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The Mouse Skin as a Model for Chemical Carcinogenesis
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
In susceptible mouse strains, the first tumors can be observed after 6 to 8 weeks of continuous promoter treatment. The nature of these tumors has been somewhat controversial. They are exophytic, noninvasive epithelial tumors resembling human and rabbit papillomas.13 For this reason they have been named papillomas and are considered by some authors as terminally benign lesions.14 However, the fate of the chemically induced papillomas seems to depend largely on the genetic background of the host. In SENCAR mice, papillomas do not behave as terminally benign lesions but as truly premalignant lesions.13 All papillomas induced in SENCAR mice by two-stage protocols develop dysplastic changes, become aneuploid, and express several markers indicative of progression, such as aberrant expression of keratin 13, the enzyme γ-Glutamyltranspeptidase (GGT), and overexpression of proteins involved in the regulation of the cell cycle.15–17
RNA methylation-related genes of m6A, m5C, and m1A predict prognosis and immunotherapy response in cervical cancer
Published in Annals of Medicine, 2023
Yan Wang, Yiwen Mao, Caizhi Wang, Xuefeng Jiang, Qionglan Tang, Lingling Wang, Jialei Zhu, Mengqiu Zhao
There are multiple transcriptional modifications of RNA [4]. The three most common RNA methylation modifications are m6A, m5C and m1A, which usually regulate gene expression at the post-transcriptional level, and the regulatory molecules are mainly methyltransferases, demethylases and methyl-binding proteins [5–7]. A recent study showed that m6A mRNA methylation plays an important role in cancer development, s such as bladder cancer [8] and stomach cancer [9]. A previous study showed the potential biological function of NSUN2, a regulator of m5C, in common gynaecological cancers, where NSUN2 promotes cervical cancer cell migration and invasion by causing m5C methylation of keratin 13 (KRT13) transcripts [10]. Zhao et al. [11] revealed that dysregulation of m1A enzymes in tumour samples from patients with five gastrointestinal (GI) cancers is associated with multiple types of genetic alterations. However, the role of the three common types of RNA methylation modifications in cervical cancer remains unknown. Therefore, it is crucial to explore the mechanisms of the roles of genes regulated by m6A, m5C and m1A methylation modifications in the prognosis and treatment of cervical cancer.
Analysis of Inflammatory and Homeostatic Roles of Tissue-resident Macrophages in the Progression of Cholesteatoma by RNA-Seq
Published in Immunological Investigations, 2021
Lian Fang, Lin Chen, Bi Lin, Liang Han, Kaiquan Zhu, Qifa Song
The homeostasis and repair functions of TRMØs were multifaceted and were affected both from up-regulated and down-regulated genes. Several genes in the homeostasis and repair processes were dramatically up-regulated, such as keratin-13 and MMP-1, MMP-7 and MMP-12. The over-expressed keratin-13 increases the fibrous structural protein of the epithelial cells in the outermost layers of the skins (Moch et al. 2013). Previous research has proved distinct expression patterns of various cytokeratins in cholesteatomas, with keratin-13 increased in the suprabasal layer of the annular external auditory canal of stage I through III of cholesteatoma (Kim and Tinling et al. 2002). This process escalates the epidermal hyperproliferation and migration in cholesteatoma pathogenesis and helped form the outer keratinizing squamous epithelial layer of cholesteatoma (Sudhoff and Tos 2007).
Endogenous lung stem cells for lung regeneration
Published in Expert Opinion on Biological Therapy, 2019
It is clear from recent studies that perceptions of stem cells existing in a hierarchical order with relatively fixed cell fate choices at each stage of differentiation were naïve. It is increasingly obvious that the lung has evolved with considerable redundancy in its reparative tool box, with duplication of stem cells that give rise to critical specialized epithelial cells and plasticity of mature specialized cells increasing the capacity for wound healing after injury. With dedicated efforts to map the cellular profile of the lung by single-cell transcriptomics, more cell subsets, and new cell types will be discovered, which I am sure will uncover unforeseen reparative routes through which the lung responds to injury and disease. Indeed, comprehensive single cell (sc)RNA-Seq analysis of the human and mouse airway epithelium by two independent research teams recently discovered a number of new cell types, including a rare type of airway cell they named pulmonary ionocytes which express the highest levels of the Cftr gene, mutations to which cause cystic fibrosis [69,70]. In a technological advance, D.T. Montoro and colleagues coupled lineage tracing with scRNA-Seq over time to provide the first evidence that new ionocytes may be derived from basal cells [69]. The team also discovered high proliferative epithelial zones in the airways (named hillocks) that are comprised of stratified epithelial layers of newly identified Trp63+ Keratin 13 (Krt13)+ basal cells and secretory cells but lacked luminal ciliated cells [69].