LncRNA FAM83H-AS1 Contributes to the Radio-resistance and Proliferation in Liver Cancer through Stability FAM83H Protein.

IF 2.5 4区 医学 Q3 ONCOLOGY
Xiaocong Jiang, Yuhong Lan, Yingchun Zhang, Yuhong Dong, Ting Song
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Abstract

Background: Liver cancer (LC) is one of China's most common malignant tumors, with a high mortality rate, ranking third leading cause of death after gastric and esophageal cancer. Recent patents propose the LncRNA FAM83H-AS1 has been verified to perform a crucial role in the progression of LC. LncRNA FAM83H-AS1 has been verified to perform a crucial role in the progression of LC. However, the concrete mechanism remains to be pending further investigation.

Objective: This study aimed to explore the embedding mechanism of FAM83H-AS1 molecules in terms of radio sensitivity of LC and provide potentially effective therapeutic targets for LC therapy.

Methods: Quantitative real-time PCR (qRT-PCR) was conducted to measure the transcription levels of genes. Proliferation was determined via CCK8 and colony formation assays. Western blot was carried out to detect the relative protein expression. A xenograft mouse model was constructed to investigate the effect of LncRNA FAM83H-AS1 on tumor growth and radio-sensitivity in vivo.

Results: The levels of lncRNA FAM83H-AS1 were remarkably increased in LC. Knockdown of FAM83H-AS1 inhibited LC cell proliferation and colony survival fraction. Deletion of FAM83H-AS1 increased the sensitivity of LC cells to 4 Gy of X-ray radiation. In the xenograft model, radiotherapy combined with FAM83H-AS1 silencing significantly reduced tumor volume and weight. Overexpression of FAM83H reversed the effects of FAM83H-AS1 deletion on proliferation and colony survival fraction in LC cells. Moreover, the over-expressing of FAM83H also restored the tumor volume and weight reduction caused by the knockdown of FAM83H-AS1 or radiation in the xenograft model.

Conclusion: Knockdown of lncRNA FAM83H-AS1 inhibited LC growth and enhanced radiosensitivity in LC. It has the potential to be a promising target for LC therapy.

LncRNA FAM83H-AS1 通过稳定 FAM83H 蛋白促进肝癌的放射抗性和增殖
背景:肝癌是中国最常见的恶性肿瘤之一,死亡率高,仅次于胃癌和食管癌,位居第三位。最近的专利提出,LncRNA FAM83H-AS1已被证实在肝癌的进展过程中起着至关重要的作用。LncRNA FAM83H-AS1 已被证实在 LC 的进展过程中发挥关键作用。然而,其具体机制仍有待进一步研究:本研究旨在探讨FAM83H-AS1分子在LC放射敏感性方面的嵌入机制,为LC治疗提供潜在有效的治疗靶点:方法:采用定量实时 PCR(qRT-PCR)检测基因的转录水平。通过 CCK8 和菌落形成试验确定增殖情况。通过 Western 印迹检测相对蛋白表达。构建了异种移植小鼠模型,以研究 LncRNA FAM83H-AS1 对体内肿瘤生长和放射敏感性的影响:结果:LC中lncRNA FAM83H-AS1的水平显著升高。结果:LC中lncRNA FAM83H-AS1的水平显著升高,敲除FAM83H-AS1可抑制LC细胞的增殖和集落存活率。FAM83H-AS1的缺失增加了LC细胞对4 Gy X射线辐射的敏感性。在异种移植模型中,放疗结合 FAM83H-AS1 沉默能显著减少肿瘤体积和重量。过表达 FAM83H 逆转了 FAM83H-AS1 基因缺失对 LC 细胞增殖和集落存活率的影响。此外,在异种移植模型中,过表达FAM83H还能恢复因敲除FAM83H-AS1或辐射导致的肿瘤体积和重量的减少:结论:敲除lncRNA FAM83H-AS1可抑制LC的生长并增强LC的放射敏感性。结论:敲除lncRNA FAM83H-AS1可抑制LC的生长并增强LC的放射敏感性,它有可能成为LC治疗的潜在靶点。
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来源期刊
CiteScore
4.50
自引率
7.10%
发文量
55
审稿时长
3 months
期刊介绍: Aims & Scope Recent Patents on Anti-Cancer Drug Discovery publishes review and research articles that reflect or deal with studies in relation to a patent, application of reported patents in a study, discussion of comparison of results regarding application of a given patent, etc., and also guest edited thematic issues on recent patents in the field of anti-cancer drug discovery e.g. on novel bioactive compounds, analogs, targets & predictive biomarkers & drug efficacy biomarkers. The journal also publishes book reviews of eBooks and books on anti-cancer drug discovery. A selection of important and recent patents on anti-cancer drug discovery is also included in the journal. The journal is essential reading for all researchers involved in anti-cancer drug design and discovery. The journal also covers recent research (where patents have been registered) in fast emerging therapeutic areas/targets & therapeutic agents related to anti-cancer drug discovery.
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