A novel long noncoding RNA HHIP-AS1 suppresses hepatocellular carcinoma progression through stabilizing HHIP mRNA

Chen, Bo; Li, Xiuli; He, Ling; Zhang, Sujing; Li, Na; An, Yonghui

doi:10.1016/j.bbrc.2019.09.137

Cited by 27 publications

(26 citation statements)

References 27 publications

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“…More recently, hedgehog-interacting protein antisense RNA 1, a novel lncRNA, was monitored to interact with and stabilize the mRNA of hedgehog-interacting protein (Hhip) to enhance Hhip expression, thereby inhibiting the progression of HCC. 11 In addition to facilitating development and regeneration, the Hedgehog (Hh) pathway results in alteration of progenitors when incessantly evoked, which might lead to small-cell lung carcinomas, prostate and digestive tract tumors. 12 Considering the aforementioned investigations, in this work, we elaborated the probable roles of DIO3OS and miR-328 in HCC progression with the intention of offering insights for the treatment of HCC.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA DIO3OS Hinders Cell Malignant Behaviors of Hepatocellular Carcinoma Cells Through the microRNA-328/Hhip Axis</p>

Wang¹,

Song²,

Ye³

et al. 2020

CMAR

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Background: The decline of a long non-coding RNA (lncRNA) DIO3OS was implicated in a plethora of cancers, while the relevance in hepatocellular carcinoma (HCC) has not been mentioned. Accordingly, we set to determine the functional role of DIO3OS and the molecular mechanism in HCC progression. Materials and Methods: The differentially expressed lncRNAs, mRNAs, and microRNAs (miRNAs) were obtained through the datasets GSE101728 and GES57555. Afterwards, DIO3OS was enhanced in HCC cells to examine the behavior changes. Subcellular localization of DIO3OS was determined through website prediction and experimental validation. The expression of Hedgehog (Hh) signaling pathway-related genes was detected. The effects of DIO3OS overexpression on tumor growth were evaluated as well. Results: DIO3OS was lower in HCC tissues and cells, while upregulation of DIO3OS repressed malignant biological behavior both in vitro and in vivo. DIO3OS, localized in the cytoplasm, inhibited the occurrence of HCC by disrupting the Hh pathway by sponging miR-328 to mediate Hh interacting protein (Hhip). Conclusion:All in all, the obtained data suggested that DIO3OS interacted with Hhipdependent Hh signaling pathway to inhibit HCC progression through binding to miR-328, which may be a potent therapeutic target for HCC.

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Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA DIO3OS Hinders Cell Malignant Behaviors of Hepatocellular Carcinoma Cells Through the microRNA-328/Hhip Axis</p>

Wang¹,

Song²,

Ye³

et al. 2020

CMAR

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“…LKB1 has been further shown to promote HuR cytoplasmic translocation, which, in turn, stabilizes the herpesvirus-associated ubiquitin-specific protease (HAUSP) mRNA, a nuclear ubiquitin-specific protease controlling the stability of P53 [ 144 , 145 ]. HuR has also been shown to be involved in Hedgehog-interacting protein antisense RNA-1 (H-AS1)-induced apoptosis by stabilizing the mRNA of HHIP , a negative regulator of the Hedgehog pathway, in Hep3B cells [ 146 ]. In contrast to these studies, HuR has been reported to inhibit arsenic trioxide (ATO)-induced apoptosis by preventing ATO-induced TGFβ/SMAD signaling.…”

Section: Aubps In the Hallmarks Of Liver Cancermentioning

confidence: 99%

mRNA Post-Transcriptional Regulation by AU-Rich Element-Binding Proteins in Liver Inflammation and Cancer

Dolicka

Sobolewski

Sousa

et al. 2020

IJMS

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AU-rich element-binding proteins (AUBPs) represent important post-transcriptional regulators of gene expression. AUBPs can bind to the AU-rich elements present in the 3’-UTR of more than 8% of all mRNAs and are thereby able to control the stability and/or translation of numerous target mRNAs. The regulation of the stability and the translation of mRNA transcripts by AUBPs are highly complex processes that occur through multiple mechanisms depending on the cell type and the cellular context. While AUBPs have been shown to be involved in inflammatory processes and the development of various cancers, their important role and function in the development of chronic metabolic and inflammatory fatty liver diseases (FLDs), as well as in the progression of these disorders toward cancers such as hepatocellular carcinoma (HCC), has recently started to emerge. Alterations of either the expression or activity of AUBPs are indeed significantly associated with FLDs and HCC, and accumulating evidence indicates that several AUBPs are deeply involved in a significant number of cellular processes governing hepatic metabolic disorders, inflammation, fibrosis, and carcinogenesis. Herein, we discuss our current knowledge of the roles and functions of AUBPs in liver diseases and cancer. The relevance of AUBPs as potential biomarkers for different stages of FLD and HCC, or as therapeutic targets for these diseases, are also highlighted.

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“…Long non-coding RNAs (LncRNAs) with a length longer than 200 nucleotides are a class of non-protein coding transcripts [12]. More and more studies indicate that lncRNAs play essential roles in oncogenesis and progression of HCC by acting on proteins, stabilizing mRNA, regulating miRNA, or signaling pathways [13][14][15]. HCC is a large proportion of tumors worldwide and China alone accounts for about 50% of the total liver cancer rates [16].…”

Section: Ivyspringmentioning

confidence: 99%

Long noncoding RNA MYLK-AS1 promotes growth and invasion of hepatocellular carcinoma through the EGFR/HER2-ERK1/2 signaling pathway

Liu¹,

Zhao²,

Jiang³

et al. 2020

Int. J. Biol. Sci.

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The epidermal growth factor receptor (EGFR) family members EGFR and HER2 play pivotal roles in oncogenesis and tumor progression. Anticancer drugs targeting EGFR and HER2 have been developed. Long noncoding RNAs (lncRNAs) have been reported to regulate cancer development and progression through signaling pathways. However, lncRNAs that regulate EGFR and HER2 expression remain unknown. Here, we show that lncRNA myosin light chain kinase-antisense RNA 1 (MYLK-AS1) promotes EGFR and HER2 expression and activates their downstream signaling pathway. MYLK-AS1 increases hepatocellular carcinoma (HCC) cell proliferation, migration, and invasion in vitro. Consistently, MYLK-AS1 knockdown hinders tumor growth in vivo. Mechanistically, MYLK-AS1 enhances HCC cell proliferation, migration, and invasion through stimulating the EGFR/HER2-extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. In addition, MYLK-AS1 is overexpressed in HCC patients and negatively correlated with HCC prognosis. Thus, MYLK-AS1 is an upstream regulator of EGFR/HER2, and acts as an oncogene, suggesting an additional target for cancer therapeutics.

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A novel long noncoding RNA HHIP-AS1 suppresses hepatocellular carcinoma progression through stabilizing HHIP mRNA

Cited by 27 publications

References 27 publications

<p>Long Noncoding RNA DIO3OS Hinders Cell Malignant Behaviors of Hepatocellular Carcinoma Cells Through the microRNA-328/Hhip Axis</p>

<p>Long Noncoding RNA DIO3OS Hinders Cell Malignant Behaviors of Hepatocellular Carcinoma Cells Through the microRNA-328/Hhip Axis</p>

mRNA Post-Transcriptional Regulation by AU-Rich Element-Binding Proteins in Liver Inflammation and Cancer

Long noncoding RNA MYLK-AS1 promotes growth and invasion of hepatocellular carcinoma through the EGFR/HER2-ERK1/2 signaling pathway

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