Long non‑coding RNA snaR is involved in the metastasis of liver cancer possibly through TGF‑β1

Shi, Zhitian; Wei, Dong; Wu, Hua‐Mei; Ge, Jiayun; Lei, Xuefen; Guo, Zhitang; Zou, Renchao; Xiao, Shufeng; Wu, Taihu; Ma, Ruicheng; Ai, Runyao; Wang, Lin

doi:10.3892/ol.2019.10258

Cited by 7 publications

(11 citation statements)

References 21 publications

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“…A number of previous studies have revealed snaR-A’s involvement in metabolic dysregulation of breast, liver, and ovarian cancers (Lee et al 2016; Lee et al 2017; Huang et al 2018; Shi et al 2019) and in drug-resistance in human colon cancer cells (Lee et al 2014). We questioned whether miR-snaR can contribute to the phenotypes associated with snaR-A.…”

Section: Resultsmentioning

confidence: 99%

“…SnaR-A is a non-coding RNA that is most highly expressed in testis, followed by brain and placenta, and is specific to higher-order primates (Parrott and Mathews 2007). Additionally, the full snaR-A transcript is upregulated in many cancer cell lines (Parrott and Mathews 2007; Lee et al 2016; Huang et al 2018; Shi et al 2019). While it would seem reasonable for miR-snaR expression to follow the expression pattern of snaR-A, we have observed instances of disproportional snaR-A and miR-snaR expression in different cell lines (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…We found that miR-snaR biogenesis is Drosha-independent, but dependent on XPO5 and Dicer. In addition, we detected Ago-bound miR-snaR in cells expressing high levels of snaR-A, which is upregulated in multiple cancer-derived cell lines and tumors, including breast, colorectal, liver, and ovarian cancers (Parrott and Mathews 2007;Lee et al 2016;Lee et al 2017;Huang et al 2018;Shi et al 2019). To investigate the potential function of this miRNA, we identified miR-snaR/target hybrids in multiple Ago-CLASH datasets and discovered that miR-snaR represses expression of non-metastatic cells 1 (NME1), which correspondingly increases mobility of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

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A non-canonical microRNA derived from the snaR-A non-coding RNA targets a metastasis inhibitor

Stribling

Lei

Guardia

et al. 2021

Preprint

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MicroRNAs (miRNAs) are small noncoding RNAs that function as critical post-transcriptional regulators in various biological processes. While most miRNAs are generated from processing of long primary transcripts via sequential Drosha and Dicer cleavage, some miRNAs that bypass Drosha cleavage can be transcribed as part of another small non-coding RNA. Here, we develop the Target-Oriented miRNA Discovery (TOMiD) bioinformatic analysis method to identify Drosha-independent miRNAs from Argonaute crosslinking and sequencing of hybrids (Ago-CLASH) datasets. Using this technique, we discovered a novel miRNA derived from a primate specific non-coding RNA, the small NF90 associated RNA A (snaR-A). The miRNA derived from snaR-A (miR-snaR) arises independent of Drosha processing, but requires Exportin-5 and Dicer for biogenesis. We identify that miR-snaR is concurrently upregulated with the full snaR-A transcript in cancer cells. Functionally, miR-snaR associates with Ago proteins and targets NME1, a key metastasis inhibitor, contributing to snaR-A’s role in promoting cancer cell migration. Our findings suggest a functional link between a novel miRNA and its precursor non-coding RNA.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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A non-canonical microRNA derived from the snaR-A non-coding RNA targets a metastasis inhibitor

Stribling

Lei

Guardia

et al. 2021

Preprint

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“…Apoptosis usually occurs in a steady state in normal cells and tissues or as a defense mechanism to eliminate defects or unwanted cells (14). It is reported that it is a necessary supplement to inhibit cell proliferation and plays an important role in the development and regulation of the immune system, the removal of damaged cells and the destruction of apoptosis.…”

Section: Colon Cancer Is One Of the Most Common Digestive Diseasesmentioning

confidence: 99%

Banxia Xiexin decoction, a traditional Chinese medicine, alleviates colon cancer in nude mice

Yan¹,

Yue²,

Wang³

et al. 2019

Ann. Transl. Med.

