Publications by authors named "Yura Song"

Glandular epithelia, including mammary gland (MG) and prostate, are composed of luminal and basal cells. During embryonic development, glandular epithelia arise from multipotent stem cells (SCs) that are replaced after birth by unipotent basal and unipotent luminal SCs. Different conditions, such as basal cell transplantation, luminal cell ablation, and oncogene expression can reinduce adult basal SC (BaSCs) multipotency in different glandular epithelia.

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Stem cells (SCs) and not progenitors (Ps) act as cells of origin of Basal Cell Carcinoma (BCC). The mechanisms promoting BCC formation in SCs or restricting tumour development in Ps are currently unknown. In this study, we transcriptionally profiled SCs and Ps and found that Survivin, a pleiotropic factor that promotes cell division and inhibits apoptosis was preferentially expressed in SCs.

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During wound healing, different pools of stem cells (SCs) contribute to skin repair. However, how SCs become activated and drive the tissue remodeling essential for skin repair is still poorly understood. Here, by developing a mouse model allowing lineage tracing and basal cell lineage ablation, we monitor SC fate and tissue dynamics during regeneration using confocal and intravital imaging.

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Article Synopsis
  • The skin constantly renews itself, but problems with this process can lead to tumors.
  • Scientists studied how a specific mutated gene (SmoM2) affects skin cells in mice, causing tumors in the ear but not in the back skin.
  • They discovered that differences in skin structure and collagen affect how easily skin cells can change and form tumors.
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Epithelial-to-mesenchymal transition (EMT) regulates tumour initiation, progression, metastasis and resistance to anti-cancer therapy. Although great progress has been made in understanding the role of EMT and its regulatory mechanisms in cancer, no therapeutic strategy to pharmacologically target EMT has been identified. Here we found that netrin-1 is upregulated in a primary mouse model of skin squamous cell carcinoma (SCC) exhibiting spontaneous EMT.

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The mammary gland (MG) is composed of three main epithelial lineages, the basal cells (BC), the estrogen receptor (ER) positive luminal cells (ER+ LC), and the ER negative LC (ER- LC). Defining the cell identity of each lineage and how it is modulated throughout the different stages of life is important to understand how these cells function and communicate throughout life. Here, we used transgenic mice specifically labelling ER+ LC combined to cell surface markers to isolate with high purity the 3 distinct cell lineages of the mammary gland and defined their expression profiles and chromatin landscapes by performing bulk RNAseq and ATACseq of these isolated populations in puberty, adulthood and mid-pregnancy.

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  • Cancer cell resistance to therapy leads to high mortality rates among patients, with epithelial-to-mesenchymal transition (EMT) linked to this resistance.
  • A study using a mouse model revealed that EMT cancer cells show strong resilience against various anti-cancer treatments due to the action of RHOJ, a small GTPase predominantly found in these cells.
  • RHOJ enhances the tumor cells' ability to handle DNA damage from chemotherapy by promoting their response to stress and maintaining DNA repair mechanisms, indicating its critical role in EMT-associated therapy resistance.
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The nongenetic mechanisms required to sustain malignant tumor state are poorly understood. During the transition from benign tumors to malignant carcinoma, tumor cells need to repress differentiation and acquire invasive features. Using transcriptional profiling of cancer stem cells from benign tumors and malignant skin squamous cell carcinoma (SCC), we identified the nuclear receptor NR2F2 as uniquely expressed in malignant SCC.

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FAT1, which encodes a protocadherin, is one of the most frequently mutated genes in human cancers. However, the role and the molecular mechanisms by which FAT1 mutations control tumour initiation and progression are poorly understood. Here, using mouse models of skin squamous cell carcinoma and lung tumours, we found that deletion of Fat1 accelerates tumour initiation and malignant progression and promotes a hybrid epithelial-to-mesenchymal transition (EMT) phenotype.

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Article Synopsis
  • Glandular epithelia, like mammary and prostate glands, consist of basal cells (BCs) and luminal cells (LCs), with adult basal stem cells (BSCs) having limited multipotency under normal conditions.
  • When LCs are removed, BSCs can regain their multipotency and follow a differentiation program akin to embryonic development, as shown through RNA sequencing.
  • The study reveals that LCs communicate with BSCs, primarily through TNF signaling, to maintain the restricted multipotency of BSCs, highlighting the importance of this interaction for proper stem cell function in glandular tissues.
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The ability of the skin to grow in response to stretching has been exploited in reconstructive surgery. Although the response of epidermal cells to stretching has been studied in vitro, it remains unclear how mechanical forces affect their behaviour in vivo. Here we develop a mouse model in which the consequences of stretching on skin epidermis can be studied at single-cell resolution.

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  • Researchers created reprogrammed H460 cancer cells (R-H460) to study how epigenetic changes contribute to drug resistance against treatments like cisplatin and paclitaxel.
  • After differentiating these cells for different time periods, they found that cells differentiated for 13 days (13dR-H460) developed short-term drug resistance, while those differentiated for 40 days (40dR-H460) lost that resistance.
  • This study indicates that the mechanisms behind short-term and medium-term drug resistance could lead to new approaches in cancer treatment by targeting the epigenetic changes in cells.
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Psoriasis is a common chronic skin disorder characterized by keratinocyte hyperproliferation with altered differentiation accompanied by inflammation and increased angiogenesis. It remains unclear whether the first events that initiate psoriasis development occur in keratinocytes or inflammatory cells. Here, using different psoriasis mouse models, we showed that conditional deletion of or in epidermal cells inhibited psoriasis mediated by overexpression or deletion.

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Background: More than 11,000 laboratories and companies developed their own next-generation sequencing (NGS) for screening and diagnosis of various diseases including cancer. Although inconsistencies of mutation calls as high as 43% in databases such as GDSC (Genomics of Drug Sensitivity in Cancer) and CCLE (Cancer Cell Line Encyclopedia) have been reported, not many studies on the reasons for the inconsistencies have been published. Methods: Targeted-NGS analysis of 151 genes in 35 cell lines common to GDSC and CCLE was performed, and the results were compared with those from GDSC and CCLE wherein whole-exome- or highly-multiplex NGS were employed.

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Circulating tumor DNA (ctDNA) has emerged as a candidate biomarker for cancer screening. However, studies on the usefulness of ctDNA for postoperative recurrence monitoring are limited. The present study monitored ctDNA in postoperative blood by employing cancer-specific rearrangements.

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Proliferation activity has already been established as a prognostic marker or as a marker for anticancer drug sensitivity. In gastric cancer, however, the prognostic significance of proliferation activity is still being debated. Several studies evaluating proliferation activity using Ki-67 have shown controversial results in terms of the relationship between proliferation activity and overall survival (OS) or drug sensitivity in gastric cancer patients.

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