LncRNA DNAJC3-AS1 Promotes Hepatocellular Carcinoma (HCC) Progression via Sponging Premature miR-27b

Fu, Changbo; Li, Jianxiu; Li, Ping; Cheng, Dan

doi:10.2147/cmar.s321111

Cited by 9 publications

(5 citation statements)

References 22 publications

(27 reference statements)

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“…Afterward, 10 μmol/L Hoechst33342 was adopted to label the nucleus. Imaging and statistical analysis were carried out by applying an inverted fluorescence microscope [ 21 ].…”

Section: Methodsmentioning

confidence: 99%

RETRACTED ARTICLE: Repressing phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma by microRNA-142-3p restrains the progression of hepatocellular carcinoma

Zeng¹,

Yuan

Hu³

et al. 2022

Bioengineered

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This paper probes the mechanisms underlying miR-142-3p’s modulation of hepatocellular carcinoma (HCC) invasion and apoptosis. Quantitative real-time PCR and Western blot monitored the miR-142-3p profile in HCC tissues and non-tumor tissues. The correlation between miR-142-3p expression and HCC patients’ clinicopathological indicators was analyzed. miR-142-3p overexpression and knockdown models were established in HCC cell lines. Cell proliferation was gauged by the colony formation assay and BrdU staining. For measuring apoptosis, flow cytometry and Western blot were implemented. Transwell assay tested cell migration and invasion. miR-142-3p mimics or inhibitors were transfected in Huh7 and HCCLM3 cells. The targeting association between miR-142-3p and PIK3CG was predicted through bioinformatics and further verified by related experiments. The influence of PIK3CG overexpression on miR-142-3p’s role in HCC was assayed. A xenografted tumor model was built in mice to validate miR-142-3p knockdown’s influence on HCC in vivo . As a result, miR-142-3p exhibited a decreased profile in HCC tissues and cells. Overexpressing miR-142-3p accelerated apoptosis and suppressed the PI3K/AKT/HIF-1α signal. Knocking down miR-142-3p presented opposite effects. PIK3CG overexpression dampened the anti-tumor effect of miR-142-3p. miR-142-3p repressed HCC invasion and intensified apoptosis to restrain HCC by abating the PIK3CG-mediated PI3K/AKT/HIF-1α pathway.

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“…Afterward, 10 μmol/L Hoechst33342 was adopted to label the nucleus. Imaging and statistical analysis were carried out by applying an inverted fluorescence microscope [ 21 ].…”

Section: Methodsmentioning

confidence: 99%

RETRACTED ARTICLE: Repressing phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma by microRNA-142-3p restrains the progression of hepatocellular carcinoma

Zeng¹,

Yuan

Hu³

et al. 2022

Bioengineered

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“…Furthermore, we found hundreds of differentially expressed genes on eccDNAs, and the majority of them (~80%) showed increased expression in HCC tumors. Notably, among the top 20 upregulated genes on eccDNAs in HCC tumors, only DNAJC3-DT has been reported to promote HCC progression, [43] while the role of the remaining 19 genes in HCC remains unknown. Interestingly, some of these genes, such as GPR183, [44] POU4F1, [45] and EDNRB, [46] play a crucial role in immunity, neuron differentiation and survival, and Hirschsprung's disease, respectively.…”

Section: Discussionmentioning

confidence: 99%

Extrachromosomal circular MiR-17-92 amplicon promotes HCC

et al. 2023

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Background and Aims: Extrachromosomal circular DNAs (eccDNAs) are prevalent in cancer genomes and emerge as a class of crucial yet less characterized oncogenic drivers. However, the structure, composition, genomewide frequency, and contribution of eccDNAs in HCC, one of the most fatal and prevalent cancers, remain unexplored. In this study, we provide a comprehensive characterization of eccDNAs in human HCC and demonstrate an oncogenic role of microRNA (miRNA)-17-92-containing eccDNAs in tumor progression.Approach and Results: Using the circle-sequencing method, we identify and characterize more than 230,000 eccDNAs from 4 paired samples of HCC tumor and adjacent nontumor liver tissues. EccDNAs are highly enriched in HCC tumors, preferentially originate from certain chromosomal hotspots, and are correlated with differential gene expression. Particularly, a series of eccDNAs carrying the miRNA-17-92 cluster are validated by outward PCR and Sanger sequencing. Quantitative PCR analyses reveal that miRNA-17-92-containing eccDNAs, along with the expression of their corresponding miRNAs, are elevated in HCC tumors and associated with poor outcomes and the age of HCC patients. More intriguingly, exogenous expression of artificial DNA circles harboring the miR-17-92 cluster, which is synthesized by the ligase-assisted minicircle

