Upregulation of miR-582-5p inhibits cell proliferation, cell cycle progression and invasion by targeting Rab27a in human colorectal carcinoma

Zhang, X; Zhang, Y; Yang, Jing; Li, S; Chen, J

doi:10.1038/cgt.2015.44

Cited by 45 publications

(40 citation statements)

References 35 publications

(35 reference statements)

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“…For example, miR-582-5p functions as a tumor suppressor by inhibiting proliferation through suppression of CDK1 expression in hepatocellular carcinoma 21. Similarly, miR-582-5p acts as the tumor suppressor by targeting Rab27a in human colorectal carcinoma 22. Recently, miR-582-5p was reported to inhibit invasion and migration of salivary adenoid cystic carcinoma cells by targeting FOXC1 23.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA UCA1 targets miR-582-5p and contributes to the progression and drug resistance of bladder cancer cells through ATG7-mediated autophagy inhibition

Wu¹,

Ning³

et al. 2019

OTT

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BackgroundRently, the incidence of bladder cancer has been on the rise. Accumulating researches have been conducted to clarify the molecular mechanisms and potential therapeutic targets of bladder cancer. The present study aims to explore the regulatory mechanism of the urothelial carcinoma-associated 1 (UCA1)-miR-582-5p-ATG7 axis in bladder cancer.MethodsQuantitative real-time polymerase chain reaction was used to detect mRNA level. Relative protein expression was detected by western blot. wound healing assay and transwell were used to determine migration and invasion of cells. in addtion, luciferase reporter assay and immunohistochemistry were performed.ResultsUCA1 expression was upregulated in bladder cancer tissues and cells, while the depletion of UCA1 by shRNA resulted in the suppression of cell proliferation, invasion, migration, and drug resistance. Further studies demonstrated that UCA1 could directly interact with miR-582-5p, and that there was an inverse correlation between miR-582-5p and UCA1. In addition, we found that ATG7 is a target of miR-582-5p and can be downregulated by either miR-582-5p overexpression or UCA1 knockdown. In particular, the autophagy is reduced when UCA1 shRNA is introduced. Moreover, the in vivo experiment further demonstrated the contribution of UCA1 in bladder cancer including tumor growth, invasion, and migration, and UCA1 knockdown can inhibit the aforementioned activities.ConclusionThese results provided evidence for a novel UCA1 interaction regulatory network in bladder cancer, that is, UCA1-miR-582-5p-ATG7-autophagy axis. Our study provides a new insight into the treatment of bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA UCA1 targets miR-582-5p and contributes to the progression and drug resistance of bladder cancer cells through ATG7-mediated autophagy inhibition

Wu¹,

Ning³

et al. 2019

OTT

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“…Jiang et al revealed a tumor suppressive role of miR-449b-5p that restricts the growth and invasion of breast cancer cells through inhibiting CREPT-mediated activation of Wnt/β-catenin [ 9 ]. In addition, miR-582-5p exerts oncogenic role in prostate cancer [ 10 ] and tumor suppressive role in colorectal cancer [ 11 ], which indicated its dual function against different tumors. Recently, miR-924 was shown to inversely regulate the expression of α-defensin 5 (DEFA5) in inflammatory bowel disease [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-924 as a tumor suppressor inhibits non-small cell lung cancer by inhibiting RHBDD1/Wnt/β-catenin signaling pathway

et al. 2020

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Background MiR-924 has been reported to be a tumor suppressor in hepatocellular carcinoma. However, the functions and mechanisms of miR-924 in non-small cell lung cancer (NSCLC) remain unclear. Methods The expression of miR-924 was determined in NSCLC tissues and cell lines using quantitative real time PCR. The Chi-squared test was used to evaluate the correlation between miR-924 levels and clinicopathological parameters in patients with NSCLC. Cell proliferation was assessed by CCK-8 assay. Cell migration and invasion were detected by transwell assay. The combination of miR-924 and RHBDD1 was analyzed via the luciferase reporter assay. The expression level of RHBDD1 was evaluated in lung cancer tissues using public microarray datasets form Oncomine and its prognostic value was assessed by Kaplan–Meier Plotter databases. A tumor xenograft mouse model was established to illustrate the effects of miR-924 on the tumorigenesis of NSCLC in vivo. Results In this study, we found miR-924 was strikingly decreased in NSCLC tissues and cell lines. Decreased miR-924 was closely correlated with advanced tumor-node-metastasis (TNM) stage and lymphatic metastasis in NSCLC patients. Noticeably, rhomboid domain-containing protein 1 (RHBDD1) was predicted and confirmed as a direct target of miR-924. Moreover, the expression level of RHBDD1 was significantly increased and inversely associated with prognosis using public microarray datasets form Oncomine and Kaplan–Meier Plotter databases. MiR-924 overexpression suppressed cell proliferation, migration and invasion. The in vivo experiments further demonstrated that miR-924 overexpression reduced NSCLC xenograft growth through inhibiting RHBDD1/Wnt/β-catenin signaling pathway. Conclusions In summary, these findings demonstrated that miR-924 blocked the progression of NSCLC by targeting RHBDD1 and miR-924/RHBDD1 axis might provide a novel therapeutic target for the treatment of NSCLC.

