Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion

Wang, Lin; Sun, Yan; Yi, Jing; Wang, Xiuwen; Liang, Jizhen; Pan, Zhaojun; Li, Li; Jiang, Gaofeng

doi:10.1080/01902148.2016.1223229

Cited by 21 publications

(19 citation statements)

References 22 publications

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“…The lncRNA H19 is an estrogen‐regulated gene whose expression is suppressed in adult liver . Aberrant expression of H19 has been associated with various cancers . H19 is also up‐regulated in BDL mice .…”

Section: Resultsmentioning

confidence: 99%

“…(14)(15)(16) Aberrant expression of H19 has been associated with various cancers. (11,13,(17)(18)(19)(20) H19 is also up-regulated in BDL mice. (16) To identify the role of H19 in the development of biliary fibrosis in Mdr2 -/mice, we first examined the expression of hepatic H19 in WT and Mdr2 -/mice.…”

Section: Aberrant Expression Of H19 Is Correlated With the Severity Omentioning

confidence: 93%

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The role of long noncoding RNA H19 in gender disparity of cholestatic liver injury in multidrug resistance 2 gene knockout mice

Liu

Yang

et al. 2017

Hepatology

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The multi-drug resistance 2 knockout (Mdr2−/−) mouse is a well-established model of cholestatic cholangiopathies. Female Mdr2−/− mice develop more severe hepatobiliary damage than male Mdr2−/− mice, which is correlated with a higher proportion of taurocholate (TCA) in bile. Although estrogen has been identified as an important player in intrahepatic cholestasis, the underlying molecular mechanisms of gender-based disparity of cholestatic injury remain unclear. The long non-coding RNA H19 is an imprinted, maternally expressed and estrogen-targeted gene, which is significantly induced in human fibrotic/cirrhotic liver and bile duct ligated mouse liver. However, whether aberrant expression of H19 accounts for gender-based disparity of cholestatic injury in Mdr2−/− mice remains unknown. The current study demonstrated that H19 was markedly induced (~200-fold) in the livers of female Mdr2−/− mice at advanced stages of cholestasis (100-day-old), but not in aged-matched male Mdr2−/− mice. During the early stages of cholestasis, H19 expression was minimal. We further determined that the hepatic H19 was mainly expressed in cholangiocytes, not hepatocytes. Both TCA and estrogen significantly activated the ERK1/2 signaling pathway and induced H19 expression in cholangiocytes. Knocking down H19 not only significantly reduced TCA/estrogen-induced expression of fibrotic genes and sphingosine 1-phosphate receptor 2 (S1PR2) in cholangiocytes, but also markedly reduced cholestatic injury in female Mdr2−/− mice. Furthermore, the expression of small heterodimer partner was substantially inhibited at advanced stages of liver fibrosis, which was reversed by H19 shRNA in female Mdr2−/− mice. Similar findings were obtained in human PSC liver samples. Conclusion H19 plays a critical role in the disease progression of cholestasis and represents a key factor that causes the gender disparity of cholestatic liver injury in Mdr2−/− mice.

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Section: Resultsmentioning

confidence: 99%

Section: Aberrant Expression Of H19 Is Correlated With the Severity Omentioning

confidence: 93%

The role of long noncoding RNA H19 in gender disparity of cholestatic liver injury in multidrug resistance 2 gene knockout mice

Liu

Yang

et al. 2017

Hepatology

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“…LncRNA H19 is firstly identified imprinting gene and plays important roles in cancers [4][5][6]. In multiple cancers including breast, kidney, stomach, ovarian, esophagus, and lung, overexpressed H19 promotes tumorigenesis and development [7][8][9][10][11][12][13]. But, it still remains mysterious about the role of H19 in lung cancer.…”

Section: Introductionmentioning

confidence: 99%

LncRNA H19-elevated LIN28B promotes lung cancer progression through sequestering miR-196b

Ren

et al. 2018

Cell Cycle

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LncRNA H19 is involved in the development of multiple cancers. Here, we firstly provide new evidence that H19 can induce LIN28B, a conserved RNA binding protein, to accelerate lung cancer growth through sponging miR-196b. Abundance in LIN28B was observed in clinical lung cancer samples. A positive link was observed between H19 and LIN28B in clinical lung cancer samples. In lung cancer cells, H19 was capable of increasing LIN28B expression. Mechanistically, miR-196b directly targeted LIN28B to inhibit LIN28B expression. H19 was capable of promoting LIN28B expression through sequestering miR-196b. Functionally, H19-increased LIN28B conferred the cell proliferation of lung cancer. Our finding indicates that H19 depresses miR-196b to elevate LIN28B, resulting in accelerating cell proliferation in lung cancer.

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“…The H19 gene is transcribed in a long non-coding RNA molecule that accumulates in fetal tissues but is repressed in the majority of adult organs (24). Dysregulation of H19 is associated with cancer, but inconsistency exists about the role of H19 in tumor development and progression (25)(26)(27). The observations in certain cancers support an oncogenic role of H19, since it is overexpressed and regulates genes involved in tumor growth, metastasis and angiogenesis (15,24,28,29).…”

Section: Discussionmentioning

confidence: 94%

H19 promotes endometrial cancer progression by modulating epithelial-mesenchymal transition

Zhao

Chen

et al. 2016

Oncology Letters

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Abstract. Endometrial cancer is one of the most common types of gynecological malignancy worldwide. Novel biomarkers and therapeutic targets are imperative for improving patients' survival. Previous studies have suggested the long non-coding RNA H19 as a potential cancer biomarker. To investigate the role of H19 in endometrial cancer, the present study examined the expression pattern of H19 in endometrial cancer tissues by quantitative polymerase chain reaction, and characterized its function in the endometrial cancer cell line via knocking down its expression with small interfering RNAs. It was found that H19 level was significantly higher in tumor tissues than in paratumoral tissues. Knockdown of H19 did not affect the growth rate of HEC-1-B endometrial cancer cells, but significantly suppressed in vitro migration and invasion of HEC-1-B cells. Furthermore, H19 downregulation decreased Snail level and increased E-cadherin expression without affecting vimentin level, indicating partial reversion of epithelial-mesenchymal transition (EMT). The present findings suggested that H19 contributed to the aggressiveness of endometrial cancer by modulating EMT process.

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Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion

Cited by 21 publications

References 22 publications

The role of long noncoding RNA H19 in gender disparity of cholestatic liver injury in multidrug resistance 2 gene knockout mice

The role of long noncoding RNA H19 in gender disparity of cholestatic liver injury in multidrug resistance 2 gene knockout mice

LncRNA H19-elevated LIN28B promotes lung cancer progression through sequestering miR-196b

H19 promotes endometrial cancer progression by modulating epithelial-mesenchymal transition

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