RECQL1 Plays an Important Role in the Development of Tongue Squamous Cell Carcinoma

Jiang, Tao; Tao, Suxiong; Han, Junli; Zhou, Zhuojun; Zhang, Xiaoping; Wang, Haining; Chen, Rongjing; Ji, Fang; Zhu, Yaqin

doi:10.1159/000358721

Cited by 10 publications

(18 citation statements)

References 30 publications

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“…RECQ1 overexpression is observed in glioblastomas and ovarian cancers and suggested to play a role in tumor cell proliferation [35–37]. Several RECQ1 polymorphisms are associated with lower pancreatic cancer survival [38], and RECQ1 is a proposed therapeutic target and proliferative marker for head and neck squamous cell carcinoma [39] and hepatocellular carcinoma [39,40].…”

Section: Discussionmentioning

confidence: 99%

Catalytic Strand Separation by RECQ1 Is Required for RPA-Mediated Response to Replication Stress

et al. 2015

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SUMMARY Three (BLM, WRN, RECQ4) of the five human RecQ helicases are linked to genetic disorders characterized by genomic instability, cancer, and accelerated aging [1]. RECQ1, the first human RecQ helicase discovered [2–4] and most abundant [5], was recently implicated in breast cancer [6,7]. RECQ1 is an ATP-dependent DNA unwinding enzyme (helicase) [8,9] with roles in replication [10–12] and DNA repair [13–16]. RECQ1 is highly expressed in various tumors and cancer cell lines (for review, see [17]) and its suppression reduces cancer cell proliferation [14], suggesting a target for anti-cancer drugs. RECQ1’s assembly state plays a critical role in modulating its helicase, branch-migration (BM), or strand annealing [18,19]. The crystal structure of truncated RECQ1 [20,21] resembles that of E. coli RecQ [22] with two RecA-like domains, a RecQ-specific zinc-binding and winged-helix domains, the latter implicated in DNA strand separation and oligomer formation. In addition, a conserved aromatic loop (AL) is important for DNA unwinding by bacterial RecQ [23,24] and truncated RECQ1 helicases [21]. To better understand the roles of RECQ1, two AL mutants (W227A, F231A) in full-length RECQ1 were characterized biochemically and genetically. The RECQ1 mutants were defective in helicase or BM, but retained DNA binding, oligomerization, ATPase, and strand annealing. RECQ1-depleted HeLa cells expressing either AL mutant displayed reduced replication tract length, elevated dormant origin firing, and increased double-strand breaks that could be suppressed by exogenously expressed Replication Protein A (RPA). Thus, RECQ1 governs RPA’s availability in order to maintain normal replication dynamics, suppress DNA damage, and preserve genome homeostasis.

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Section: Discussionmentioning

confidence: 99%

Catalytic Strand Separation by RECQ1 Is Required for RPA-Mediated Response to Replication Stress

et al. 2015

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“…The target proteins were extracted by EpiQuik Total Histone Extraction Kit (Epigentek, Farmingdale, NY, USA) and quantified by a BCA Protein Quantification Kit (vazyma, Nanjing, Jiangsu, China) with bovine serum albumin (BSA) as standard as described previously [17,18]. The sample (= 50 mg) containing target protein were processed by electrophoretic separation before being transferred to PVDF membrane (EMD Millipore, Billerica, MA, USA).…”

Section: Western Blotting Analysismentioning

confidence: 99%

CD47 is a Potential Target for the Treatment of Laryngeal Squamous Cell Carcinoma

