Anillin is required for tumor growth and regulated by miR-15a/miR-16-1 in HBV-related hepatocellular carcinoma

Lian, Yi Fan; Huang, Yan; Wang, Jia Liang; Deng, Mei Hai; Xia, Tian Liang; Zeng, Mu Sheng; Chen, Minshan; Wang, Hong; Huang, Yue

doi:10.18632/aging.101510

Cited by 45 publications

(44 citation statements)

References 38 publications

(44 reference statements)

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“…These validation experiments used wild-type and target site mutant 3'UTRs for known miR-16 targets that are expected to be shared with miR-K6-5p (CDC25A, BCL2L2 (Chang et al, 2007), CCND3, and PDCD4 (Fu et al, 2018), Fig. S3B-E); three known miR-16 targets with preferential regulation by miR-16 over miR-K6-5p (MYB (Chung et al, 2008), ANLN (Lian et al, 2018), and CCND1 (Chen et al, 2008), Fig. S3 F-H); and three candidates for miR-K6-5p targets that are unlikely to be shared by miR-16 (BCL7B, VASP, and STAT3, Fig.…”

Section: Mir-k6-5p Shares Binding Sites With Mir-16mentioning

confidence: 99%

The oncogenic Kaposi’s sarcoma-associated herpesvirus encodes a mimic of the tumor suppressive miR-15/16 miRNA family

Morrison

Manzano

Chung

et al. 2019

Preprint

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Many tumor viruses encode oncogenes of cellular origin. Here, we report the first instance of an oncoviral mimic of a cellular tumor suppressor. The Kaposi's sarcoma-associated herpesvirus (KSHV) miRNA miR-K6-5p shares sequence similarity to the tumor suppressive cellular miR-15/16 miRNA family. We show that miR-K6-5p inhibits cell cycle progression, a hallmark function of miR-16. miR-K6-5p regulates conserved miR-15/16 targets, including many cell cycle regulators. Inhibition of miR-K6-5p in KSHV-transformed B cells conferred a significant growth advantage. Altogether, our data show that KSHV encodes a functional mimic of the miR-15/16 miRNA family. While it is exceedingly well established that oncogenic viruses encode oncogenes of cellular origin, this is the first example of an oncogenic virus that encodes a viral mimic of a cellular tumor suppressor. Encoding a tumor suppressive miRNA could help KSHV balance viral oncogene expression and thereby avoid severe pathogenesis in the healthy host.

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Section: Mir-k6-5p Shares Binding Sites With Mir-16mentioning

confidence: 99%

The oncogenic Kaposi’s sarcoma-associated herpesvirus encodes a mimic of the tumor suppressive miR-15/16 miRNA family

Morrison

Manzano

Chung

et al. 2019

Preprint

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“…ANLN , an actin-binding protein, is essential for assembly of the cleavage furrow during the late stages of mitosis and acts as the central organizer at the cytokinetic machinery hub [ 23 ]. Owing to its critical role, studies have observed overexpressed ANLN in several types of cancers [ 24 – 26 ], and it has also been proven to be correlated with poor prognoses in breast cancer, lung cancer and hepatocellular carcinoma [ 27 – 29 ]. However, the role of ANLN in PC remains unclear.…”

Section: Discussionmentioning

confidence: 99%

A two-gene-based prognostic signature for pancreatic cancer

Zhou

Yan

Chen

et al. 2020

Aging

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The purpose of this study was to identify a vital gene signature that has prognostic value for pancreatic cancer based on gene expression datasets from the Cancer Genome Atlas and Gene Expression Omnibus. A total of 34 genes were obtained by the univariate analysis, which were significantly associated with the overall survival of PC patients. After further analysis, Anillin (ANLN) and Histone H1c (HIST1H1C) were identified and considered to be the most significant prognostic genes among the 34 genes. A prognostic model based on these two genes was constructed, and successfully distinguished pancreatic cancer survival into high-risk and low-risk groups in the training set and testing set. Subsequently, independent predictive factors, including the age, margin condition and risk score, were then employed to construct the nomogram model. The area under curve for the nomogram model was 0.826 at 0.5 years and 0.726 at 1 year, and the C-index of the nomogram model was 0.664 higher than the others variables alone. These findings have indicated that high expression of ANLN and HIST1H1C predicted poor outcomes for patients with pancreatic cancer. The nomogram model based on the expression of two genes could be valuable for the guidance of clinical treatment.

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“…The differential expression of ANLN has been reported in various cancers [7][8][9][10][11]. According to previous studies, the high ANLN level is associated with the dismal prognosis for HCC patients [5]. Using the MYCinduced, DEN-induced liver tumorigenesis and tumor engraftment mouse models, Zhang et al concluded that ANLN knockdown in liver cells inhibited the development of liver cancer [12].…”

Section: Discussionmentioning

confidence: 99%

“…Remarkably, ANLN expression is also reported to be disordered during HCC development and progression. Lian et al elaborated that ANLN was essential for HCC tumor growth, and that it was regulated by miR-15a/miR-16-1 [5]. Meanwhile, another study also suggests that, ANLN expression in HCC is up-regulated, and the positive protein expression indicates dismal prognosis for the long-term survival of patients undergoing liver transplantation [6].…”

Section: Introductionmentioning

confidence: 99%

Up-regulated Expression and Related Gene Regulatory Networks of ANLN Predict Poor Prognosis and Correlate with Immune Infiltration in Hepatocellular Carcinoma

Hu¹,

Yang²,

Sang³

2020

Preprint

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Background: The aberrant Anillin (ANLN) expression is reported to be associated with carcinogenesis. In this study, sequencing data collected from the Cancer Genome Atlas database were utilized to analyze ANLN expression in hepatocellular carcinoma (HCC).Methods: The relationships of clinicopathological features with ANLN were investigated, and gene set enrichment analysis (GSEA) was performed to reveal the ANLN-related functions. LinkedOmics was employed to identify the co-expressed genes of ANLN and to examine the target networks of kinases, microRNAs (miRNAs) and transcription factors (TFs). Besides, the correlation of ANLN expression with cancer immune infiltrates was analyzed by TIMER. Results: ANLN over-expression predicted dismal prognosis, and GESA results revealed several functions that were related to cell cycle and mRNA binding. Moreover, functional network analysis indicated that, ANLN might regulate DNA replication and cell cycle signaling through pathways that involved several cancer-related kinases, miRNAs and E2F1. Additionally, ANLN was suggested to be associated with the infiltration of several immune cells, which was proved to be upregulated in both HCC cells and tissues. Conclusion: Those efficiently mined data reveal information regarding ANLN expression, the potential regulatory networks and the relationship with immune infiltration in HCC, which lay a foundation for further study on the role of ANLN in carcinogenesis.

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Anillin is required for tumor growth and regulated by miR-15a/miR-16-1 in HBV-related hepatocellular carcinoma

Cited by 45 publications

References 38 publications

The oncogenic Kaposi’s sarcoma-associated herpesvirus encodes a mimic of the tumor suppressive miR-15/16 miRNA family

The oncogenic Kaposi’s sarcoma-associated herpesvirus encodes a mimic of the tumor suppressive miR-15/16 miRNA family

A two-gene-based prognostic signature for pancreatic cancer

Up-regulated Expression and Related Gene Regulatory Networks of ANLN Predict Poor Prognosis and Correlate with Immune Infiltration in Hepatocellular Carcinoma

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