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慢病毒介导的[具体基因]基因沉默对非小细胞肺癌干性能力的影响

The Effects of Lentivirus-Mediated Gene Silencing of on the Stemness Capability of Non-Small Cell Lung Cancer.

作者信息

Abu Halim Noor Hanis, Zakaria Norashikin, Theva Das Kumitaa, Lin Juntang, Lim Moon Nian, Fakiruddin Kamal Shaik, Yahaya Badrul Hisham

机构信息

Lung Stem Cell and Gene Therapy Group, Regenerative Medicine Cluster, Advanced Medical and Dental Institute (IPPT), Sains@Bertam, Universiti Sains Malaysia, Kepala Batas Penang, 13200, Malaysia.

Infectomics Cluster, Advanced Medical and Dental Institute (IPPT), Sains@Bertam, Universiti Sains Malaysia, Kepala Batas Penang, 13200, Malaysia.

出版信息

J Cancer. 2021 Apr 19;12(12):3468-3485. doi: 10.7150/jca.50793. eCollection 2021.

DOI:10.7150/jca.50793
PMID:33995625
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8120186/
Abstract

Retinoic acid receptor beta is a nuclear receptor protein that binds to retinoic acid (RA) to mediate cellular signalling in embryogenic morphogenesis, cell growth, and differentiation. However, the function of in cancer stem cells (CSCs) has yet to be determined. This study aimed to understand the role of in regulating cell growth and differentiation of lung cancer stem cells. Based on the clonogenic assay, spheroid assay, mRNA levels of stem cell transcription factors, and cell cycle being arrested at the G0/G1 phase, the suppression of resulted in significant inhibition of A549 parental cell growth. This finding was contradictory to the results seen in CSCs, where inhibition enhanced the cell growth of putative and non-putative CSCs. These results suggest that suppression may act as an essential regulator in A549 parental cells, but not in the CSCs population. The findings in this study demonstrated that the loss of promotes tumorigenicity in CSCs. Microarray analysis revealed that various cancer pathways were significantly activated following the suppression of . The changes seen might compensate for the loss of function, CSCs population's aggressiveness, which led to the CSCs population's aggressiveness. Thus, understanding the role of in regulating the stemness of CSCs may lead to targeted therapy for lung CSCs.

摘要

维甲酸受体β是一种核受体蛋白，它与维甲酸（RA）结合，在胚胎形态发生、细胞生长和分化过程中介导细胞信号传导。然而，其在癌症干细胞（CSCs）中的功能尚未确定。本研究旨在了解其在调节肺癌干细胞的细胞生长和分化中的作用。基于克隆形成试验、球体形成试验、干细胞转录因子的mRNA水平以及细胞周期停滞在G0/G1期，其抑制导致A549亲本细胞生长受到显著抑制。这一发现与在癌症干细胞中观察到的结果相矛盾，在癌症干细胞中，其抑制增强了假定的和非假定的癌症干细胞的细胞生长。这些结果表明，其抑制在A549亲本细胞中可能起重要调节作用，但在癌症干细胞群体中并非如此。本研究结果表明，其缺失促进了癌症干细胞的致瘤性。微阵列分析显示，在其抑制后，各种癌症相关通路被显著激活。所观察到的变化可能补偿了其功能丧失后癌症干细胞群体的侵袭性，从而导致癌症干细胞群体的侵袭性。因此，了解其在调节癌症干细胞干性中的作用可能会为肺癌癌症干细胞带来靶向治疗方法。

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