miR-101 Inhibits Proliferation and Promotes Apoptosis of Gastric Cancer Cells Through Inhibition of Angiopoietin-Like Protein 2

2019 ◽  
Vol 9 (9) ◽  
pp. 1298-1303
Author(s):  
Jiping Xie ◽  
Qin Zhou
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cells ◽  
Qrt Pcr ◽  
Gastric Cancer Cell Proliferation ◽  
Cancer Tissues ◽  
Relationship Of

ANGPTL2 abnormal expression is associated with various tumors. miR-101 abnormalities are associated with gastric cancer. There is a targeted relationship of miR-101 with ANGPTL2. This study intends to assess miR-101’s role gastric cancer cells. The gastric cancer tissues and adjacent tissues were collected to detect miR-101 and ANGPTL2 by qRT-PCR. Gastric cancer SGC7901 cells were divided into miR-NC group and miR-101 mimic group followed by analysis of ANGPTL2 expression by qRT-PCR and western blot, apoptosis by flow cytometry, and cell proliferation by EdU staining. Gastric cancer tissues had significantly decreased miR-101 and increased ANGPTL2 mRNA expression than adjacent tissues. The survival of patients with lower miR-101 level was significantly lower than higher miR-101 patients. There was a relationship between miR-101 and ANGPTL2. miR-101 mimic transfection significantly reduced ANGPTL2 expression, reduced cell proliferation and increased cell apoptosis. Abnormal miR-101 and ANGPTL2 expression is found in gastric cancer. miR-101 inhibits ANGPTL2 expression and gastric cancer cell proliferation and induces apoptosis.

scholarly journals Long Noncoding RNA KLF3-AS1 Acts as an Endogenous RNA of miR-223 to Attenuate Gastric Cancer Progression and Chemoresistance

2021 ◽  
Vol 11 ◽  
Author(s):  
Houxiang Jiang ◽  
KaiFeng Hu ◽  
Yabing Xia ◽  
Linhu Liang ◽  
Xiaoli Zhu
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Inhibitory Effects ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Proliferation

Gastric cancer is a deadly disease, and the low rate of early diagnosis and chemoresistance largely contributed to the poor prognosis of gastric cancer. LncRNAs have been extensively reported for their roles in regulating cancer progression. In this study, we found that KLF3-AS1 was down-regulated in gastric cancer cells. Overexpression of KLF3-AS1 repressed gastric cancer cell proliferation, growth. In addition, KLF3-AS1 overexpression also exerted inhibitory effects on the gastric cancer cell invasion, migration and EMT, but promoted chemosensitivity of gastric cancer cells to cisplatin. The mechanistic studies showed that KLF3-AS1 could act as the “sponge” for miR-223 and to repress miR-223 expression in gastric cancer cells. Overexpression of miR-223 reversed the inhibitory effects of KLF3-AS1 overexpression on gastric cancer cell proliferation, invasion, migration and EMT, and attenuated the enhanced effects of KLF3-AS1 overexpression on gastric cancer cell chemosensitivity to cisplatin. The in vivo studies showed that KLF3-AS1 overexpression suppressed the tumor growth of SGC-7901 in the nude mice. In conclusion, our results for the first time demonstrated that KLF3-AS1 was down-regulated in gastric cancer cells and repressed gastric cancer cell proliferation, invasion, migration and EMT, and enhanced chemosensitivity to cisplatin. Further mechanistic results indicated that KLF3-AS1 exerted its biological function in gastric cancer cells by inhibiting miR-223 expression. Future studies are still required to decipher the detailed molecular mechanisms of KLF3-AS1 in gastric cancer.

scholarly journals miR-504 Promoted Gastric Cancer Cell Proliferation and Inhibited Cell Apoptosis by Targeting RBM4

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Yi Zhang ◽  
Hongmei Yong ◽  
Jing Fu ◽  
Guangyi Gao ◽  
Huichang Shi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
Normal Group ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Proliferation

Background. The purpose of this study was to explore the role and underlying mechanism of miR-504 and RBM4 in gastric cancer. Methods. The qRT-PCR or Western blot was performed to determine the expressions of miR-504 and RBM4 in the gastric cancer tissues and normal tissues. Human SGC-7901 cells were transfected with miR-504 mimic/inhibitor or pcDNA-RBM4. Cell proliferation and cell apoptosis were assessed by colony formation assay and flow cytometry, respectively. Luciferase reporter gene assays were used to investigate interactions between miR-504 and RBM4 in SGC-7901 cells. Results. The relative expression of miR-504 was significantly upregulated in the gastric cancer group ( n = 25 ) than in the paired normal group ( n = 25 ), but the relative RBM4 expression was remarkably downregulated in the gastric tumor group, compared with the normal group. Additionally, miR-504 overexpression increased the viability of gastric cancer cells. Moreover, RBM4 is a functional target of miR-504 in gastric cancer cells. miR-504 was further confirmed to promote SGC-7901 cell proliferation and inhibit cell apoptosis by downregulation RBM4 in vitro. Conclusions. miR-504 promotes gastric cancer cell proliferation and inhibits cell apoptosis by targeting RBM4, and this provides a potential diagnostic biomarker and treatment for patients with gastric cancer.

