Lung cancer (LC) is the leading cause of cancer-related deaths worldwide. On the other hand, idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease showing a prevalence of 20 new cases per 100,000 persons per year. Despite differences in cellular origin and pathological phenotypes, LC and IPF are lung diseases that share common features, including hyperproliferation of specific cell types in the lung, involvement of epithelial-mesenchymal transition (EMT) and enhanced activity of signaling pathways, such as tissue growth factor (TGFB), epidermal growth factor (EGF), fibroblast growth factor (FGF), wingless secreted glycoprotein (WNT) signaling, among others. EMT is a process during which epithelial cells lose their cell polarity and cell-cell adhesion, and acquire migratory and invasive properties to become mesenchymal cells. EMT involves numerous morphological hallmarks of hyperproliferative diseases, like cell plasticity, resistance to apoptosis, dedifferentiation and proliferation, thereby playing a central role during organ fibrosis and cancer progression. EMT was considered as an “all-or-none” process. In contrast to these outdated dichotomist interpretations, recent reports suggest that EMT occurs gradually involving different epithelial cell intermediate states with mesenchyme-like characteristics. These cell intermediate states of EMT differ from each other in their cell plasticity, invasiveness and metastatic potential, which in turn are induced by signals from their microenvironment. EMT is regulated by several transcription factors (TFs), which are members of prominent families of master regulators of transcription. In addition, there is increasing evidence for the important contribution of noncoding RNAs (ncRNAs) to EMT. In our review we highlight articles dissecting the function of different ncRNAs subtypes and nuclear architecture in cell intermediate states of EMT, as well as their involvement in LC and IPF.

肺癌 (LC) 是全球癌症相关死亡的主要原因。另一方面，特发性肺纤维化 (IPF) 是最常见的间质性肺病，每年每 100,000 人中有 20 例新病例。尽管细胞起源和病理表型存在差异，但 LC 和 IPF 是具有共同特征的肺部疾病，包括肺中特定细胞类型的过度增殖、上皮间充质转化 (EMT) 的参与和信号通路活性增强，例如组织生长因子 (TGFB)、表皮生长因子 (EGF)、成纤维细胞生长因子 (FGF)、无翅分泌糖蛋白 (WNT) 信号等。EMT是上皮细胞失去细胞极性和细胞间粘附的过程，并获得迁移和侵袭特性，成为间充质细胞。EMT 涉及过度增殖性疾病的许多形态学特征，如细胞可塑性、抗凋亡、去分化和增殖，从而在器官纤维化和癌症进展过程中发挥核心作用。EMT 被认为是一个“全有或全无”的过程。与这些过时的二分法解释相反，最近的报告表明 EMT 的发生逐渐涉及具有间充质样特征的不同上皮细胞中间状态。EMT 的这些细胞中间状态在细胞可塑性、侵袭性和转移潜能方面彼此不同，而这些又是由来自其微环境的信号诱导的。EMT 受多种转录因子 (TF) 的调控，它们是转录主要调节因子的重要家族成员。此外，越来越多的证据表明非编码 RNA (ncRNA) 对 EMT 的重要贡献。在我们的评论中，我们重点介绍了剖析不同 ncRNA 亚型和细胞核结构在 EMT 细胞中间状态中的功能的文章，以及它们在 LC 和 IPF 中的参与。