Yang

Gao

Zhang

et al. 2016

Cell Physiol Biochem

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Background/Aims: This study aims to investigate the effect of CD47 on the development of laryngeal squamous cell carcinoma (LSCC) and the therapeutic potential of monoclonal antibody against CD47 and its ligand SIRPα in the treatment of LSCC. Methods: We firstly detected the expressions of CD47 mRNA and protein in LSCC and para-carcinoma tissues, introduced the most efficient CD47siRNA sequence into LSCC cells by lentiviral transfection and employed three monoclonal antibodies to evaluate their anti-LSCC effects in vitro and in vivo. Results: We observed that the mRNA and protein expressions of CD47 in LSCC tissue had significant increase in LSCC tissues compared with those in para-carcinoma tissue (p < 0.05). After the treatments of three monoclonal antibodies, i.e. anti-SIRPα, anti-CD47 BRIC126, anti-CD47 B6H12.2, in rats transfected with Hep-2 cell, it has been showed that the mRNA and protein expressions of CD47 in LSCC tissue decreased, macrophage efficiency was promoted when anti-SIRPα and/or CD47siRNA were used, the amounts, viabilities and expressions of CD47 protein of tumor cell were significantly inhibited. Additionally, combined use of CD47siRNA and anti-SIRPα seemed more efficient than solo use of CD47siRNA/anti-SIRPα. Conclusion: The results suggested a critical role of CD47 in LSCC development and the promising treatment of antiCD47/SIRPα and/or CD47siRNA in LSCC.

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“…In fact, both specific small molecular weight inhibitors of RecQ helicases ( Aggarwal et al, 2011 , 2013 ; Rosenthal et al, 2013 ; Shadrick et al, 2013 ) and RNAi-mediated gene silencing with siRNA suppress the growth of cancer cells in various model systems. In the following sections, we introduce both cases, while placing a greater emphasis on the recently established RNAi-mediated strategy that proved to act specifically on cancer cells that contain impaired checkpoint functions and represent high expressions of RecQ helicases ( Futami et al, 2008a , c , 2010 , Arai et al, 2011 ; Mendoza-Maldonado et al, 2011 , Sanada et al, 2013 ; Tao et al, 2014 ).…”

Section: Increased Expression Of Recq Helicases In Cancer Cellsmentioning

confidence: 99%

RECQL1 and WRN DNA repair helicases: potential therapeutic targets and proliferative markers against cancers

Futami

Furuichi

2015

Front. Genet.

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RECQL1 and WRN helicases in the human RecQ helicase family participate in maintaining genome stability, DNA repair, replication, and recombination pathways in the cell cycle. They are expressed highly in rapidly proliferating cells and tumor cells, suggesting that they have important roles in the replication of a genome. Although mice deficient in these helicases are indistinguishable from wild-type mice, their embryonic fibroblasts are sensitive to DNA damage. In tumor cells, silencing the expression of RECQL1 or WRN helicase by RNA interference induces mitotic catastrophe that eventually kills tumor cells at the mitosis stage of the cell cycle. By contrast, the same gene silencing by cognate small RNA (siRNA) never kills normal cells, although cell growth is slightly delayed. These findings indicate that RECQL1 and WRN helicases are ideal molecular targets for cancer therapy. The molecular mechanisms underlying these events has been studied extensively, which may help development of anticancer drugs free from adverse effects by targeting DNA repair helicases RECQL1 and WRN. As expected, the anticancer activity of conventional genotoxic drugs is significantly augmented by combined treatment with RECQL1- or WRN-siRNAs that prevents DNA repair in cancer cells. In this review, we focus on studies that clarified the mechanisms that lead to the specific killing of cancer cells and introduce efforts to develop anticancer RecQ-siRNA drugs free from adverse effects.

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RECQL1 Plays an Important Role in the Development of Tongue Squamous Cell Carcinoma

Cited by 10 publications

References 30 publications

Catalytic Strand Separation by RECQ1 Is Required for RPA-Mediated Response to Replication Stress

Catalytic Strand Separation by RECQ1 Is Required for RPA-Mediated Response to Replication Stress

CD47 is a Potential Target for the Treatment of Laryngeal Squamous Cell Carcinoma

RECQL1 and WRN DNA repair helicases: potential therapeutic targets and proliferative markers against cancers

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