Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression

Rong, Zhonghou; Wang, Zhiyi; Wang, Xinxing; Qin, Chengkun; Geng, Wei

doi:10.1186/s13046-020-01551-9

Cited by 34 publications

(45 citation statements)

References 33 publications

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“…Among these lncRNAs, RHPN1-AS1 was reported to act as an oncogene in multiple human cancers, including nonsmall cell lung cancer [19], uveal melanoma [20], and breast cancer [21]. LINC01134 and MKLN1-AS were found to promote HCC progression or metastasis by previous studies [24][25][26][27][28], suggesting that the two lncRNAs might be more specific in HCC, while NRAV and CMB9-22P13.1 were 13 BioMed Research International rarely reported as an oncogene in cancers. Similar with RHPN1-AS1, MAPKAPK5-AS1 was frequently reported to act as tumor-promoting lncRNAs in multiple cancers like thyroid cancer, colorectal cancer, glioma, lung cancer, and HCC [29][30][31][32][33].…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Screening Identifies Prognostic Long Noncoding RNAs in Hepatocellular Carcinoma

Feng

et al. 2021

BioMed Research International

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Hepatocellular carcinoma (HCC) is a common malignancy with a poor prognosis. Therefore, there is an urgent call for the investigation of novel biomarkers in HCC. In the present study, we identified 6 upregulated lncRNAs in HCC, including LINC01134, RHPN1-AS1, NRAV, CMB9-22P13.1, MKLN1-AS, and MAPKAPK5-AS1. Higher expression of these lncRNAs was correlated to a more advanced cancer stage and a poorer prognosis in HCC patients. Enrichment analysis revealed that these lncRNAs played a crucial role in HCC progression, possibly through a series of cancer-related biological processes, such as cell cycle, DNA replication, histone acetyltransferase complex, fatty acid oxidation, and lipid modification. Moreover, competing endogenous RNA (ceRNA) network analysis revealed that these lncRNAs could bind to certain miRNAs to promote HCC progression. Loss-of-function assays indicated that silencing of RHPN1-AS1 significantly suppressed HCC proliferation and migration. Though further validations are still needed, these identified lncRNAs could serve as valuable potential biomarkers for HCC prognosis.

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Section: Discussionmentioning

confidence: 99%

Genome-Wide Screening Identifies Prognostic Long Noncoding RNAs in Hepatocellular Carcinoma

Feng

et al. 2021

BioMed Research International

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“…Through regulating NF-κB signaling, the effects of LINC01134 and AKT1S1 on HCC cell proliferation and apoptosis need further investigation. During our revision, another group reported that LINC01134 promotes EMT and metastasis of HCC through the LINC01134/miR-324-5p/IGF3BP1/YY1 axis (Rong et al, 2020). We both reported the pro-metastatic roles of LINC01134 in HCC.…”

Section: Discussionmentioning

confidence: 65%

Long Noncoding RNA LINC01134 Promotes Hepatocellular Carcinoma Metastasis via Activating AKT1S1 and NF-κB Signaling

Wang

Chen

et al. 2020

Front. Cell Dev. Biol.

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Hepatocellular carcinoma (HCC) is one of the most common malignancies with poor outcomes. The main causes of HCC-related deaths are recurrence and metastasis. Long noncoding RNAs (lncRNAs) are recently identified as critical regulators in cancers. However, the lncRNAs involved in HCC recurrence and metastasis are poorly understood. In this study, via analyzing The Cancer Genome Atlas Liver Hepatocellular Carcinoma dataset, we identified a novel lncRNA LINC01134, which is highly expressed in HCC tissues and correlated with microvascular invasion, macrovascular invasion, recurrence, and poor overall survival of HCC patients. Functional experiments revealed that ectopic expression of LINC01134 promotes HCC cell migration and invasion in vitro and HCC liver metastasis and lung metastasis in vivo. Knockdown of LINC01134 represses HCC cell migration and invasion in vitro and HCC liver metastasis and lung metastasis in vivo. Mechanistically, we found that LINC01134 directly binds the promoter of AKT1S1 and activates AKT1S1 expression. Via activating AKT1S1, LINC01134 further activates NF-κB signaling. The expression of LINC01134 is significantly positively correlated with that of AKT1S1 in HCC tissues. In line with LINC01134, AKT1S1 is also highly expressed in HCC tissues and correlated with poor survival of HCC patients. Functional rescue experiments showed that repressing AKT1S1 or NF-κB signaling abrogates the roles of LINC01134 in HCC. Taken together, these findings recognized LINC01134 as a novel oncogenic lncRNA, which indicates vascular invasion, recurrence, and poor overall survival of HCC patients. LINC01134 promotes HCC metastasis via activating AKT1S1 expression and subsequently activating NF-κB signaling. This study suggested LINC01134 as a potential prognostic biomarker and therapeutic target for HCC.

