background: We aimed to investigate the relationship between miR-596, BCL-2, and apoptosis of gastric cancer cells, and to explore the mechanism of miR-596 in gastric cancer. Besides, this study aimed to find the target of miR-596 and explore the mechanism of action of miR-596 in gastric cancer. Methods: Eighteen samples of gastric cancer tissues and 18 samples of corresponding tumor-adjacent tissues were collected from 18 gastric cancer patients (aged from 40 to 55 yr) admitted to Zhuji People's Hospital, Zhuji, China from March 2017 to May 2018. The expression levels of miR-596 and BCL-2 were detected to verify the regulation of miR-596 on the apoptosis and proliferation of gastric cancer cell lines MKN-45 and HGC-27 and its effect on BCL-2 expression. Results: The expression level of miR-596 was notably lower in gastric cancer tissues than in adjacent tissues, and BCL-2 level was notably higher in gastric cancer tissues than in adjacent tissues. After the up-regulation of miR-596 expression, the proliferation of MKN-45 and HGC-27 cells was significantly decreased, the level of apoptosis was significantly increased (P<0.05), and the expression of BCL-2 was decreased. The dual-luciferase report showed that miR-596 had a targeting inhibition of BCL-2. Gastric cancer cells with up-regulated miR596 and BCL-2 had significantly higher proliferation and lower apoptosis than cells with up-regulated miR-596. Conclusions: miR-596 can inhibit the proliferation of gastric cancer cells and promote the apoptosis through its targeting inhibition of BCL-2 expression.

scholarly journals Tenascin-c Knockdown Suppresses Vasculogenic Mimicry of Gastric Cancer by Inhibiting ERK- Triggered EMT

2021 ◽  
Author(s):  
Xing Kang ◽  
en xu ◽  
Xingzhou wang ◽  
Lulu Qian ◽  
Zhi Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Vasculogenic Mimicry ◽  
Gastric Cancer Cells ◽  
Tenascin C ◽  
Gastric Cancer Patients ◽  
Cancer Tissues

Abstract BackgroundGastric cancer is one of the most common malignancies worldwide and vasculogenic mimicry (VM) is considered to be the leading cause for the failure of anti-angiogenesis therapy in advanced gastric cancer patients. Tenascin-c (TNC) plays a pivotal role in VM. Thus, we explored the role of TNC in VM formation in gastric cancer.MethodsGastric cancer tissues and corresponding adjacent tissues were collected from gastric cancer patients after surgery. We used western blot and immunohistochemistry to examine the expression of TNC in tissues and used siRNA and lentivirus to knockdown the TNC expression in gastric cancer cell lines. Then three-dimensional culturing, CCK-8, Edu assay, flow cytometry, trasnwell and pseudopodia formation assay were used to evaluate the function of TNC in gastric cancer cells and bioinformatic prediction was used to explore the mechanism underlying TNC modulating the VM in gastric cancer. Xenograft and peritoneal dissemination model were used to further explore the role of TNC in vivo.ResultsIn this study, we demonstrated that TNC was highly expressed in gastric cancer tissues and correlated with poor prognosis of gastric cancer. Furthermore, knockdown of TNC significantly inhibited VM formation and proliferation of gastric cancer cells in vitro and in vivo, with a reduction in cell migration and invasion. Mechanistically, TNC knockdown suppressed the phosphorylation of ERK and subsequently inhibited the process of EMT, both of which play an important role in VM formation. What’s more, rescue experiments showed that activation of p-ERK could reverse the suppressive role of TNC knockdown in gastric cancer cells.ConclusionsTNC plays an important role in VM formation in gastric cancer. Combining inhibition of TNC and ERK may be a potential therapeutic approach to inhibit gastric cancer growth and metastasis and decrease anti-angiogenic therapeutic resistance.

scholarly journals SOX13 Dependent PAX8 Expression Promotes the Proliferation of Gastric Carcinoma Cells

2019 ◽  
Author(s):  
Liang-Yu Bie ◽  
Dan Li ◽  
Yan Wei ◽  
Ning Li ◽  
Xiao-Bing Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cyclin B1 ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Pax8 Expression ◽  
Mgc803 Cell ◽  
Gastric Cancer Patients ◽  
Cancer Tissues

