MiR-128-3p suppresses tumor proliferation and metastasis via targeting CDC6 in hepatocellular carcinoma cells

Yu, Shaojun; Yan, Fuguo; Wang, Fangping; Pan, Linfeng

doi:10.1016/j.tice.2021.101534

Cited by 15 publications

(9 citation statements)

References 34 publications

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“…In breast cancer tumor tissues and cell lines, it can be founded that miR-128-3p was declined and miR-128-3p acted as tumor inhibitor. This result is consistent with previous studies of down-regulated expression of miR-128-3p in many cancers, 17,21 such as hepatocellular carcinoma, breast cancer, and glioma, and its anticancer function. In particular, miR-128-3p has been previously reported to inhibit proliferation and metastasis of colorectal cancer and breast cancer.…”

Section: Discussionsupporting

confidence: 93%

RETRACTED: Circular forms of dedicator of cytokinesis 1 promotes breast cancer progression by derepressing never in mitosis related kinase 2 via sponging miR‐128‐3p

Liu

Pan

et al. 2023

Environmental Toxicology

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The conjecture of breast cancer is uncertain because of its explosive growth and the complicated molecular mechanisms. Circular RNAs (circRNAs) are regulatory RNA sequences present in the genome and their regulatory mechanism involves the sponging of microRNAs (miRNAs). In this study, we explored the regulation between circular forms of dedicator of cytokinesis 1 (circDOCK1) (hsa_circ_0007142) and miR‐128‐3p, and its implication on the pathogenesis of breast cancer modulated by never in mitosis (NIMA) related kinase 2 (NEK2). We revealed an increase in circDOCK1 and NEK2 expression, and a decrease in miR‐128‐3p expression in breast cancer tissues and cell lines. Bioinformatics analysis and experimental validation indicated a positive correlation between circDOCK1 and NEK2 expression but a negative correlation was recorded between miR‐128‐3p and circDOCK1 or NEK2, respectively. Furthermore, inhibition of circDOCK1 expression was followed by an increase in miR‐128‐3p and a decrease in NEK2 levels in vitro and in vivo. The luciferase assay concluded that miR‐128‐3p was a direct target of circDOCK1 while NEK2 was the direct target of miR‐128‐3p. Furthermore, circDOCK1 inhibition hindered breast cancer development by repressing NEK2 and thus promoting the increased expression of miR‐128‐3p both in vitro and in vivo. We therefore conclude that circDOCK1 promotes breast cancer progression by targeting miR‐128‐3p‐mediated downregulation of NEK2 and that the circDOCK1/hsa‐miR‐128‐3p/NEK2 axis may be a novel therapeutic target for breast cancer treatment.

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Section: Discussionsupporting

confidence: 93%

RETRACTED: Circular forms of dedicator of cytokinesis 1 promotes breast cancer progression by derepressing never in mitosis related kinase 2 via sponging miR‐128‐3p

Liu

Pan

et al. 2023

Environmental Toxicology

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“…The CDC6 gene is a key gene in the regulation of the human cell cycle, and it plays an important role in DNA replication and cell division ( Hofmann et al., 2011 ; Shi et al., 2021 ; Zhang et al., 2023 ). Recent studies have shown that the CDC6 gene plays an important role in a variety of tumors, including gliomas ( Wang et al., 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Effect of gut microbiome regulated Taohong Siwu Decoction metabolism on glioma cell phenotype

Feng

Wan

et al. 2023

Front. Cell. Infect. Microbiol.

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IntroductionTo establish a new model for exploring the mechanism of the gut microbiome and drug metabolism, we explored whether Taohong Siwu Decoction acts after metabolism by intestinal flora under the premise of clarifying the interaction between intestinal flora and drug metabolism.MethodsTaohong Siwu Decoction (TSD) was fed to germ-free mice and conventional mice, respectively. The serum from both groups of mice was removed and co-cultured with glioma cells in vitro. The co-cultured glioma cells were compared separately for changes at the RNA level using RNA-seq technology. The genes of interest in the comparison results were selected for validation.ResultsThe differences in the phenotypic alterations of glioma cells between serum from TSD-fed germ-free mice and normal mice were statistically significant. In vitro experiments showed that Taohong Siwu Decoction-fed normal mouse serum-stimulated glioma cells, which inhibited proliferation and increased autophagy. RNA-seq analysis showed that TSD-fed normal mouse serum could regulate CDC6 pathway activity in glioma cells. The therapeutic effect of TSD is significantly influenced by intestinal flora.ConclusionThe treatment of tumors by TSD may be modulated by intestinal flora. We established a new method to quantify the relationship between intestinal flora and the regulation of TSD efficacy through this study.

