Department of Science Education, Korea National University of Education, Cheongju-si, Chungbuk, Republic of Korea.
Department of Biology Education, Korea National University of Education, Cheongju-si, Chungbuk, Republic of Korea.
Cancer Biomark. 2021;32(2):175-188. doi: 10.3233/CBM-210242.
Lung cancer accounts for a large proportion of cancer-related deaths worldwide. Personalized therapeutic medicine based on the genetic characteristics of non-small cell lung cancer (NSCLC) is a promising field, and discovering clinically applicable biomarkers of NSCLC is required. LINC00472 is a long non-coding RNA and has been recently suggested to be a biomarker of NSCLC, but little is known of its mechanism in NSCLC. Thus, the current study was performed to document changes in gene expression after LINC00472 overexpression in NSCLC cells. As a result of cell viability and migration assay, LINC00472 downregulated cell survival, proliferation, and motility. Transcriptome sequencing analysis showed 3,782 genes expression were changed in LINC00472 overexpressing cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed most genes were associated with intracellular metabolism. The PPP1R12B, RGS5, RBM5, RBL2, LDLR and PTPRM genes were upregulated by LINC00472 overexpression and these genes functioned as tumor suppressors in several cancers. In contrast, SPSB1, PCNA, CD24, CDK5, CDC25A, and EIF4EBP1 were downregulated by LINC00472, and they functioned as oncogenes in various cancers. Consequently, the function of LINC00472 in tumorigenesis might be related to changes in the expressions of other oncogenes and tumor suppressors.
肺癌占全球癌症相关死亡的很大比例。基于非小细胞肺癌（NSCLC）遗传特征的个性化治疗药物是一个很有前途的领域，需要发现 NSCLC 的临床适用生物标志物。LINC00472 是一种长非编码 RNA，最近被认为是 NSCLC 的生物标志物，但人们对其在 NSCLC 中的机制知之甚少。因此，本研究旨在记录 NSCLC 细胞中 LINC00472 过表达后基因表达的变化。通过细胞活力和迁移试验，LINC00472 下调了细胞的存活、增殖和迁移。转录组测序分析显示，LINC00472 过表达细胞中有 3782 个基因的表达发生了变化。基因本体论（GO）和京都基因与基因组百科全书（KEGG）富集分析表明，大多数基因与细胞内代谢有关。PPP1R12B、RGS5、RBM5、RBL2、LDLR 和 PTPRM 基因被 LINC00472 过表达上调，这些基因在几种癌症中作为肿瘤抑制因子发挥作用。相反，SPSB1、PCNA、CD24、CDK5、CDC25A 和 EIF4EBP1 被 LINC00472 下调，它们在各种癌症中作为癌基因发挥作用。因此，LINC00472 在肿瘤发生中的功能可能与其他癌基因和肿瘤抑制基因表达的变化有关。
