scholarly journals RNA Binding Protein RNPC1 Promotes Gastric Cancer Progression via Stabilizing the Aurora Kinase B mRNA

2021 ◽  
Author(s):  
Chunmei Ji ◽  
Xu Zhang ◽  
Wentong Fang ◽  
Ling Meng ◽  
Xiaolong Wei ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Mrna Stability ◽  
Rna Binding ◽  
Aurora Kinase ◽  
Luciferase Reporter ◽  
Gastric Cancer Cells ◽  
Aurora Kinase B ◽  
Potential Biomarker

Abstract BackgroundRNPC1, was reported to act as a tumor suppressor by binding and regulating the expression of the target genes in various cancers. However, the role of RNPC1 on the gastric cancer and the underly mechanisms were still unclear.MethodsGastric cancer cells were stably transfected with lentivirus. Proliferation, migration, invasion, cell cycle in vitro as well as tumorigenesis in vivo were performed to assess the role of RNPC1. Quantitative real-time PCR, western blot and immunohistochemistry were used to detect the relation between RNPC1 and Aurora kinase B (AURKB). RNA immunoprecipitation(RIP), RNA electrophoretic mobility shift assay (REMSA), dual-luciferase reporter assay were employed to identify the direct binding sites of RNPC1 with AURKB mRNA. CCK-8 assay conducted to confirm the function of AURKB in RNPC1-induced growth promotion. ResultsHigh RNPC1 expression was found in gastric cancer tissues and cell lines, associated with high TNM stage. RNPC1 overexpression could significantly promote the proliferation, migration, invasion of gastric cancer cells. Knockdown of RNPC1 could impede gastric cancer tumorigenesis in nude mice. AURKB expression was positively related with RNPC1. RNPC1 binded to the 3'-untranslated region (3'-UTR) of AURKB directly and enhanced AURKB mRNA stability. AURKB could reversed the proliferation induced by RNPC1 in gastric cancer cells. RNPC1 resulted in mitotic defects, aneuploidy and chromosomal instability in gastric cancer cells, as AURKB did. ConclusionRNPC1 acted as an oncogene in gastric cancer by influencing cell mitosis by regulating AURKB mRNA stability, which may provide a potential biomarker and therapeutic target for gastric cancer.

Aurora kinase B inhibitor barasertib (AZD1152) inhibits glucose metabolism in gastric cancer cells

2019 ◽  
Vol 30 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Jian He ◽  
Zihao Qi ◽  
Xiaofei Zhang ◽  
Yufei Yang ◽  
Fei Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Glucose Metabolism ◽  
Cancer Cells ◽  
Aurora Kinase ◽  
Gastric Cancer Cells ◽  
Aurora Kinase B

scholarly journals CircCNIH4 inhibits gastric cancer progression via regulating DKK2 and FRZB expression and Wnt/β-catenin pathway

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Qi Shi ◽  
Chuanwen Zhou ◽  
Rui Xie ◽  
Miaomiao Li ◽  
Peng Shen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Gastric Cancer Cells ◽  
Potential Biomarker

Abstract Background Circular RNAs (circRNAs) have been reported to play an important role in tumor progression in various cancer types, including gastric cancer. The aim of this study was to investigate the role of circCNIH4 (hsa_circ_0000190) in gastric cancer and the underlying mechanism. Methods The expression levels of circCNIH4 and Wnt antagonist genes were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of β-catenin, Ki67, Dickkopf 2 (DKK2) and Frizzled related protein (FRZB) were measured by western blot. Ectopic overexpression or knockdown of circCNIH4, proliferation, apoptosis, migration and invasion by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry and transwell assay in vitro, and in vivo experiment, were employed to assess the role of circCNIH4 in gastric cancer. Results CircCNIH4 was downregulated in gastric cancer tissues and cells. Overexpression of circCNIH4 inhibited gastric cancer cell proliferation, migration and invasion and promoted apoptosis by inactivating Wnt/β-catenin pathway in vitro. CircCNIH4 induced the expression of DKK2 and FRZB in gastric cancer cells. Moreover, silencing of DKK2 or FRZB reversed circCNIH4 overexpression-mediated effects on gastric cancer cells. Additionally, circCNIH4 suppressed tumor growth via regulating DKK2 and FRZB expression in gastric cancer in vivo. Conclusion Our study demonstrated that circCNIH4 played a tumor-inhibiting role through upregulating DKK2 and FRZB expression and suppressing Wnt/β-catenin pathway in gastric cancer, which might provide a potential biomarker for the diagnosis and treatment of gastric cancer.

scholarly journals miR-206 inhibits estrogen-induced proliferation and invasion of ER-α36 positive gastric cancer cells

2021 ◽  
Author(s):  
Xia sheng ◽  
Chunyan Yuan ◽  
Yunyuan Yang ◽  
Xuebing Jiang ◽  
Xiaoli Xie ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Therapeutic Option ◽  
Luciferase Reporter ◽  
Rt Pcr ◽  
Invasive Ability ◽  
Gastric Cancer Cells ◽  
Encoding Gene ◽  
Proliferation And Invasion

