Elevated expression of NFE2L3 promotes the development of gastric cancer through epithelial-mesenchymal transformation

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.

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Silencing of circ_0078607 prevents development of gastric cancer and inactivates the ERK1/2/AKT pathway through the miR-188-3p/RAP1B axis

Anti-Cancer Drugs ◽

10.1097/cad.0000000000001083 ◽

2021 ◽

Vol Publish Ahead of Print ◽

Author(s):

Weixin Bian ◽

Zhiqiang Liu ◽

Yanjie Chu ◽

Xiaofang Xing

Keyword(s):

Gastric Cancer ◽

Akt Pathway ◽

Development Of Gastric Cancer

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The Role of Polymorphic Variants of Several Genes of Matrix Metalloproteinases and Their Tissue Inhibitors in the Development of Gastric Cancer

Russian Journal of Genetics ◽

10.1134/s1022795421050021 ◽

2021 ◽

Vol 57 (5) ◽

pp. 607-619

Author(s):

L. F. Gallyamova ◽

A. Kh. Nurgalieva ◽

I. I. Khidiyatov ◽

T. R. Nasibullin ◽

F. R. Munasypov ◽

...

Keyword(s):

Gastric Cancer ◽

Matrix Metalloproteinases ◽

Tissue Inhibitors ◽

Polymorphic Variants ◽

Development Of Gastric Cancer

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CanHelicobacter pyloriEradication Prevent the Development of Gastric Cancer?

The Korean Journal of Helicobacter and Upper Gastrointestinal Research ◽

10.7704/kjhugr.2016.16.4.238 ◽

2016 ◽

Vol 16 (4) ◽

pp. 238

Author(s):

Chang Seok Bang ◽

Gwang Ho Baik

Keyword(s):

Gastric Cancer ◽

Development Of Gastric Cancer

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miR-491-5p, mediated by Foxi1, functions as a tumor suppressor by targeting Wnt3a/β-catenin signaling in the development of gastric cancer

Cell Death and Disease ◽

10.1038/cddis.2017.134 ◽

2017 ◽

Vol 8 (3) ◽

pp. e2714-e2714 ◽

Cited By ~ 24

Author(s):

Ruifang Sun ◽

Zhigang Liu ◽

Dongdong Tong ◽

Yang Yang ◽

Bo Guo ◽

...

Keyword(s):

Gastric Cancer ◽

Tumor Suppressor ◽

Development Of Gastric Cancer

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SLCO4A1-AS1 Facilitates the Malignant Phenotype via miR-149-5p/STAT3 Axis in Gastric Cancer Cells

Journal of Oncology ◽

10.1155/2021/1698771 ◽

2021 ◽

Vol 2021 ◽

pp. 1-12

Author(s):

Qing Li ◽

Dachuan Zhang ◽

Hui Wang ◽

Jun Xie ◽

Lei Peng ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Organic Anion ◽

Organic Anion Transporter ◽

Gastric Cancer Cells ◽

Anion Transporter ◽

Transporter Family ◽

Cancer Tissues ◽

Development Of Gastric Cancer

Solute carrier organic anion transporter family member 4A1 (SLCO4A1-AS1), a newly discovered lncRNA, may exert effects in tumors. Since its role in gastric cancer remains obscure, we sought to explore the mechanism of SLCO4A1-AS1 in gastric cancer. The relationship among SLCO4A1-AS1, miR-149-5p, and STAT3 was detected by bioinformatics, dual luciferase analysis, and Pearson’s test, and the expressions of these genes were determined by quantitative real-time PCR and Western blot. Moreover, CCK-8, flow cytometry, wound healing assay, and Transwell analysis were performed to verify the function of SLCO4A1-AS1 in gastric cancer. Rescue experiments were used to detect the role of miR-149-5p. The expressions of SLCO4A1-AS1 and STAT3 were increased, while the expression of miR-149-5p was suppressed in gastric cancer tissues and cell lines. In addition, STAT3 expression was negatively correlated with miR-149-5p expression but was positively correlated with SLCO4A1-AS1 expression. Overexpression of SLCO4A1-AS1 promoted cell viability, migration, invasion, and STAT3 expression but suppressed apoptosis, while knockdown of SLCO4A1-AS1 had the opposite effect. SLCO4A1-AS1 bound to miR-149-5p and targeted STAT3. Moreover, miR-149-5p mimic inhibited the malignant development of gastric cancer cells and obviously reversed the function of SLCO4A1-AS1 overexpression. Our research reveals that abnormally increased SLCO4A1-AS1 expression may be an important molecular mechanism in the development of gastric cancer.

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