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“…10 While miR-134-5p overexpression has been confirmed to be capable of reducing SGC7901 cells' proliferation, colony formation and invasion. 11 All these studies verify the value of miRNAs in regulating GC progression. As an ubiquitous transcription factor, Yin Yang 1 (YY1) can drive tumorigenesis, metastasis and drug resistance, and targeting YY1 is deemed to be a potential therapeutic option for various malignant tumors.…”

Section: Introductionmentioning

confidence: 62%

<p>Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells</p>

Zhong

Wang

et al. 2020

OTT

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Objective: To explore the related influencing mechanism of miR-384 and miR-134-5p acting on Yin Yang 1 (YY1) signaling transduction on the biological function of gastric cancer (GC) cells. Methods: miR-384, miR-134-5p and YY1 levels in human GC cell lines KATO III, MKN-45, SNU-1 and normal gastric cell line GES-1 were measured by polymerase chain reaction (PCR). Dual luciferase reporter (DLR) gene assay and Western blot (WB) were employed for correlation analysis between miR-384, miR-134-5p and YY1. miR-384-inhibitor, miR-384mimics, empty plasmid (miRNA-NC) and sh-YY1 were transfected into KATO III cells. Cell proliferation was determined by 3-(4,5-Dimethylthiazolyl-2)-2,5-Diphenyl Tetrazolium Bromide (MTT), cell invasion was measured by Transwell, and apoptosis was analyzed by flow cytometry (FC). Results: In KATO III, MKN-45 and SNU-1 cell lines, YY1 was upregulated while miR-384 and miR-134-5p were downregulated (P<0.001). The expression of miR-134-5p in the miR-134-5p-inhibitor group was significantly lower (P<0.001), while that in the miR-134-5pmimics group was significantly higher (P<0.001). The expression of miR-384 in the miR-384-inhibitor group was significantly lower (P<0.001), and that in the miR-384-mimics group was significantly higher as compared to the NC group (P<0.001). Both miR-384 and miR-134-5p overexpression could inhibit cell proliferation and invasion, and promote apoptosis. As detected by WB, overexpressed miR-384 and miR-134-5p inhibited the expression of EMT-related molecular markers. Compared with sh-YY1, the number of cells in S phase decreased, the pro-apoptotic proteins boosted statistically, and the anti-apoptotic proteins declined notably after transfecting miR-134-5p-mimics/sh-YY1 or miR-384-mimics/sh-YY1 (P<0.05). The tumor growth rate of nude mice in miR-134-5p/sh-YY1 and miR-384/sh-YY1 groups were significantly lower than those in sh-YY1 group (all P<0.001). Conclusion: By targeting YY1 signaling transduction, miR-134-5p and miR-384 can alter the growth and apoptosis of GC cells, which are promising targets for new therapeutics of GC.

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Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression

Cited by 34 publications

References 33 publications

Genome-Wide Screening Identifies Prognostic Long Noncoding RNAs in Hepatocellular Carcinoma

Genome-Wide Screening Identifies Prognostic Long Noncoding RNAs in Hepatocellular Carcinoma

Long Noncoding RNA LINC01134 Promotes Hepatocellular Carcinoma Metastasis via Activating AKT1S1 and NF-κB Signaling

<p>Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells</p>

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