Objective To explore the biological role of miR-206 in inhibiting the proliferation and invasion of estrogen-induced ER-α36 positive gastric cancer cells and its related mechanisms. Methods MTT and tranwell assays were used to detect the proliferation and invasion of BGC-823 cells under different concentrations and time of ER stimulation. RT-PCR was used to detect the effect of ER stimulation on the content of miR-206 in gastric cancer cells. miR-206 mimics were transfected into BGC-823 cells to detect cell proliferation and invasion; luciferase reporter assay was used to determine whether miR-206 targets the 3'-untranslated region of the CDK14-encoding gene (3' -UTR). Results We confirmed that estrogen promoted the proliferation and invasion of BGC-823 cells; As the concentration of estrogen increases, the level of miR206 in the cell gradually rises.Overexpression of miR-206 significantly decreased the estrogen-induced BGC-823 cells. Proliferative and invasive ability; miR-206 inhibits the expression of CDK14 by directly binding to the 3'-UTR of CDK14 mRNA, thereby inhibiting the proliferation and invasion of gastric cancer cells. Conclusions Our results suggest that miR-206 inhibits estrogen-induced proliferation and invasion of ER-α36-positive gastric cancer cells by inhibiting CDK14 and may be a promising therapeutic option for anticancer therapy.

scholarly journals Lnc RNA MALAT 1 increases the stemness of gastric cancer cells via enhancing SOX 2 mRNA stability

FEBS Open Bio ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 1212-1222 ◽  
Author(s):  
Yiwen Xiao ◽  
Jingjing Pan ◽  
Qian Geng ◽  
Ge Wang
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Mrna Stability ◽  
Gastric Cancer Cells

scholarly journals RNA-binding protein RNPC1 acts as an oncogene in gastric cancer by stabilizing Aurora kinase B mRNA

2021 ◽  
pp. 112741
Author(s):  
Chun-Mei Ji ◽  
Xu Zhang ◽  
Wentong Fang ◽  
Ling Meng ◽  
Xiaolong Wei ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Aurora Kinase ◽  
Aurora Kinase B

scholarly journals Restoration of klotho gene expression induces apoptosis and autophagy in gastric cancer cells: tumor suppressive role of klotho in gastric cancer

2013 ◽  
Vol 13 (1) ◽  
pp. 18 ◽  
Author(s):  
Biao Xie ◽  
Jianping Zhou ◽  
Guoshun Shu ◽  
Dong-cai Liu ◽  
Jiapeng Zhou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Klotho Gene

scholarly journals MicroRNA-154 Inhibits the Growth and Invasion of Gastric Cancer Cells by Targeting DIXDC1/WNT Signaling

2018 ◽  
Vol 26 (6) ◽  
pp. 847-856 ◽  
Author(s):  
Jifu Song ◽  
Zhibin Guan ◽  
Maojiang Li ◽  
Sha Sha ◽  
Chao Song ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Wnt Signaling ◽  
Cancer Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Inverse Correlation ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Gastric Cancer Cells ◽  
Cancer Cell Growth ◽  
Cancer Tissues

MicroRNAs (miRNAs) have emerged as pivotal regulators of the development and progression of gastric cancer. Studies have shown that miR-154 is a novel cancer-associated miRNA involved in various cancers. However, the role of miR-154 in gastric cancer remains unknown. Here we aimed to investigate the biological function and the potential molecular mechanism of miR-154 in gastric cancer. We found that miR-154 was significantly downregulated in gastric cancer tissues and cell lines. The overexpression of miR-154 significantly repressed the growth and invasion of gastric cancer cells. Bioinformatics analysis and Dual-Luciferase Reporter Assay data showed that miR-154 directly targeted the 3′-untranslated region of Dishevelled‐Axin domain containing 1 (DIXDC1). Real-time quantitative polymerase chain reaction and Western blot analyses showed that miR-154 overexpression inhibited DIXDC1 expression. An inverse correlation of miR-154 and DIXDC1 was also demonstrated in gastric cancer specimens. Overexpression of miR-154 also significantly suppressed the activation of WNT signaling. Moreover, restoration of DIXDC1 expression significantly reversed the inhibitory effect of miR-154 overexpression on the cell proliferation, invasion, and WNT signaling in gastric cancer cells. Overall, these results suggest that miR-154 inhibits gastric cancer cell growth and invasion by targeting DIXDC1 and could serve as a potential therapeutic target for the treatment of gastric cancer.

scholarly journals The tRNA-derived fragment 5026a inhibits the proliferation of gastric cancer cells by regulating the PTEN/PI3K/AKT signaling pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Linwen Zhu ◽  
Zhe Li ◽  
Xiuchong Yu ◽  
Yao Ruan ◽  
Yijing Shen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Gastric Cancer Cells ◽  
Qrt Pcr