Abstract PAX8 is identified as a regulator in the pathogenesis of human tumors and an indicator of the prognosis for patients. However, the role of PAX8 on proliferation in gastric cancer have not been studied. This study was aimed to explore the expression pattern of PAX8 in gastric cancer, and investigate the effect of PAX8 on the proliferation of gastric cancer cells. PAX8 and SOX13 were identified to be synchronously upregulated in primary gastric cancer in human gastric cancer tissues and the gastric cancer datasets of TCGA, and gastric cancer patients of combined high PAX8 and SOX13 expression showed poor prognosis. Furthermore, SOX13 can mediate PAX8 and its targeted genes, Aurora B and Cyclin B1, expression in AGS and MGC803 cell lines. Flow cytometry and EdU incorporation assays showed that silencing PAX8 can block the cell cycle of gastric cancer cell in G1 phase and SOX13 expression can rescue the arrested proliferative process induced by PAX8 silenced in CCK8 and colony formation assays. Thus, combined SOX13 and PAX8 expression regulate the proliferation of gastric cancer cells, and both SOX13 and PAX8 play an oncogene function in gastric cancer.

Gene’s co-expression network and experimental validation of molecular markers associated with the drug resistance of gastric cancer

2020 ◽  
Vol 14 (9) ◽  
pp. 761-773
Author(s):  
Wenqian Qi ◽  
Qian Zhang
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Molecular Markers ◽  
Human Gastric Cancer ◽  
Cancer Resistance ◽  
Gastric Cancer Cells ◽  
Network Analyses ◽  
Potential Factors ◽  
Function Enrichment

Aim: Chemotherapy can significantly improve the overall survival rate of patients with gastric cancer; however, so far little is known about the molecular mechanism of resistance to chemotherapy. Therefore, this study was proposed to elucidate molecular markers of resistance to chemotherapeutic agent in gastric cancer. Materials & methods: Weighted gene co-expression network analyses were performed in gastric cancer cohort. The most relevant genes modules for gastric cancer resistance were selected. Gene oncology function enrichment of genes was conducted. The biological function of resistant genes were identified in vitro. Results & conclusion: Two resistant hub genes, SPTBN1 and LAMP1, were selected. Experiments showed that downregulation of SPTBN1and LAMP1 proteins significantly enhanced the sensitivity of human gastric cancer cells SGC7901 to 5-FU and cisplatin. Thus, our results provide a baseline about the potential factors of drug resistance in gastric cancer.

scholarly journals E2F1 Maintains Gastric Cancer Stemness Properties by Regulating Stemness-Associated Genes

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yan Fu ◽  
Cheng’en Hu ◽  
Peizhun Du ◽  
Guangjian Huang
Keyword(s):  
Gastric Cancer ◽  
Overall Survival ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Close Association ◽  
Gastric Cancer Cells ◽  
Cancer Stemness ◽  
Gastric Cancer Patients ◽  
Cancer Tissues ◽  
E2f1 Expression

Purpose. To determine the regulatory role of E2F1 in maintaining gastric cancer stemness properties and the clinical significance of E2F1 in gastric cancer. Materials and Methods. We conducted a tumor spheroid formation assay to enrich gastric cancer stem-like cells. The protein and mRNA expression levels of genes were measured using Western Blot and qRT-PCR. Lentivirus-mediated overexpression and downregulation of E2F1 were performed to evaluate the effect of E2F1 on the stemness properties of gastric cancer cells. The effect of E2F1 on gastric cancer cell sensitivity of 5-Fu was evaluated using cell viability assay and TdT-mediated dUTP Nick-End Labeling staining. We also analyzed the association between E2F1 expression and clinical characteristics in gastric cancer patients. The KM plotter database was used to analyze the relationship between E2F1 and overall survival in GC patients. Results. We found that E2F1 expression was significantly higher in gastric cancer tissues than in the paired adjacent normal tissues ( p < 0.05 ) and was positively correlated with tumor size ( p < 0.05 ), T stage ( p < 0.05 ), and differentiation degree ( p < 0.05 ). KM plotter database demonstrated a close association between higher E2F1 expression level and worse overall survival of gastric cancer patients ( p < 0.05 ). In vitro assay illustrated that E2F1 could regulate the expression of stemness-associated genes, such as BMI1, OCT4, Nanog, and CD44, and maintain the tumor spheroid formation ability of gastric cancer cells. E2F1 enhanced 5-Fu resistance in gastric cancer cells, and the E2F1 expression level was correlated with the prognosis of gastric cancer patients receiving 5-Fu therapy. The expression levels of stemness-associated genes were also significantly higher in gastric cancer tissues than the paired adjacent normal tissues ( p < 0.05 ). A positive correlation was observed between E2F1 and BMI1 (r = 0.422, p < 0.05 ), CD44 (r = 0.634, p < 0.05 ), OCT4 (r = 0.456, p < 0.05 ), and Nanog (r = 0.337, p < 0.05 ) in gastric cancer tissues. The co-overexpression of E2F1 and stemness-associated genes was associated with worse overall survival. Conclusion. E2F1 plays a significant role in gastric cancer progression by maintaining gastric cancer stemness properties through the regulation of stemness-associated genes. The close association between E2F1 and poor prognosis of patients suggests that E2F1 could serve as a prognostic biomarker and a therapeutic target in gastric cancer patients.

