miR-133a acts as a tumor suppressor in colorectal cancer by targeting eIF4A1

Li, Wenfeng; Chen, Anqi; Xiong, Lingling; Chen, Ting; Tao, Fengxing; Lu, Yiyi; He, Qiaojun; Zhao, Liang; Ou, Rongying; Xu, Yunsheng

doi:10.1177/1010428317698389

Cited by 38 publications

(34 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, we found that EIF4A1 was a target of miR-599. Li et al unraveled that miR-133a could decelerate the progression of colorectal cancer by targeting EIF4A1 [30]. Wei et al demonstrated that EIF4A1 could function as a target of miR-1284 to participate in the regulation of GC [20].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Circ_0008035 contributes to cell proliferation and inhibits apoptosis and ferroptosis in gastric cancer via miR-599/EIF4A1 axis

Tian

Liang

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background: Currently, multiple circular RNAs (circRNAs) have been verified to act as essential regulators in the progression of gastric cancer (GC). We aimed to investigate the role of circ_0008035 in GC progression. Methods:Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to measure the expression of circ_0008035 and miR-599. 3-(4,5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay was employed to evaluate cell proliferation and ferroptosis. Western blot assay was performed to measure the levels of cyclin D1, proliferating cell nuclear antigen (PCNA) and eukaryotic initiation factor 4A1 (EIF4A1). Flow cytometry analysis was conducted to assess cell apoptosis. The iron accumulation, lipid peroxidation and mitochondrial membrane potential were examined by relevant kits. Dual-luciferase reporter assay was conducted to determine the targeting relationship between miR-599 and circ_0008035 or EIF4A1. A murine xenograft model was established to investigate the function of circ_0008035 in vivo. Results:Circ_0008035 was up-regulated in GC tissues and cells. Silencing of circ_0008035 repressed cell proliferation and induced cell apoptosis and ferroptosis in GC cells. Circ_0008035 acted as a sponge of miR-599. The effects of circ_0008035 knockdown on GC cell proliferation, apoptosis and ferroptosis were abolished by miR-599 inhibition. EIF4A1 was confirmed to be a target gene of miR-599. Circ_0008035 knockdown inhibited EIF4A1 expression by targeting miR-599. Moreover, the suppressive role of circ_0008035 deficiency in GC progression could be restored by EIF4A1. Additionally, circ-0008035 knockdown hampered tumorigenesis in vivo. Conclusion:Circ_0008035 promoted GC cell growth and repressed apoptosis and ferroptosis by up-regulating EIF4A1 through sponging miR-599.

show abstract

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Circ_0008035 contributes to cell proliferation and inhibits apoptosis and ferroptosis in gastric cancer via miR-599/EIF4A1 axis

Tian

Liang

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

show abstract

“…MiR-133a has been reported as a tumor suppressor in several cancer types, such as glioma, colorectal cancer, etc. ( 31 , 32 ). For OS, miR-133a down-regulation is associated to unfavorable prognosis in patients with OS ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Astragalus polysaccharides decrease proliferation, migration, and invasion but increase apoptosis of human osteosarcoma cells by up-regulation of microRNA-133a

Chu

Yuan

Chi

et al. 2018

Braz J Med Biol Res

View full text Add to dashboard Cite

Osteosarcoma (OS) has a high incidence, malignity, and frequency of recurrence and metastasis. In this study, we aimed to explore the potential anti-cancer effects of Astragalus polysaccharides (APS) on human OS MG63 cells as well as underlying mechanisms. Viability of MG63 cells was assessed by CCK-8 assay to determine the adequate concentration of APS. Then, effects of APS on MG63 cell proliferation, cell cycle distribution, apoptosis, and migration and invasion were analyzed by BrdU incorporation, PI staining, flow cytometry, and transwell assays, respectively. The expression levels of proteins involved in these physiological processes were assessed by western blot analysis. Afterwards, miR-133a level in APS-treated cells was determined by qRT-PCR, and whether APS affected MG63 cells through regulation of miR-133a was determined. Finally, the activation of c-Jun N-terminal protein kinase (JNK) pathway was detected. We found that APS treatment suppressed the viability, proliferation, migration, and invasion of MG63 cells, as well as induced cell apoptosis. Moreover, APS enhanced the expression of miR-133a in MG63 cells. Knockdown of miR-133a reversed the APS treatment-induced MG63 cell proliferation, migration and invasion inhibition, as well as cell apoptosis. Furthermore, APS inactivated JNK pathway in MG63 cells. Knockdown of miR-133a reversed the APS treatment-induced inactivation of JNK pathway in MG63 cells. To conclude, APS repressed proliferation, migration, and invasion while induced apoptosis of OS MG63 cells by up-regulating miR-133a and then inactivating JNK pathway.