Identification of novel 3-nitroacridines as autophagy inducers in gastric cancer cells

2017 ◽  
Vol 41 (10) ◽  
pp. 4087-4095
Author(s):  
Jia Yu ◽  
Xiaoqing Zhao ◽  
Nanmengzi Zhang ◽  
Chaoqun You ◽  
Gang Yao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cells ◽  
Cell Death Pathway ◽  
Gastric Cancer Cell Proliferation

Nine novel 3-nitroacridines were synthesized, of which 3 compounds inhibited gastric cancer cell proliferation via an autophagy-associated cell death pathway.

MiR-203 Affects Proliferation, Apoptosis and Cisplatin Resistance of Gastric Cancer Cells Through DJ-1-PTEN-PI3K/AKT Pathway

2019 ◽  
Vol 9 (11) ◽  
pp. 1557-1562
Author(s):  
Liangrun Zhu ◽  
Nan Zhang ◽  
Xia Shao ◽  
Ning Zhang Lili Dong ◽  
Liya Song
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
Cancer Drug ◽  
Akt Pathway ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Proliferation

DJ-1 negatively regulates phosphatase and tensin homolog gene (PTEN). Abnormal miR-203 expression is associated with gastric cancer. Bioinformatics analysis showed a targeting relationship between miR-203 and DJ-1 3′-UTR. Our study evaluated the role of miR-203 gastric cancer cell proliferation, apoptosis, and cisplatin (DDP) resistance. The CDDP-resistant cell line SGC7901/CDDP was established and divided into miR-NC group and miR-203 mimic group followed by detecting DJ-1, PTEN and p-AKT expression, and cell apoptosis and proliferation by flow cytometry. There was a targeted relationship between miR-203 and DJ-1 mRNA. miR-203 expression in SGC7901/CDDP cells was significantly reduced compared with SGC7901 cells with elevated DJ-1 mRNA and protein level. Compared with miR-NC group, DJ-1 and p-AKT in SGC7901/CDDP cells was significantly downregulated in miR-203 mimic transfection group, while PTEN expression was significantly increased, cell apoptosis was increased, and proliferation and CDDP resistance were reduced. Decreased miR-203 and increased DJ-1 level is associated with gastric cancer drug resistance. Elevated miR-203 can downregulate DJ-1, affect the activity of PTEN-PI3K/AKT pathway, inhibit gastric cancer cell proliferation, promote cell apoptosis, and enhance the drug sensitivity to CDDP.

The Effect of LncRNA Zinc Finger E-Box-Binding Homeobox 1 Antisense 1 on the Biological Characteristics of Gastric Cancer Cells by Regulating the MiR-200b/Wnt1 Axis

2021 ◽  
Vol 11 (3) ◽  
pp. 541-547
Author(s):  
Minghai Shen ◽  
Weidong Zhang ◽  
Bei Wang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Molecular Axis ◽  
Luciferase Reporter ◽  
Cancer Cell Proliferation ◽  
Qrt Pcr ◽  
Gastric Cancer Cell Proliferation ◽  
Proliferation And Invasion

In recent decades, most gastric cancer patients are diagnosed in the advanced disease stage with poor prognosis, and more than half of the advanced-stage patients will relapse. This research explores lncRNA ZEB1-AS1’s effect on gastric cancer cell proliferation, invasion, apoptosis via regulating the miR-200b/Wnt1 molecular axis. ZEB1-AS1 and miR-200b expressions in BGC-803, SGC-7901, MKN-45, and AGS cells were measured by qRT-PCR. ZEB1-AS1 siRNA, miR-200b mimics, and miR-200b mimics + pcDNA3.1-ZEB1-AS1 were transfected into BGC-803 cells to study their respective effect on cell proliferation, invasion, apoptosis using CCK-8 and Transwell assays and flow cytometry, respectively. Dual-luciferase reporter gene assay is used to detect the luciferase activity of ZEB1-AS1 WT or MUT and Wnt1 WT or MUT after co-transfecting with miR-200b mimics. The expression of miR-200b in BGC-803 cells with knocked down or overexpressed ZEB1-AS1 was quantified with qRT-PCR. Western blot analysis was used to detect the protein level of Wnt1 in BGC-803 cells with upregulated or downregulated miR-200b expression. Data showed that ZEB1-AS1 expression was significantly raised when miR-200b expression was reduced (P < 0.05). BGC-803 cells were selected for follow-up experiments. ZEB1-AS1, Wnt1, and miR-200b were found to have a targeted regulatory relationship. The knockdown of ZEB1-AS1 and upregulation of miR-200b can hinder BGC-803 cell proliferation and invasion and expedite apoptosis. ZEB1-AS1 and miR-200b overexpression can reverse the effect of miR-200b upregulation on BGC-803 cell proliferation, invasion, and apoptosis. Therefore, lncRNA ZEB1-AS1 could impede gastric cancer cell proliferation and invasion and accelerate apoptosis via the regulation of the miR-200b/Wnt1 molecular axis.