LncRNA CRYM-AS1 Inhibits Gastric Cancer Progression via Epigenetically Regulating CRYM

2021 ◽  
Author(s):  
Peipei Zhang ◽  
Changyu Chen ◽  
Jiajia Zhang ◽  
Xin Yu
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Aerobic Glycolysis ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Immunoprecipitation Assay ◽  
Gastric Cancer Patients

Abstract Objective: To study the role of long non-coding RNA (lncRNA) CRYM-AS1 in human gastric cancer. Methods: Expression levels of CRYM-AS1 in cell lines and clinical tissues were examined by RT-qPCR. The association between CRYM-AS1 levels and clinicopathological parameters / survival rates of gastric cancer patients was analyzed.Cell functional experiments including MTT assay, glucose consumption / lactate production / ATP production detection were performed to examine the role of CRYM-AS1 in cell aerobic glycolysis and cell proliferation of gastric cancer cells. Subcellular fractionation location detection, western blot, RIP (RNA binding protein immunoprecipitation) assay, CHIP (Chromatin immunoprecipitation) assay and BSP (Bisulfite sequencing PCR) assay were carried out to explore the molecular mechanism of CRYM-AS1 in gastric cancer cells.Results: CRYM-AS1 was low expressed in gastric cancer cells and tissues compared with normal gastric cells and tissues respectively. CRYM-AS1 was negatively correlated with TNM staging, tumor size and overall survival (OS) rate in gastric cancer patients. CRYM-AS1 inhibited gastric cancer cell aerobic glycolysis and cell proliferation. CRYM-AS1 directly bound to EZH2 and mediated the CRYM promoter methylation and consequently negatively regulated the expression of CRYM. Forced expression of CRYM rescued the decreased aerobic glycolysis and cell proliferation induced by CRYM-AS1 in gastric cancer cells.Conclusion: CRYM-AS1 was an important biomarker and could be used for human gastric cancer treatment.

scholarly journals Circular RNA circ_0026359 Enhances Cisplatin Resistance in Gastric Cancer via Targeting miR-1200/POLD4 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Zongyao Zhang ◽  
Xin Yu ◽  
Bo Zhou ◽  
Jiajia Zhang ◽  
Jiacong Chang
Keyword(s):  
Gastric Cancer ◽  
Malignant Tumors ◽  
Acquired Resistance ◽  
Circular Rna ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Free Survival ◽  
Gastric Cancer Patients ◽  
Cancer Tissues

Human gastric cancer is one of the most common malignant tumors with a poor prognosis. Cisplatin (CDDP) is a well-known first-line chemotherapeutic drug. Acquired resistance retards the clinical application of CDDP in gastric cancer. In this study, circular RNA circ_0026359 was demonstrated to be overexpressed in gastric cancer tissues/cells compared with normal gastric tissues/cells and was overexpressed in CDDP-resistant gastric cancer tissues/cells compared with CDDP-sensitive gastric cancer tissues/cells. High levels of circ_0026359 were associated with low overall survival (OS) and relapse-free survival (RFS) rates in gastric cancer patients. circ_0026359 was examined to promote CDDP resistance in gastric cancer cells. circ_0026359 directly interacted and negatively regulated miR-1200. POLD4 was a direct target of miR-1200. miR-1200/POLD4 pathway mediated the promoting role of circ_0026359 in CDDP resistance of gastric cancer. circ_0026359 could be used as a potential target for CDDP-resistant gastric cancer therapy.

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