miR‑939‑3p promotes epithelial‑mesenchymal transition and may be used as a prognostic marker in hepatocellular carcinoma

Chen, Fei; Ni, Xiaoying; Chen, Lingxiu; Wang, Xiaoyan; Xu, Jianping

doi:10.3892/ol.2020.11361

Cited by 8 publications

(8 citation statements)

References 31 publications

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“…MEG3 can bind a few miRNAs at the sites that undergo editing (among them, miR-939-39 and miR-331-3p). Interestingly, miR-331-3p can inhibit glioma progression [ 43 ], while miR-939-3p can promotes hepatocellular carcinoma and lung cancer [ 44 , 45 ]. We believe that editing loss in lncRNA in GBM can play an important role in either releasing miRNAs that can promote cancer (miR-939-3p) and/or binding tumor suppressor miRNAs (miR-331-3p).…”

Section: Discussionmentioning

confidence: 99%

De Novo A-to-I RNA Editing Discovery in lncRNA

Silvestris

Scopa

Hanchi

et al. 2020

Cancers

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Background: Adenosine to inosine (A-to-I) RNA editing is the most frequent editing event in humans. It converts adenosine to inosine in double-stranded RNA regions (in coding and non-coding RNAs) through the action of the adenosine deaminase acting on RNA (ADAR) enzymes. Long non-coding RNAs, particularly abundant in the brain, account for a large fraction of the human transcriptome, and their important regulatory role is becoming progressively evident in both normal and transformed cells. Results: Herein, we present a bioinformatic analysis to generate a comprehensive inosinome picture in long non-coding RNAs (lncRNAs), using an ad hoc index and searching for de novo editing events in the normal brain cortex as well as in glioblastoma, a highly aggressive human brain cancer. We discovered >10,000 new sites and 335 novel lncRNAs that undergo editing, never reported before. We found a generalized downregulation of editing at multiple lncRNA sites in glioblastoma samples when compared to the normal brain cortex. Conclusion: Overall, our study discloses a novel layer of complexity that controls lncRNAs in the brain and brain cancer.

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Section: Discussionmentioning

confidence: 99%

De Novo A-to-I RNA Editing Discovery in lncRNA

Silvestris

Scopa

Hanchi

et al. 2020

Cancers

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“…It has been confirmed that miRNAs could exert their biological function mainly by binding their target mRNAs. 30,31 In the current study, we found cyclin E1 was a direct target of miR-1231, which has been regarded as a key regulator in cell cycle. 32 In addition, CDK2 was found to be downregulated in pancreatic cancer cells in the presence of ABHD11-AS1 shRNA1.…”

Section: Discussionmentioning

confidence: 57%

<p>Knockdown of lncRNA ABHD11-AS1 Suppresses the Tumorigenesis of Pancreatic Cancer via Sponging miR-1231</p>

Liu¹,

Wang²,

Sun³

et al. 2020

OTT

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Background Pancreatic cancer ranks first among the most aggressive malignancies. Long non-coding RNA (LncRNA) ABHD11-AS1 is known to be upregulated in pancreatic cancer. However, the mechanism by which ABHD11-AS1 mediates the tumorigenesis of pancreatic cancer remains unclear. Methods Gene and protein expressions in pancreatic cancer cells were detected by qRT-PCR and Western blot, respectively. Cell viability was measured by CCK-8 assay. Cell apoptosis and cycle were tested by flow cytometry. In addition, cell migration and invasion were tested by wound healing and transwell assay, respectively. The correlation between ABHD11-AS1, miR-1231 and cyclin E1 was confirmed by dual-luciferase report and RNA pull-down. Finally, xenograft mice model was established to investigate the role of ABDH-AS1 in pancreatic cancer in vivo. Results ABHD11-AS1 was found to be negatively correlated with the survival rate of patients with pancreatic cancer. ABHD11-AS1 silencing significantly inhibited the proliferation and induced the apoptosis of pancreatic cancer cells. Additionally, knockdown of ABHD11-AS1 greatly inhibited the migration and invasion of pancreatic cancer cells. Meanwhile, ABHD11-AS1 bound to miR-1231 and cyclin E1 was found to be the target of miR-1231. Moreover, ABHD11-AS1 knockdown-induced G1 arrest in pancreatic cancer cells was reversed by miR-1231 antagomir. Finally, knockdown of ABHD11-AS1 obviously inhibited the tumor growth of pancreatic cancer in vivo. Conclusion ABHD11-AS1 silencing significantly inhibited the tumorigenesis of pancreatic cancer in vitro and in vivo. Thus, ABHD11-AS1 may serve as a potential target for the treatment of pancreatic cancer.

