MiR-30b suppresses tumor migration and invasion by targeting EIF5A2 in gastric cancer

Tian, Shu-bo; Yu, Jian-chun; Liu, Yuqin; Kang, Weiming; Ma, Zhiqiang; Ye, Xin; Yan, Chao

doi:10.3748/wjg.v21.i31.9337

Cited by 41 publications

(36 citation statements)

References 30 publications

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“…Among the results in this research, one of them implied that miR‐30b and miR‐30d were poorly expressed, and CEACAM1 was highly expressed in liver tissues of FHF mice and serum of FHF patients. Similarly, down‐regulation of miR‐30b in gastric cancer cell lines and tissues has been unraveled in a recent literature . Xiong et al have pointed out that members of the miR‐30 family, particularly miR‐30b was depleted in triple‐positive pancreatic cancer stem cells .…”

Section: Discussionmentioning

confidence: 88%

Up‐regulation of microRNA‐30b/30d cluster represses hepatocyte apoptosis in mice with fulminant hepatic failure by inhibiting CEACAM1

et al. 2020

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Recently, impacts of microRNAs have been unraveled in human diseases, and we aimed to confirm the role of miR‐30b/30d in fulminant hepatic failure (FHF). Expression of miR‐30b/30d and CEACAM1 in serum of FHF patients and healthy people was measured by reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and Western blot analysis. Mice FHF models were established by injection of D‐Galn and lipopolysaccharide, and were treated with miR‐30b/30d mimics. Oxidative stress, liver injury, and inflammatory reaction in mouse liver tissues were measured using oxidative stress‐related factor kits, hematoxylin–eosin staining and enzyme‐linked immunosorbent assay, respectively. Moreover, cell cycle distribution and apoptosis of hepatocytes of mice were determined by flow cytometry, and the target relation between miR‐30b/30d and CEACAM1 was confirmed by bioinformatic method and dual luciferase reporter gene assay. MiR‐30b/30d expression was positively, and CEACAM1 expression was negatively related to prognosis of FHF patients. Up‐regulation of miR‐30b/30d attenuated oxidative stress, liver injury, and inflammatory reaction, and improved survival rate of FHF mice. Furthermore, elevated miR‐30b/30d ameliorated apoptosis and cell cycle arrest of hepatocytes of FHF mice. CEACAM1 was a target gene of miR‐30b/30d. This study highlights that up‐regulated miR‐30b/30d attenuates the progression of FHF by targeting CEACAM1, which may be helpful to FHF treatment.

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Section: Discussionmentioning

confidence: 88%

Up‐regulation of microRNA‐30b/30d cluster represses hepatocyte apoptosis in mice with fulminant hepatic failure by inhibiting CEACAM1

et al. 2020

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“…Previous studies have demonstrated that EIF5A2 exhibits its tumorigenic effects via activation of the phosphoinositide-3-kinase/Rac-α serine/threonine-protein kinase signaling pathway (15,25) and its induction of matrix metalloproteinase 2 protein expression (26). In addition, EIF5A2 reduces expression of E-cadherin and increases expression of Vimentin (26,27), and may activate transforming protein RhoA precursor/Rac1 signaling pathways (24). Additionally, a previous study identified zinc finger protein Gli1 as a putative transcription factor for EIF5A2 (28).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of EIF5A2 inhibits the malignant potential of non-small cell lung cancer cells