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“…By analysing the TCGA database (372 HCC tissues versus 50 normal adjacent liver tissues) and using qRT-PCR assay of 68 pairs of HCC specimens (patients with hepatitis B virus and without metastases), Liang et al also determined that the level of hsa-miR-27b were decreased in HCC. Besides, Fu et al showed that hsa-miR-27b was downregulated at mature miRNA level but upregulated at premature level (66 pairs of tissue samples) [18]. However, opposite results were obtained by Sun et al [14] and He et al [15].…”

Section: Discussionmentioning

confidence: 95%

“…Interestingly, Fu et al showed that premature hsa-miR-27b was frequently upregulated, while mature hsa-miR-27b was downregulated in HCC tissues compared with ANTs. Mechanistically, long non-coding RNA DNAJC3 anti-sense RNA 1 sponged premature hsa-miR-27b in the nucleus to suppress its maturation and promote cell proliferation [18]. To date, the expression pattern of hsa-miR-27b and its exact roles in HCC are unclear, and therapeutic applications of hsa-miR-27b in HCC remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Hsa-microRNA-27b-3p inhibits hepatocellular carcinoma progression by inactivating transforming growth factor-activated kinase-binding protein 3/nuclear factor kappa B signalling

et al. 2022

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Background MicroRNAs (miRNAs) play crucial roles in the development of hepatocellular carcinoma (HCC). Hsa-microRNA-27b-3p (hsa-miR-27b) is involved in the formation and progression of various cancers, but its role and clinical value in HCC remain unclear. Methods The expression of hsa-miR-27b in HCC was examined by quantitative real-time PCR (qRT-PCR) and in situ hybridization (ISH) assays of clinical samples. Cell Counting Kit-8 assays (CCK-8), 5-ethynyl-2′-deoxyuridine (EdU) incorporation assays, Transwell assays, filamentous actin (F-actin) staining and western blot analyses were used to determine the effects of hsa-miR-27b on HCC cells in vitro. Subcutaneous xenograft and lung metastatic animal experiments were conducted to verify the role of hsa-miR-27b in HCC in vivo. In silico prediction, qRT-PCR, western blot, anti-Argonaute 2 (AGO2) RNA immunoprecipitation (RIP) and dual luciferase reporter assays were applied to identify the target genes of hsa-miR-27b. To detect the impacts of hsa-miR-27b on nuclear factor kappa B (NF-кB) signalling cascades mediated by transforming growth factor-activated kinase-binding protein 3 (TAB3), we performed qRT-PCR, western blot assays, immunofluorescence staining, immunohistochemistry (IHC) and dual-luciferase reporter assays. Recombinant oncolytic adenovirus (OncoAd) overexpressing hsa-miR-27b was constructed to detect their therapeutic value in HCC. Results The expression of hsa-miR-27b was lower in HCC than in adjacent non-tumourous tissues (ANTs), and the reduced expression of hsa-miR-27b was associated with worse outcomes in patients with HCC. Hsa-miR-27b significantly inhibited the proliferation, migration, invasion, subcutaneous tumour growth and lung metastasis of HCC cells. The suppression of hsa-miR-27b promoted the nuclear translocation of NF-κB by upregulating TAB3 expression. TAB3 was highly expressed in HCC compared with ANTs and was negatively correlated with the expression of hsa-miR-27b. The impaired cell proliferation, migration and invasion by hsa-miR-27b overexpression were recovered by ectopic expression of TAB3. Recombinant OncoAd with overexpression of hsa-miR-27b induced anti-tumour activity compared with that induced by negative control (NC) OncoAd in vivo and in vitro. Conclusions By targeting TAB3, hsa-miR-27b acted as a tumour suppressor by inactivating the NF-кB pathway in HCC in vitro and in vivo, indicating its therapeutic value against HCC. Graphical Abstract

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LncRNA DNAJC3-AS1 Promotes Hepatocellular Carcinoma (HCC) Progression via Sponging Premature miR-27b

Cited by 9 publications

References 22 publications

RETRACTED ARTICLE: Repressing phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma by microRNA-142-3p restrains the progression of hepatocellular carcinoma

RETRACTED ARTICLE: Repressing phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma by microRNA-142-3p restrains the progression of hepatocellular carcinoma

Extrachromosomal circular MiR-17-92 amplicon promotes HCC

Hsa-microRNA-27b-3p inhibits hepatocellular carcinoma progression by inactivating transforming growth factor-activated kinase-binding protein 3/nuclear factor kappa B signalling

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