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“…Our findings are in agreement with those of Mazza et al, who demonstrated that hsa-miR-6126 was one of the most significantly increased miRNAs in the plasma of PDAC patients [41], and the same hsa-miR-6126 has been found in the tumor tissues of five patients with stage II colon cancer but not in cancer-free tissues [42]. hsa-miR-939-5p, of potential interest for its role in invasive cancer, is reportedly upregulated in lung adenocarcinomas [43], hepatocellular carcinomas [44,45], ovarian cancer tissue [46] and in the promotion of blood vessel invasion in breast cancer [47]. The recent study by Shen et al [48] shed some light on the role of this hsa-miR-939-5p in PDAC biology and prognosis.…”

Section: Discussionmentioning

confidence: 96%

Serum miRNA Profiling for Early PDAC Diagnosis and Prognosis: A Retrospective Study

et al. 2021

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Background: Tumor stage predicts pancreatic cancer (PDAC) prognosis, but prolonged and short survivals have been described in patients with early-stage tumors. Circulating microRNA (miRNA) are an emerging class of suitable biomarkers for PDAC prognosis. Our aim was to identify whether serum miRNA signatures predict survival of early-stage PDAC. Methods: Serum RNA from archival 15 stage I-III PDAC patients and 4 controls was used for miRNAs expression profile (Agilent microarrays). PDAC patients with comparable age, gender, diabetes, jaundice and surgery were classified according to survival: less than 14 months (7/15 pts, group A) and more than 22 months (8/15 pts, group B). Bioinformatic data analysis was performed by two-class Significance Analysis of Microarray (SAM) algorithm. Binary logistic regression analyses considering PDAC diagnosis and outcome as dependent variables, and ROC analyses were also performed. Results: 2549 human miRNAs were screened out. At SAM, 76 differentially expressed miRNAs were found among controls and PDAC (FDR = 0.4%), the large majority (50/76, 66%) of them being downregulated in PDAC with respect to controls. Six miRNAs were independently correlated with early PDAC, and among these, hsa-miR-6821-5p was associated with the best ROC curve area in distinguishing controls from early PDAC. Among the 71 miRNAs differentially expressed between groups A and B, the most significant were hsa-miR-3135b expressed in group A only, hsa-miR-6126 and hsa-miR-486-5p expressed in group B only. Eight miRNAs were correlated with the presence of lymph-node metastases; among these, hsa-miR-4669 is of potential interest. hsa-miR-4516, increased in PDAC and found as an independent predictor of survival, has among its putative targets a series of gens involved in key pathways of cancer progression and dissemination, such as Wnt and p53 signalling pathways. Conclusions: A series of serum miRNAs was identified as potentially useful for the early diagnosis of PDAC, and for establishing a prognosis.

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miR‑939‑3p promotes epithelial‑mesenchymal transition and may be used as a prognostic marker in hepatocellular carcinoma

Cited by 8 publications

References 31 publications

De Novo A-to-I RNA Editing Discovery in lncRNA

De Novo A-to-I RNA Editing Discovery in lncRNA

<p>Knockdown of lncRNA ABHD11-AS1 Suppresses the Tumorigenesis of Pancreatic Cancer via Sponging miR-1231</p>

Serum miRNA Profiling for Early PDAC Diagnosis and Prognosis: A Retrospective Study

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