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Backgrounds: Banxia Xiexin decoction (BXD) is widely used in the treatment of acute and chronic gastritis, peptic ulcer, dyspepsia, gastrointestinal dysfunction, chronic hepatitis, oral ulcer and other diseases, but there are few reports on its treatment of colon cancer. The current study was designed to investigate the effect of BXD on colon cancer and its possible molecular mechanisms.Methods: Fifty SPF BALB/c nude mice were selected to establish an animal model of colon cancer bearing nude mice. Establishment of nude mice intestinal cancer model by subcutaneous injection of intestinal cancer cells. Serum superoxide dismutase (SOD) and malondialdehyde (MDA) were detected by commercial kits. Pro-inflammatory cytokines in serum were detected. Western blotting was used to demonstrate the expression levels of related apoptosis proteins, inflammation and oxidative stress proteins.Results: Our results showed that BXD could decrease SOD and increased MDA in nude mice bearing tumors. BXD increased pro-inflammatory cytokines in serum in nude mice bearing tumors. Western blotting revealed that the protein expressions of Bax, Caspase-3, Caspase-9 were increased by different concentrations of BXD, while Bcl-2 was decreased. BXD also decreased Nrf-2 and HO-1, and increased the levels of MAPK/NF-κB pathway in tumor tissue.Conclusions: BXD has an obvious tumor inhibiting effect on SW 480 colon cancer transplanted tumor in nude mice via apoptotic pathway and MAPK/NF-κB pathway.

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“…Additional classes of Pol III-transcribed genes, whose functions remain less well understood, include vault RNA (regulation of apoptosis and autophagy) 16,17 , Y RNA (replication initiation; translation regulation) 18, 19 , BC200 (translation regulation) 20 , and SNAR RNA, which interacts with RNA-binding protein ILF3 21,22 . BC200 and SNAR RNA are both aberrantly upregulated in a variety of cancer contexts, yet the underlying mechanisms and disease contributions of these RNA species remain poorly understood [23][24][25][26][27] .…”

Section: Introductionmentioning

confidence: 99%

A cancer-associated RNA polymerase III identity drives robust transcription and expression of SNAR-A noncoding RNA

Bortle

Marciano

et al. 2021

Preprint

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Dysregulation of the RNA polymerase III (Pol III) transcription program, which synthesizes tRNA and other classes of small noncoding RNA critical for cell growth and proliferation, is associated with cancer and human disease. Previous studies have identified two distinct Pol III isoforms defined by the incorporation of either subunit POLR3G (RPC7α) during early development, or POLR3GL (RPC7β) in specialized tissues. Though POLR3G is re-established in cancer and immortalized cell lines, the contributions of these isoforms to transcription potential and transcription dysregulation in cancer remain poorly defined. Using an integrated Pol III genomic profiling approach in combination with in vitro differentiation and subunit disruption experiments, we discover that loss of subunit POLR3G is accompanied by a restricted repertoire of genes transcribed by Pol III. In particular, we observe that a specific class of small noncoding RNA, SNAR-A, is exquisitely sensitive to the availability of subunit POLR3G in proliferating cells. Taken further, large-scale analysis of Pol III subunit expression and downstream chromatin features identifies concomitant loss of POLR3G and SNAR-A activity across a multitude of differentiated primary immune cell lineages, and conversely, coordinate re-establishment of POLR3G expression and SNAR-A features in a variety of human cancers. These results altogether argue against strict redundancy models for subunits POLR3G and POLR3GL, and instead support a model in which Pol III identity itself functions as an important transcriptional regulatory mechanism. Upregulation of POLR3G, which is driven by MYC, identifies a subgroup of patients with unfavorable survival outcomes in specific cancers, further implicating the POLR3G-enhanced transcription repertoire as a potential disease factor.

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Long non‑coding RNA snaR is involved in the metastasis of liver cancer possibly through TGF‑β1

Cited by 7 publications

References 21 publications

A non-canonical microRNA derived from the snaR-A non-coding RNA targets a metastasis inhibitor

A non-canonical microRNA derived from the snaR-A non-coding RNA targets a metastasis inhibitor

Banxia Xiexin decoction, a traditional Chinese medicine, alleviates colon cancer in nude mice

A cancer-associated RNA polymerase III identity drives robust transcription and expression of SNAR-A noncoding RNA

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