Autophagy suppresses tumorigenesis of hepatitis B virus‐associated hepatocellular carcinoma through degradation of microRNA‐224

Lan, Sheng Hui; Wu, Sihan; Zuchini, Roberto; Lin, Xi Zhang; Su, Ih Jen; Tsai, Ting Fen; Lin, Yen Ju; Wu, Chih Chiang; Liu, Hsiao Sheng

doi:10.1002/hep.26659

Cited by 169 publications

(161 citation statements)

References 33 publications

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“…MiR-224 promotes HCC tumorigenesis through targeting and silencing Smad4 gene. Smad4 contains two miR-224-binding sites in the 3′untranslated region and acts as a tumor suppressor role [21]. It was also reported that miR-224 acts as an oncogenic role in the cellular processes by targeting Smad4 in CRC [22].…”

Section: Mir-224 In Tumorigenesismentioning

confidence: 98%

MicroRNA-224: as a potential target for miR-based therapy of cancer

et al. 2015

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MicroRNAs (miRNAs) are small noncoding RNA molecules which regulate the target gene expression posttranscriptionally. Increasing studies have shown that microRNAs play important roles in multiple biological pathways. For instance, aberrant expression of microRNA-224 (miR-224) plays a vital role in tumor biology in various types of human cancer. Here, we aim to summarize the molecular mechanisms that lead to the overexpression of miR-224 in cancers, analyze the effect of miR-224 on tumor biology, and reveal the clinical significance of miR-224. MiR-224 regulates its targets by modulating messenger RNA (mRNA) stability and/or protein translation, and it would provide new insight into molecular targeting cancer treatment.

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Section: Mir-224 In Tumorigenesismentioning

confidence: 98%

MicroRNA-224: as a potential target for miR-based therapy of cancer

et al. 2015

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“…Previous studies have shown that the canonical autophagy machinery can function in antibacterial and antiviral host defense by delivering intracellular pathogens or components of intracellular pathogens to the lysosome for degradation (2,36). Moreover, Beclin 1 and the autophagy pathway has been proposed to function in controlling viral oncogenesis in at least two contexts: monoallelic deletion of Becn1 accelerates neoplastic lesions in the livers of mice that transgenically express hepatitis B envelope protein autophagy (30) and decreased autophagic degradation of a microRNA (miR-224) is postulated to contribute to hepatitis B virus-associated hepatocellular carcinoma in mice and in humans (42). Our findings suggest that independently of the autophagy machinery, the delivery of viral oncoproteins to the lysosome for degradation (via an endolysosomal trafficking route) may play a crucial role in innate immunity.…”

Section: Discussionmentioning

confidence: 99%

Endolysosomal trafficking of viral G protein-coupled receptor functions in innate immunity and control of viral oncogenesis

Dong

Cheng

Zou

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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The ubiquitin-proteasome system degrades viral oncoproteins and other microbial virulence factors; however, the role of endolysosomal degradation pathways in these processes is unclear. Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma, and a constitutively active viral G protein-coupled receptor (vGPCR) contributes to the pathogenesis of KSHV-induced tumors. We report that a recently discovered autophagy-related protein, Beclin 2, interacts with KSHV GPCR, facilitates its endolysosomal degradation, and inhibits vGPCR-driven oncogenic signaling. Furthermore, monoallelic loss of Becn2 in mice accelerates the progression of vGPCR-induced lesions that resemble human Kaposi's sarcoma. Taken together, these findings indicate that Beclin 2 is a host antiviral molecule that protects against the pathogenic effects of KSHV GPCR by facilitating its endolysosomal degradation. More broadly, our data suggest a role for host endolysosomal trafficking pathways in regulating viral pathogenesis and oncogenic signaling.

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“…(Lan et al, 2014a) Autophagy specifically has been shown to suppress HBV-associated tumor formation by degrading microRNA-224. (Lan et al, 2014b)…”

Section: Autophagic Membranes In Classical Viral Envelope Formationmentioning

confidence: 99%

Viruses and the autophagy pathway

2015

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Studies of the cellular autophagy pathway have exploded over the past twenty years. Now appreciated as a constitutive degradative mechanism that promotes cellular homeostasis, autophagy is also required for a variety of developmental processes, cellular stress responses, and immune pathways. Autophagy certainly acts as both an anti-viral and pro-viral pathway, and the roles of autophagy depend on the virus, the cell type, and the cellular environment. The goal of this review is to summarize, in brief, what we know so far about the relationship between autophagy and viruses, particularly for those who are not familiar with the field. With a massive amount of relevant published data, it is simply not possible to be comprehensive, or to provide a complete “parade of viruses”, and apologies are offered to researchers whose work is not described herein. Rather, this review is organized around general themes regarding the relationship between autophagy and animal viruses.

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Autophagy suppresses tumorigenesis of hepatitis B virus‐associated hepatocellular carcinoma through degradation of microRNA‐224

Cited by 169 publications

References 33 publications

MicroRNA-224: as a potential target for miR-based therapy of cancer

MicroRNA-224: as a potential target for miR-based therapy of cancer

Endolysosomal trafficking of viral G protein-coupled receptor functions in innate immunity and control of viral oncogenesis

Viruses and the autophagy pathway

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