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“…LncRNA XLOC_006390 potentiates the malignancy of cervical cancer cells through miR-331-3p and miR-338-3p sponging [34]. MiR-582-5p serves as a tumor suppressor in many cancers, including hepatocellular carcinoma, colorectal carcinoma, gastric cancer and NSCLC [20,21,[35][36][37]. MiR-582-5p suppresses the proliferation and metastasis of colorectal cancer cells via Ras-related protein Rab27a [36], and impedes the proliferation and motility of NSCLC cells [21].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-582-5p serves as a tumor suppressor in many cancers, including hepatocellular carcinoma, colorectal carcinoma, gastric cancer and NSCLC [20,21,[35][36][37]. MiR-582-5p suppresses the proliferation and metastasis of colorectal cancer cells via Ras-related protein Rab27a [36], and impedes the proliferation and motility of NSCLC cells [21]. MiR-582-5p was found to be a direct target of NEAT1, and functional experiments showed that NEAT1 undermined NSCLC by sponging miR-582-5p.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

Zhang

Sun

Zou

2020

ARCH BIOL SCI BELGRA

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In this study, we aimed to elucidate the role of long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the abundance of NEAT1, microRNA-582-5p (miR-582-5p) and eukaryotic translation initiation factor 4 gamma 2 (EIF4G2). Proliferation, apoptosis, metastasis and glycolytic metabolism were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) flow cytometry, transwell assays and fluorescence-based glucose and lactate assay kits. The targets of NEAT1 and miR-582-5p were predicted by the starBase website, and dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to verify these predictions. Western blot analysis was conducted to detect the protein expression of EIF4G2. A xenograft tumor model was built to clarify the role of NEAT1 in vivo. Results showed that NEAT1 interference inhibited proliferation, metastasis and glycolysis, and facilitated the apoptosis of NSCLC cells. MiR-582-5p was a functional target of NEAT1, and the biological influence of NEAT1 intervention on NSCLC cells was alleviated by transfection with anti-miR-582-5p. MiR-582-5p could bind to EIF4G2 messenger RNA (mRNA); it exerted its antitumor role in NSCLC cells by inhibiting EIF4G2. EIF4G2 was regulated by NEAT1/miR-582-5p signaling. NEAT1 accelerated NSCLC tumor growth via the miR-582-5p/EIF4G2 axis in vivo. In conclusion, NEAT1 affected NSCLC by elevating their malignant potential via the miR-582-5p/EIF4G2 axis.Abbreviations: long non-coding RNA (lncRNA); nuclear enriched abundant transcript 1 (NEAT1); non-small cell lung cancer (NSCLC); eukaryotic translation initiation factor 4 gamma (EIF4G); eukaryotic initiation factor 4F (EIF4F) Arch Biol Sci. 2020;72(2):243-252 https://doi.

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Upregulation of miR-582-5p inhibits cell proliferation, cell cycle progression and invasion by targeting Rab27a in human colorectal carcinoma

Cited by 45 publications

References 35 publications

Long noncoding RNA UCA1 targets miR-582-5p and contributes to the progression and drug resistance of bladder cancer cells through ATG7-mediated autophagy inhibition

Long noncoding RNA UCA1 targets miR-582-5p and contributes to the progression and drug resistance of bladder cancer cells through ATG7-mediated autophagy inhibition

MiR-924 as a tumor suppressor inhibits non-small cell lung cancer by inhibiting RHBDD1/Wnt/β-catenin signaling pathway

LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

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