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客戶采用我司磁珠進行RNA pull-down實驗，SCI論文發(fā)表在《IUBMB LIFE》。

2.10 | RNA pull-down assay
The probe targeting the junction site of circ-ARL3 was synthesized and labeled with biotin, followed by addition into HCC cell lysates and incubation overnight at 4
C. The next day, above cell lysates were incubated with PuriMag G-streptavidin beads (Invitrogen) for 2 hr. After being washed five times, the purified RNA was collected and quantified by qRT-PCR to analyze the enrichment of circ-ARL3 and the indicated miRNAs.

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本文更多內容請參考：

N6‐methyladenosine modification of circular RNA circ‐ARL3 facilitates Hepatitis B virus‐associated hepatocellular carcinoma via sponging miR‐1305

環(huán)狀RNA circ-ARL3的N6-甲基腺苷修飾可通過海綿miR-130促進乙型肝炎病毒相關的肝細胞癌
Xi Rao  Lingling Lai  Xiaopeng Li  Liang Wang  Ai Li  Qian Yang
First published: 28 December 2020 https://doi.org/10.1002/iub.2438
IUBMB LIFE, Volume73, Issue2, February 2021, Pages 408-417

ABSTRACT: Hepatitis B virus (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC), whether circular RNA (circRNA) is involved in this process remains unknown. In this study, we performed circRNA microarray profile and found an HBV‐related circRNA, circ‐ARL3 (hsa_circ_0092493). Stable knockdown of circ‐ARL3 inhibited the proliferation and invasion of HBV+ HCC cells. High circ‐ARL3 was positively correlated with malignant clinical features and poor prognosis. In terms of mechanism, HBx protein upregulated N6‐methyladenosine (m6A) methyltransferases METTL3 expression, increasing the m6A modification of circ‐ARL3; then, m6A reader YTHDC1 bound to m6A‐modified of circ‐ARL3 and favored its reverse splicing and biogenesis. Furthermore, circ‐ARL3 was able to sponge miR‐1305, antagonizing the inhibitory effects of miR‐1305 on a cohort of target oncogenes, thereby promoting HBV+ HCC progression. Importantly, depletion of circ‐ARL3 significantly retarded HBV+ HCC cell growth in vivo, whereas this effect was evidently blocked after silencing of miR‐1305. Collectively, our data suggest that circ‐ARL3 is a critical regulator in HBV‐related HCC, targeting the axis of circ‐ARL3/miR‐1305 may be a promising treatment for HBV+ HCC patients.

乙型肝炎病毒（HBV）感染是肝細胞癌（HCC）的主要危險因素，目前尚不清楚環(huán)狀RNA（circRNA）是否參與該過程。在這項研究中，我們進行了circRNA微陣列分析，并發(fā)現(xiàn)了與HBV相關的circRNA，circ-ARL3（hsa_circ_0092493）。 circ-ARL3的穩(wěn)定敲低抑制了HBV + HCC細胞的增殖和侵襲。 circ-ARL3高與惡性臨床特征和預后不良呈正相關。在機制上，HBx蛋白上調N6-甲基腺苷（m6A）甲基轉移酶METTL3的表達，從而增加circ-ARL3的m6A修飾。然后，m6A閱讀器YTHDC1與circ-ARL3的m6A修飾結合，并支持其反向剪接和生物發(fā)生。此外，circ-ARL3能夠抑制miR-1305，從而拮抗miR-1305對目標癌基因群的抑制作用，從而促進HBV + HCC的進展。重要的是，circ-ARL3的耗竭可顯著延緩體內HBV + HCC細胞的生長，而在miR-1305沉默后，這種作用明顯被阻止。總體而言，我們的數據表明，circ-ARL3是HBV相關HCC的關鍵調節(jié)劑，靶向circ-ARL3 / miR-1305的軸可能是HBV + HCC患者的有希望的治療方法。