Overexpression of Hiwi Promotes Growth of Human Breast Cancer Cells

Wang, Dawei; Wang, Zhaohui; Wang, Lingling; Yang, Song; Zhang, Guizhen

doi:10.7314/apjcp.2014.15.18.7553

Cited by 40 publications

(25 citation statements)

References 41 publications

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“…To further investigate the functional potential of these piRNAs, we assessed these piRNAs in the context of PIWI proteins. Using mRNA expression data for 253 patients from The Cancer Genome Atlas, we identified PIWIL1 to be significantly upregulated in current smoker vs. lifelong nonsmoker samples, in accordance with previous studies identifying overexpression of this gene in other carcinomas ( p < 0.05, FDR < 0.05) [33–36]. Correlations of our 13-member piRNA panel to PIWIL1 indicated that NONHSAT081250 , a piRNA downregulated in smoking-associated HNSCCs, exhibited significantly reduced expression with upregulation of PIWIL1 , suggesting a potential mechanistic interaction between these elements ( p < 0.05).…”

Section: Discussionsupporting

confidence: 88%

Smoking status regulates a novel panel of PIWI-interacting RNAs in head and neck squamous cell carcinoma

et al. 2017

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Objective Smoking remains a primary etiological factor in head and neck squamous cell carcinoma (HNSCC). Given that non-coding RNAs (ncRNAs), including PIWI-interacting RNAs (piRNAs), have emerged as mediators of initiation and progression in head and neck malignancies, we undertook a global study of piRNA expression patterns in smoking-associated HNSCC. Materials and Methods Using RNA-sequencing data from 256 current smoker and lifelong nonsmoker samples in The Cancer Genome Atlas (TCGA), we analyzed the differential expression patterns of 27,127 piRNAs across patient cohorts stratified by tobacco use, with HPV16 status and tumor status taken into account. We correlated their expression to clinical characteristics and to smoking-induced alteration of PIWI proteins, the functional counterparts of piRNAs. Finally, we correlated our identified piRNAs and PIWI proteins to known chromosomal aberrations in HNSCC to understand their wider-ranging genomic effects. Results and Conclusion Our analyses implicated a 13-member piRNA panel in smoking-related HNSCC, among which NONHSAT123636 and NONHSAT113708 are associated with tumor stage, NONHSAT067200 with patient survival, and NONHSAT081250 with smoking-altered PIWIL1 protein expression. 6 piRNAs as well as PIWIL1 correlated with genomic alterations common to HNSCC, including TP53 mutation, TP53-3p co-occurrence, and 3q26, 8q24, and 11q13 amplification. Collectively, our findings provide novel insights into the etiology-specific piRNA landscape of smoking-induced HNSCC.

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Section: Discussionsupporting

confidence: 88%

Smoking status regulates a novel panel of PIWI-interacting RNAs in head and neck squamous cell carcinoma

et al. 2017

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“…The involvement of PIWI proteins in cancer was first reported in seminomas in which PIWILI might participate in enhancing the proliferation of germ cells but not somatic cells [33]. Very recently, the hiwi gene was also reported to promote the growth of human breast tumors [46], gastric tumors [40], and hepatocellular carcinoma cells [72]. The piwil2 gene was suggested to modulate the proliferation of colon cancer [58] and breast cancer [51,53].…”

Section: Piwis Are Involved In Promoting Cell Proliferationmentioning

confidence: 99%

Emerging roles for PIWI proteins in cancer

Tan¹,

Liu²,

Liao³

et al. 2015

ABBS

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It is generally accepted that PIWI proteins are predominately expressed in the germline but absent in somatic tissues. Their best-characterized role is to suppress transposon expression, which ensures genomic stability in the germline. However, increasing evidence has suggested that PIWI proteins are linked to the hallmarks of cancer defined by Weinberg and Hanahan, such as cell proliferation, anti-apoptosis, genomic instability, invasion and metastasis. This provides new possibilities for anticancer therapies through the targeting of PIWI proteins, which may have fewer side effects due to their potential classification as a CTA (cancer/testis antigen). Furthermore, PIWI has been proposed to act as a diagnostic and prognostic marker for many types of cancer, and even to differentiate early-and late-stage cancers. We herein summarize the latest progress in this exciting field, hoping to encourage new investigations of PIWIs in cancer biology that will help to develop new therapeutics for clinical application.

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“…PIWIL1 (Piwi‐like RNA‐mediated gene silencing 1), also known as HIWI, contains two conserved domains: the PAZ domain in middle and the PIWI domain in C‐terminal . Current discoveries have shown that PIWIL1 is involved in tumorigenesis in various cancers, including proliferation, migration and invasion of cancers . Meanwhile, evidences have demonstrated that the dysfunction of circadian rhythms is associated with tumours .…”

Section: Introductionmentioning

confidence: 99%

PIWIL1 suppresses circadian rhythms through GSK3β‐induced phosphorylation and degradation of CLOCK and BMAL1 in cancer cells

Tan

Zhu

Zheng

et al. 2019

J Cellular Molecular Medi

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Circadian rhythms are maintained by series of circadian clock proteins, and post‐translation modifications of clock proteins significantly contribute to regulating circadian clock. However, the underlying upstream mechanism of circadian genes that are responsible for circadian rhythms in cancer cells remains unknown. PIWIL1 participates in many physiological processes and current discoveries have shown that PIWIL1 is involved in tumorigenesis in various cancers. Here we report that PIWIL1 can suppress circadian rhythms in cancer cells. Mechanistically, by promoting SRC interacting with PI3K, PIWIL1 can activate PI3K‐AKT signalling pathway to phosphorylate and inactivate GSK3β, repressing GSK3β‐induced phosphorylation and ubiquitination of CLOCK and BMAL1. Simultaneously, together with CLOCK/BMAL1 complex, PIWIL1 can bind with E‐BOX region to suppress transcriptional activities of clock‐controlled genes promoters. Collectively, our findings first demonstrate that PIWIL1 negatively regulates circadian rhythms via two pathways, providing molecular connection between dysfunction of circadian rhythms and tumorigenesis.

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Overexpression of Hiwi Promotes Growth of Human Breast Cancer Cells

Cited by 40 publications

References 41 publications

Smoking status regulates a novel panel of PIWI-interacting RNAs in head and neck squamous cell carcinoma

Smoking status regulates a novel panel of PIWI-interacting RNAs in head and neck squamous cell carcinoma

Emerging roles for PIWI proteins in cancer

PIWIL1 suppresses circadian rhythms through GSK3β‐induced phosphorylation and degradation of CLOCK and BMAL1 in cancer cells

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