Abstract Background Recently, tRNA-derived fragments (tRFs) have been shown to serve important biological functions. However, the role of tRFs in gastric cancer has not been fully elucidated. This study aimed to identify the tumor suppressor role of tRF-5026a (tRF-18-79MP9P04) in gastric cancer. Methods Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was first used to detect tRF-5026a expression levels in gastric cancer tissues and patient plasma. Next, the relationship between tRF-5026a levels and clinicopathological features in gastric cancer patients was assessed. Cell lines with varying tRF-5026a levels were assessed by measuring tRF-5026a using qRT-PCR. After transfecting cell lines with a tRF-5026a mimic or inhibitor, cell proliferation, colony formation, migration, apoptosis, and cell cycle were evaluated. The expression levels of related proteins in the PTEN/PI3K/AKT pathway were also analyzed by Western blotting. Finally, the effect of tRF-5026a on tumor growth was tested using subcutaneous tumor models in nude mice. Results tRF-5026a was downregulated in gastric cancer patient tissues and plasma samples. tRF-5026a levels were closely related to tumor size, had a certain diagnostic value, and could be used to predict overall survival. tRF-5026a was also downregulated in gastric cancer cell lines. tRF-5026a inhibited the proliferation, migration, and cell cycle progression of gastric cancer cells by regulating the PTEN/PI3K/AKT signaling pathway. Animal experiments showed that upregulation of tRF-5026a effectively inhibited tumor growth. Conclusions tRF-5026a (tRF-18-79MP9P04) is a promising biomarker for gastric cancer diagnostics and has tumor suppressor effects mediated through the PTEN/PI3K/AKT signaling pathway.

scholarly journals Has-miR-875-5p Inhibits Tumorigenesis by Targeting USF2 via TGF-β Signaling Pathway in Gastric Cancer

2021 ◽  
Author(s):  
Shenshuo Gao ◽  
Zhikai Zhang ◽  
Xubin Wang ◽  
Yan Ma ◽  
Chensheng Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Signaling Pathway ◽  
Research Direction ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
New Research

Abstract Background: Gastric cancer (GC) is one of the most common malignancies, and more and more evdiences show that the pathogenesis is regulated by various miRNAs.In this study, we investigated the role of miR-875 in GC. Methods:The expression of miR-875-5p was detected in human GC specimens and cell lines by miRNA RT-PCR. The effect of miR-875-5p on GC proliferation was determined by CCK-8 proliferation assay and EDU assay. Migration and invasion were examined by transwell migration and invasion assay and wound healing assay. The interaction between miR-875-5p and its target gene USF2 was verified by a dual luciferase reporter assay. The effects of miR-875-5p in vivo were studied in xenograft nude mice models.Related proteins were detected by Western blot.Results:The results showed that miR-875-5p inhibited the proliferation, migration and invasion of gastric cancer cells in vitro, and inhibited tumorigenesis in vivo. USF2 proved to be a direct target of miR-875-5p. Knockdown of USF2 partially counteracts the effects of miR-875-5p inhibitors.Overexpression of miR-875-5p can inhibit proliferation, migration, and invasion through the TGF-β signaling pathway by down-regulation of USF2 in GC, providing a new research direction for the diagnosis and targeted therapy of GC.Conclusions: MiR-875-5pcan inhibited the progression of GC by directly targeting USF2 and negatively regulating TGF-β signaling pathway.In the future, miR-875-5p is expected to be used as a potential therapeutic target for GC therapy.

scholarly journals miR-335-5p Suppresses Gastric Cancer Progression by Targeting MAPK10

2020 ◽  
Author(s):  
Yi Gao ◽  
Yanfeng Wang ◽  
Xiaofei Wang ◽  
Changan Zhao ◽  
Fenghui Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Progression ◽  
Target Gene ◽  
Luciferase Reporter ◽  
Gastric Cancer Cells ◽  
Aberrant Expression ◽  
Related Target

Abstract Background: In recent years, many microRNAs(miRNAs) involved in cancer progression. The aberrant expression of miR-335-5p in tumorigenesis has been demonstrated. The present study aimed to investigate the molecular mechanisms underlying miR-335-5p- regulated MAPK10 expression in human gastric cancer（GC）.Methods: The quantitative real-time PCR was used to study the level of miR-335-5p expression in gastric cancer cell lines and tissues. Subsequently, the MTT and cloning formation assays were used to detect cell proliferation, while transwell and wound-healing assays were used to identify invasion and migration of the gastric cancer cells. The correlation between the miR-335-5p and the cell cycle-related target gene mitogen‑activated protein kinase 10 (MAPK10) in gastric cancer was analyzed based on the website. In addition, the target gene of miR-335-5p was detected by luciferase reporter assay, qRT-PCR, and western blotting.Results: The miR-335-5p level was down-regulated in GC tissues and cell lines. Furthermore, miR-335-5p inhibited proliferation, migration of gastric cancer cells, and induced apoptosis. During the G1/S phase, miR-335-5p arrested the cycle of gastric cancer cells in vitro. The correlation between the miR-335-5p and the cell cycle-related target gene MAPK10 in GC was analyzed, MAPK10 was directly targeted by the miR-335-5p.Conclusion: These data suggested that miR-335-5p acts as a tumor suppressor, and go through the MAPK10 to inhibit the GC progression.

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