Chen

Zhang

et al. 2018

Oncol Lett

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Abstract. Eukaryotic translation initiation factor 5A2(EIF5A2) has been demonstrated to be upregulated in numerous types of human cancer and is associated with cancer progression. However, the expression and role of EIF5A2 in non-small cell lung cancer (NSCLC) remains unclear. In the present study, the role of EIF5A2 in NSCLC was investigated, in addition to the underlying molecular mechanisms by which EIF5A2 acts. Relative EIF5A2 expression levels were determined in NSCLC cells and compared with levels in non-cancerous lung tissues. Short interfering (si)RNA targeted against EIF5A2 was used to knock down EIF5A2 levels in NSCLC cells. Cell proliferation, apoptosis rate, migration ability and invasion ability were determined in untreated and siRNA-treated NSCLC cells, in addition to the relative protein expression levels of various tumorigenic proteins and E-cadherin. EIF5A2 expression was significantly higher in NSCLC tissues compared with adjacent normal tissues. Knockdown of EIF5A2 in the NSCLC cells significantly inhibited cell proliferation and induced apoptosis. Furthermore, EIF5A2 silencing suppressed cell migratory and invasive capacities in vitro. Silencing of EIF5A2 in the NSCLC cells resulted in the downregulation of the tumorigenic proteins, apoptosis regulator Bcl-2 and myc proto-oncogene protein, and upregulation of E-cadherin, suggesting that EIF5A2 promotes proliferation and metastasis through these proteins. EIF5A2 may therefore serve as a novel therapeutic target for the treatment of NSCLC.

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“…miR-30b has been previously described as a tumor suppressor in certain types of cancer, including NSCLC, gastric cancer and colorectal cancer (CRC) (14,21,22). Conversely, miR-30b has been described as an oncogene in bladder cancer (23), oral squamous cell cancer (10) and medulloblastoma (24).…”

Section: Discussionmentioning

confidence: 99%

“…In certain types of cancer, the mechanism of miR-30b is understood. Tian et al (22) demonstrated that miR-30b regulated gastric cancer cell processes by targeting eukaryotic translation initiation factor 5A2. In gastric cancer, Zhu et al (15) indicated that miR-30b could promote cell apoptosis and suppress tumor growth in vivo by targeting plasminogen activator inhibitor-1.…”

Section: Discussionmentioning

confidence: 99%

Identification of miR-30b as an oncogene in renal cell carcinoma

Jin

et al. 2017

Molecular Medicine Reports

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microRNAs (miRs) have been investigated as a novel class of regulators of cellular processes, including proliferation, apoptosis and metabolism. In particular, miR‑30b has been demonstrated to be deregulated in certain types of cancer, including lung, colorectal and gastric cancer. Previous studies of miR‑30b in renal clear cell carcinoma demonstrated that the expression level of miR‑30b was associated with distant metastasis. However, the function of miR‑30b in renal cell carcinoma (RCC) remained to be elucidated. In the present study, the expression of miR‑30b in 31 paired RCC tissues from four cell lines (786‑O, 769‑P, ACHN and 293T) was detected by reverse transcription‑quantitative polymerase chain reaction. In addition, the effect of miR‑30b on cell proliferation in RCC cells was also determined using MTT and Cell Counting Kit‑8 assay analyses. Furthermore, the function of miR‑30b in cell migration and invasion was determined by wound scratch and Transwell assays. Flow cytometry was also performed to quantify the effect of miR‑30b on cell apoptosis. The results of the current study indicated that miR‑30b was upregulated in RCC tissues from affected cell lines when compared with adjacent normal tissues and a normal kidney cell line, which is different to the downregulation of miR‑30b as observed in other types of cancer. miR‑30b is associated with RCC cell proliferation, invasion, migration and apoptosis, which indicated that miR‑30b acts as an oncogene in RCC. To the best of our knowledge, the present study is the first to demonstrate the upregulation of miR‑30b in RCC tissues and describe miR‑30b as an oncogene in RCC in the regulation of cell proliferation, migration, invasion and apoptosis. Further studies will define the target gene of miR‑30b in RCC and investigate the potential role of miR‑30b as a biomarker for RCC.

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MiR-30b suppresses tumor migration and invasion by targeting EIF5A2 in gastric cancer

Abstract: Our findings describe a link between miR-30b and EIF5A2, which plays an important role in mediating epithelial-mesenchymal transition.

Cited by 41 publications

References 30 publications

Up‐regulation of microRNA‐30b/30d cluster represses hepatocyte apoptosis in mice with fulminant hepatic failure by inhibiting CEACAM1

Up‐regulation of microRNA‐30b/30d cluster represses hepatocyte apoptosis in mice with fulminant hepatic failure by inhibiting CEACAM1

Knockdown of EIF5A2 inhibits the malignant potential of non-small cell lung cancer cells

Identification of miR-30b as an oncogene in renal cell carcinoma

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