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“…More precisely, miR-128 is an anti-oncomiR or suppressor oncomiR in HCC as its overexpression suppresses the proliferation and metastasis of HCC cells and positively correlates with the prognosis of HCC patients. 28 , 29 Studies have also shown that miR-128-3p increases the chemosensitivity of oxaliplatin-resistant colorectal cancer, 30 confers chemoresistance-associated metastasis in lung cancer, 31 enhances the sensitivity of temozolomine in glioma, 32 and sensitizes HCC cells to sorafenib-induced apoptosis 33 through regulating various targets. The present study demonstrates that miR-128-3p is downregulated in LR-HCC cells, and miR-128-3p mimics enhances the sensitivity of LR-HCC cells to lenvatinib by downregulating the expression of c-Met, further supporting the involvement of miR-128-3p in chemoresistance though it targets different genes from the above studies possibly because the role of miRNAs is complex, and cell- and disease-dependent.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-128-3p Mediates Lenvatinib Resistance of Hepatocellular Carcinoma Cells by Downregulating c-Met

Xu¹,

Jiang²,

Han³

et al. 2022

JHC

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Objective Lenvatinib is a first-line multikinase inhibitor for advanced hepatocellular carcinoma (HCC), but resistance to the drug remains a major hurdle for its long-term anti-cancer activity. This resistance is thought to be due to overexpression of c-Met. This study aims to identify potential upstream microRNAs (miRNAs) that regulate c-Met, investigate the underlying mechanisms, and seek potential strategies that may reverse such resistance. Methods Lenvatinib-resistant HCC (LR-HCC) cells were established from human HCC Huh7 and SMMC-7721 cells. Assays of cell proliferation, cell cycle distribution, apoptosis, RT-qPCR, Western blot analysis and immunohistochemistry were employed. Potential miRNAs were screened by miRNA-target prediction tools and their regulatory effects were evaluated by luciferase reporter assays. Xenograft tumor models were used to evaluate the therapeutic effects. Results LR-HCC cells were refractory to lenvatinib-induced growth inhibition and apoptosis in vitro and in vivo. Sustained exposure of cells to lenvatinib resulted in increased expression and phosphorylation of c-Met, and c-Met inhibition enhanced the effects of lenvatinib in suppressing LR-HCC cells. Among eleven miRNA candidates, miR-128-3p displayed the most vigorous activity to negatively regulate c-Met and was downregulated in LR-HCC cells. MiR-128-3p mimics inhibited proliferation and induced apoptosis of LR-HCC cells, and enhanced the effects of lenvatinib in cell culture and animal models. MiR-128-3p and c-Met participate in the mechanisms underlying lenvatinib resistance through regulating Akt that mediates the apoptotic pathway and ERK (extracellular-signal-regulated kinase) modulating cell cycle progression. Conclusion The present results indicate that the miR-128-3p/c-Met axis may be potential therapeutic targets for circumventing lenvatinib resistance in HCC and warrant further investigation.

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MiR-128-3p suppresses tumor proliferation and metastasis via targeting CDC6 in hepatocellular carcinoma cells

Cited by 15 publications

References 34 publications

RETRACTED: Circular forms of dedicator of cytokinesis 1 promotes breast cancer progression by derepressing never in mitosis related kinase 2 via sponging miR‐128‐3p

RETRACTED: Circular forms of dedicator of cytokinesis 1 promotes breast cancer progression by derepressing never in mitosis related kinase 2 via sponging miR‐128‐3p

Effect of gut microbiome regulated Taohong Siwu Decoction metabolism on glioma cell phenotype

MicroRNA-128-3p Mediates Lenvatinib Resistance of Hepatocellular Carcinoma Cells by Downregulating c-Met

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