show abstract

“…miRNAs typically bind to the mRNA 3′-UTR of its target gene or directly cut the mRNA at a post-transcriptional level, thereby inhibiting the expression of the target gene ( 5 , 6 ). miR-133a has been reported to be an antioncogene, which was correlated with cell development, proliferation and prognosis in colon cancer, oral squamous cell carcinoma and gastric cancer ( 14 , 16 , 27 ). In the present study, we verified that USP39 was a direct target of miR-133a in gastric cancer cell lines GC-27 and MGC-803.…”

Section: Discussionmentioning

confidence: 99%

“…In oral squamous cell carcinoma, miR-133a inhibits cell proliferation and invasion by suppressing COL1A1 ( 14 ). Furthermore, in colorectal cancer, miR-133a acts as a tumor suppressor to inhibit cell growth and migration by targeting elF4A1 in vitro ( 15 ). In addition, miR-133a had a low expression and inhibited cell proliferation, invasion and induced apoptosis in gastric carcinoma cells ( 12 , 16 , 17 ).…”

Section: Introductionmentioning

confidence: 99%

miR‑133a, directly targeted USP39, suppresses cell proliferation and predicts prognosis of gastric cancer

Dong

Jiang

et al. 2018

Oncol Lett

View full text Add to dashboard Cite

Gastric cancer has high incidence and mortality, and the mortality ranks second only to lung cancer. Downregulation of miR-133a has been observed in certain types of tumors, and it is involved in gastric cancer. The aim of the present study was to explore the molecular mechanisms of miR-133a and ubiquitin-specific protease 39 (USP39) in gastric cancer. Western blot analysis and RT-PCR were employed to measure miR-133a and USP39 expression. To confirm whether miR-133a targeted USP39, we conducted a luciferase reporter assay. We utilized 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay to detect the effects of miR-133a on gastric cell proliferation. miR-133a was significantly downregulated in cancer tissues and cell lines (HGC-27 and MGC-803), while the expression level of USP39 was higher in tumor tissues than in paracancerous tissues. Upregulated expression of miR-133a and/or USP39 downregulation could inhibit cell proliferation in gastric cancer cells. Furthermore, USP39 was identified as a direct target of miR-133a and the inverse relationship between them was also observed. USP39 was a firsthand target of miR-133a and there was a negative correlation between them. In addition, a low expression of miR-133a or overexpression of USP39 predicted poor prognosis. In conclusion, miR-133a may be a novel therapeutic target of microRNA-mediated suppression of cell proliferation in CC, but the role of the miR-133a/USP39 axis in CC progression needs further study.

show abstract

miR-133a acts as a tumor suppressor in colorectal cancer by targeting eIF4A1

Cited by 38 publications

References 21 publications

RETRACTED ARTICLE: Circ_0008035 contributes to cell proliferation and inhibits apoptosis and ferroptosis in gastric cancer via miR-599/EIF4A1 axis

RETRACTED ARTICLE: Circ_0008035 contributes to cell proliferation and inhibits apoptosis and ferroptosis in gastric cancer via miR-599/EIF4A1 axis

Astragalus polysaccharides decrease proliferation, migration, and invasion but increase apoptosis of human osteosarcoma cells by up-regulation of microRNA-133a

miR‑133a, directly targeted USP39, suppresses cell proliferation and predicts prognosis of gastric cancer

Contact Info

Product

Resources

About