<scp>LINC</scp>01287 regulates tumorigenesis and invasion via miR‐298/<scp>MYB</scp> in hepatocellular carcinoma

Mo, Yichao; He, Longguang; Lai, Zeru; Wan, Zhiheng; Chen, Qinshou; Pan, Sibo; Li, Liangfu; Li, Dasheng; Huang, Jun; Xue, Fan; Che, Siyao

doi:10.1111/jcmm.13818

Cited by 14 publications

(14 citation statements)

References 22 publications

(31 reference statements)

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“…In addition, lncRNAs also act as “miRNA sponges” and sequester miRNAs to modify miRNAs target genes transcription, which has been identified as the lncRNA-miRNA-mRNA regulatory network in cancer tumorigenesis and progression [ 21 , 22 ]. For examples, LINC01287 regulates tumorigenesis of hepatocellular carcinoma via miR-298/MYB axis [ 23 ]. LncRNA SNHG15 promotes the proliferation and migration of lung cancer through targeting microRNA-211-3p [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

Tian

Cui

et al. 2020

Cancer Cell Int

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Background LncRNAs act as functional regulators in tumor progression through interacting with various signaling pathways in multiple types of cancer. However, the effect of LINC02418 on colorectal cancer (CRC) progression and the underling mechanisms remain unclear. Methods LncRNA expression profile in CRC tissues was investigated by the TCGA database. The expressional level of LINC02418 in CRC patients was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Kaplan–Meier analyses was used to investigate the correlation between LINC02418 and overall survival (OS) of CRC patients. Cell proliferative, migratory and invasive abilities were detected by CCK-8 assays, colony formation assays and trans-well assays in HCT116 and LoVo cells which were stably transduced with sh-LINC02418 or sh-NC. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assays. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418/miR-34b-5p/BCL2 axis in CRC progression. Results LINC02418 was upregulated in human colon cancer samples when compared with adjacent tissue, and its high expressional level correlated with poor prognosis of CRC patients. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently affect BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, while transfection of miR-34b-5p inhibitor or BCL2 into LINC02418-silenced CRC cells significantly promoted CRC cells growth. Conclusions LINC02418 was upregulated in human CRC samples and could be used as the indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418/miR-34b-5p/BCL2 axis in CRC.

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Section: Introductionmentioning

confidence: 99%

LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

Tian

Cui

et al. 2020

Cancer Cell Int

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“…Many reports have recommended lncRNAs as vital regulators of gene expression and cancer development over the past few decades. From our previous studies, for example, we reported that LINC01287 and XIST could function as oncogenic lncRNA in human HCC [ 5 , 7 ]. LINC01419 was shown to promote tumor progression, this led to substandard prognosis in different types of cancers [ 8 – 10 ].…”

Section: Discussionmentioning

confidence: 99%

“…Currently, researchers have identified a lncRNAs that are associated with HCC. Similarly, previous studies have reported that abnormal expression of lncRNAs contributes to HCC progression [5][6][7]. However, the underlying mechanisms have not been properly determined.…”

Section: Introductionmentioning

confidence: 95%

LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK

Zhang¹,

Chen

et al. 2020

Aging

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This study aims to investigate the biological role of LINC01419 and the underlying mechanism in HCC. RESULTS LINC01419 expression level is elevated in HCC tissues and is associated with a malignant phenotype In investigating the role of lncRNAs in HCC progression, the lncRNA expression profile was analyzed in HCC samples and non-HCC liver samples. The samples were obtained from TCGA datasets via circlncRNAnet (http://app.cgu.edu.tw/circlnc/) and TANRIC (http://ibl.mdanderson.org/tanric/_design/ basic/index.html). Several abnormal lncRNAs were detected and showed significant statistical differences. This study focused on LINC01419 because it showed the most significant difference (Figure 1A, Supplementary Figure 1A). The LINC01419 expression level was higher in HCC cell lines when compared to LO2 (normal liver cell line), (Figure 1B). To confirm whether

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“…Hepatocellular carcinoma (HCC) is one of the common malignant tumors and remains the leading cause of cancer-related death worldwide 1,2. Multiple genes influence the tumorigenesis and progression of HCC and accumulation of multiple molecular changes are involved in the progression of HCC 3,4.…”

Section: Introductionmentioning

confidence: 99%

Tanshinol inhibits the growth, migration and invasion of hepatocellular carcinoma cells via regulating the PI3K-AKT signaling pathway

Zhu

Liu

Zhou

et al. 2018

OTT

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BackgroundTanshinol is an active constituent of Salvia miltiorrhiza and possess anti-inflammatory, antioxidant, and anti-bacterial activity. Herein, we explored the role of tanshinol on the growth and aggressiveness of hepatocellular carcinoma (HCC) cells in vitro and in vivo.Materials and methodsThe proliferation of a panel of HCC cell lines was measured using MTT assay. The expressions of phosphatidylinositol 3 kinase (PI3K) and protein kinase B (AKT) were detected by immunofluorescence staining and immunohistochemical assay. The levels of Bcl-2 and Bax were determined using immunoblotting assay. The secretions of matrix metalloproteinase-2 (MMP-2) and MMP-9 were detected by ELISA. The migration and invasion abilities of HepG2 cell were determined using wound healing and Transwell invasion assays. The apoptosis of HepG2 cell induced by tanshinol was analyzed by Annexin V/propidium iodide staining. A xenograft model was constructed to investigate the inhibitory effect of tanshinol on HepG2 cell growth in vivo. To further investigate the role of tanshinol on the metastasis of HepG2 cell in vivo, an experimental metastasis assay was performed.ResultsTanshinol inhibited the growth and colony formation of HCC cell in vitro. Tanshinol also induced the apoptosis of HepG2 cell and inhibited the migration and invasion of HepG2 cell. In in vivo experiments, tanshinol suppressed the tumor growth and metastasis of HepG2 cell. Furthermore, the phosphorylation of PI3K and AKT was decreased by tanshinol in vitro and in vivo.ConclusionTanshinol exerts its anti-cancer effects via regulating the PI3K-AKT signaling pathway in HCC.

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LINC01287 regulates tumorigenesis and invasion via miR‐298/MYB in hepatocellular carcinoma

Cited by 14 publications

References 22 publications

LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK

Tanshinol inhibits the growth, migration and invasion of hepatocellular carcinoma cells via regulating the PI3K-AKT signaling pathway

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