scholarly journals LncRNA UCA1 promotes development of gastric cancer via the miR-145/MYO6 axis

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
An Yang ◽  
Xin Liu ◽  
Ping Liu ◽  
Yunzhang Feng ◽  
Hongbo Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Development Of Gastric Cancer

Abstract Background Long noncoding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1) is aberrantly expressed in multiple cancers and has been verified as an oncogene. However, the underlying mechanism of UCA1 in the development of gastric cancer is not fully understood. In the present study, we aimed to identify how UCA1 promotes gastric cancer development. Methods The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to analyze UCA1 and myosin VI (MYO6) expression in gastric cancer. Western blot and quantitative real-time PCR (QPCR) were performed to test the expression level of the UCA1/miR-145/MYO6 axis in gastric cancer cell lines and tissues. The roles of the UCA1/miR-145/MYO6 axis in gastric cancer in vitro and in vivo were investigated by CCK-8 assay, flow cytometry, siRNAs, immunohistochemistry, and a mouse xenograft model. The targeted relationship among UCA1, miR-145, and MYO6 was predicted using LncBase Predicted v.2 and TargetScan online software, and then verified by luciferase activity assay and RNA immunoprecipitation. Results UCA1 expression was higher but miR-145 expression was lower in gastric cancer cell lines or tissues, compared to the adjacent normal cell line or normal tissues. Function analysis verified that UCA1 promoted cell proliferation and inhibited cell apoptosis in the gastric cancer cells in vitro and in vivo. Mechanistically, UCA1 could bind directly to miR-145, and MYO6 was found to be a downstream target gene of miR-145. miR-145 mimics or MYO6 siRNAs could partly reverse the effect of UCA1 on gastric cancer cells. Conclusions UCA1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-145 to upregulate MYO6 expression in gastric cancer, indicating that the UCA1/miR-145/MYO6 axis may serve as a potential therapeutic target for gastric cancer.

scholarly journals Carnosic Acid Induces Apoptosis and Inhibits Akt/mTOR Signaling in Human Gastric Cancer Cell Lines

2021 ◽  
Vol 14 (3) ◽  
pp. 230
Author(s):  
Waseem El-Huneidi ◽  
Khuloud Bajbouj ◽  
Jibran Sualeh Muhammad ◽  
Arya Vinod ◽  
Jasmin Shafarin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Carnosic Acid ◽  
Human Gastric Cancer ◽  
Cancer Cell Proliferation ◽  
Human Gastric Cancer Cell ◽  
Gastric Cancer Cell Lines ◽  
Gastric Cancer Cell Proliferation

Gastric cancer is among the most common malignancies worldwide. Due to limited availability of therapeutic options, there is a constant need to find new therapies that could target advanced, recurrent, and metastatic gastric cancer. Carnosic acid is a naturally occurring polyphenolic abietane diterpene derived from Rosmarinus officinalis and reported to have numerous pharmacological effects. In this study, the cytotoxicity assay, Annexin V-FITC/PI, caspases 3, 8, and 9, cell cycle analysis, and Western blotting were used to assess the effect of carnosic acid on the growth and survival of human gastric cancer cell lines (AGS and MKN-45). Our findings showed that carnosic acid inhibited human gastric cancer cell proliferation and survival in a dose-dependent manner. Additionally, carnosic acid is found to inhibit the phosphorylation/activation of Akt and mTOR. Moreover, carnosic acid enhanced the cleavage of PARP and downregulated survivin expression, both being known markers of apoptosis. In conclusion, carnosic acid exhibits antitumor activity against human gastric cancer cells via modulating the Akt-mTOR signaling pathway that plays a crucial role in gastric cancer cell proliferation and survival.

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