Mir-30d suppresses cell proliferation of colon cancer cells by inhibiting cell autophagy and promoting cell apoptosis

Zhang, Rui; Xu, Jian; Zhao, Jian; Bai, Jinghui

doi:10.1177/1010428317703984

Cited by 56 publications

(32 citation statements)

References 26 publications

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“…Downregulation of miR-30d correlated with aggressive cancer progression while its ectopic expression contributed to suppression of cancer development in colorectal carcinoma [28]. miR-30d functioned as a tumor suppressor by facilitating cancer cell apoptosis [29]. Partially consistent with our finding, miR-30d was determined to be one of downregulated miRNA in ATC, the least common but the most fatal thyroid cancer [30].…”

Section: Discussionsupporting

confidence: 81%

WITHDRAWN: Contribution of microRNA-30d to the prevention of the thyroid cancer progression: mechanism and implications

Shao¹,

Zhang²,

Wang³

et al. 2020

Preprint

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Background Thyroid cancer is a major endocrine tumor and represents an emerging health problem worldwide. MicroRNAs (miRNAs) have been addressed to be associated with the pathogenesis and progression of thyroid cancer. However, it remains largely unknown what functions miR-30d may exert on thyroid cancer. This study herein aimed to identify the functional significance and mechanism of miR-30d in the progression of thyroid cancer. Methods The expression of miR-30d and ubiquitin-specific protease 22 (USP22) in cancerous tissues of patients with thyroid cancer was measured using RT-qPCR and Western blot analysis. In response to the gain- or loss-of-function of miR-30d and USP22, cell apoptosis was evaluated by flow cytometry and TUNEL staining in combination with the measurement of apoptosis-related proteins. The interactions among miR-30d, USP22, SIRT1, FOXO3a and PUMA were explored using a series of assays, including dual-luciferase reporter gene assay, Co-IP and ChIP assay. The effects of miR-30d and USP22 on thyroid tumorigenesis were finally validated in vivo. Results MiR-30b presented aberrant low expression in thyroid cancer tissues and this low expression correlated with poor prognosis of thyroid cancer patients. miR-30d promoted apoptosis of thyroid cancer cells through targeting USP22, an up-regulated gene in thyroid cancer. USP22 could enhance the stability of SIRT1 by inducing deubiquitination which consequently contributed to FOXO3a deacetylation-induced PUMA repression. It was verified that this regulatory mechanism was responsible for the pro-apoptotic effect of miR-30d by the in vivo tumorigenicity assay. Conclusion To conclude, the progression of thyroid cancer can be suppressed by miR-30d-mediated inhibition of USP22, provides a promising therapeutic target for thyroid cancer treatment.

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Section: Discussionsupporting

confidence: 81%

WITHDRAWN: Contribution of microRNA-30d to the prevention of the thyroid cancer progression: mechanism and implications

Shao¹,

Zhang²,

Wang³

et al. 2020

Preprint

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“…We showed low expression of miR30d, 133b, and 451a (0.51-, 0.52-, and 0.68fold; P=0.038, P=0.044, P=0.032) was tumor-suppressive in the patient group, as previously demonstrated by other reports. [41][42][43] Our data show that circulating miRNAs might have great potential as diagnostic and therapeutic biomarkers in CLL. Although our results suggest the mentioned roles for miR25-3p and miR19a-3p, further investigations are needed.…”

Section: Discussionmentioning

confidence: 70%

<p>Serum Expression of Seven MicroRNAs in Chronic Lymphocytic Leukemia Patients</p>

Farzadfard¹,

Kalantari²,

Tamaddon³

2020

JBM

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Purpose: MicroRNAs are small single-strand noncoding RNAs that can be deregulated in a variety of cancers. Over the past few years, multiple markers have been discovered in chronic lymphocytic leukemia (CLL). Among these, miRNAs seem to have important roles in the pathogenesis of CLL. The development and validation of miRNA-expression patterns as biomarkers should have a significant impact in cancer diagnosis, therapeutic success, and increasing the life expectancy of patients. In this study, to specify the utility of circulatory miRNA expression as noninvasive and useful biomarkers for CLL, we analyzed the dysregulation of seven miRNAs: miR30d, miR25-3p, miR19a-3p, miR133b, miR451a, miR145, and miR144 in CLL-patient sera. Methods: Thirty untreated patients with flow-cytometry confirmation of CLL were chosen. Serum samples were collected from 30 newly diagnosed CLL patients. Fifteen healthy samples were taken for comparison as controls. RNA was extracted using Trizol. RNA from CLL patient specimens was compared to controls with real-time PCR. Results: Seven miRNAs were differently expressed between CLL and normal specimens using the comparative 2 −ΔΔ Ct method. miRNAs 133b, 25-3p, 451a, 145, 19a-3p, and 144 were overexpressed in sera obtained from CLL patients, and miRNA-30d was underexpressed in patient samples. Among these seven miRNAs, miR19a-3p and miR25-3p showed the most deregulation in CLL patients. Conclusion: Real-time PCR is an applied means to perform high-throughput investigation of serum-RNA samples. We assessed the expression of seven miRNAs in CLL patients by this method. The results demonstrated that the use of miRNA-expression profiling may have an impressive role in the diagnosis of CLL. In addition, miRNA 19a-3p and 25-3p are known oncogenes with therapeutic and potential biomarkers.

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“…The low expression of miR‐30d has also been found in non‐small cell lung cancer (NSCLC) tissues and cell lines . It has been suggested by Zhang et al that miR‐30d was degraded in human colon cancer cell lines in contrast to normal colon epithelial cell line . As for dysregulation of CEACAM1, a recent study has unveiled that CEACAM1 exerted a high expression in multiple myeloma, and Ueshima et al have provided evidence that expression of CEACAM1 was heightened in both neoplastic mast cells and medullary thyroid carcinoma cell lines …”

Section: Discussionmentioning

confidence: 99%

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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Mir-30d suppresses cell proliferation of colon cancer cells by inhibiting cell autophagy and promoting cell apoptosis

Cited by 56 publications

References 26 publications

WITHDRAWN: Contribution of microRNA-30d to the prevention of the thyroid cancer progression: mechanism and implications

WITHDRAWN: Contribution of microRNA-30d to the prevention of the thyroid cancer progression: mechanism and implications

<p>Serum Expression of Seven MicroRNAs in Chronic Lymphocytic Leukemia Patients</p>

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

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