Tanja Čugura, Emanuela Boštjančič, Sara Uhan, Nina Hauptman, Jera Jeruc
{"title":"透明细胞肾细胞癌肉瘤样转化中的上皮-间质转化相关标记物","authors":"Tanja Čugura, Emanuela Boštjančič, Sara Uhan, Nina Hauptman, Jera Jeruc","doi":"10.1016/j.yexmp.2024.104909","DOIUrl":null,"url":null,"abstract":"<div><p>Epithelial-mesenchymal transition (EMT) plays a pivotal role in the development and progression of many cancers. Partial EMT (pEMT) could represent a critical step in tumor migration and dissemination. Sarcomatoid renal cell carcinoma (sRCC) is an aggressive form of renal cell carcinoma (RCC) composed of a carcinomatous (sRCC-Ca) and sarcomatous (sRCC-Sa) component. The role of (p)EMT in the progression of RCC to sRCC remains unclear. The aim of this study was to investigate the involvement of (p)EMT in RCC and sRCC. Tissue samples from 10 patients with clear cell RCC (ccRCC) and 10 patients with sRCC were selected. The expression of main EMT markers (<em>miR-200</em> family, <em>miR-205</em>, <em>SNAI1/2, TWIST1/2, ZEB1/2</em>, <em>CDH1/2, VIM</em>) was analyzed by qPCR in ccRCC, sRCC-Ca, and sRCC-Sa and compared to non-neoplastic tissue and between both groups. Expression of E-cadherin, N-cadherin, vimentin and ZEB2 was analyzed using immunohistochemistry. <em>miR-200c</em> was downregulated in sRCC-Ca compared to ccRCC, while <em>miR-200a</em> was downregulated in sRCC-Sa compared to ccRCC. <em>CDH1</em> was downregulated in sRCC-Sa when compared to any other group. <em>ZEB2</em> was downregulated in ccRCC and sRCC compared to corresponding non-neoplastic kidney. A positive correlation was observed between <em>CDH1</em> expression and <em>miR-200a/b/c</em>. Our results suggest that full EMT is not present in sRCC. Instead, discreet molecular differences exist between ccRCC, sRCC-Ca, and sRCC-Sa, possibly representing distinct intermediary states undergoing pEMT.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":2.8000,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480024000285/pdfft?md5=7eb7984eba7d085c7bc82bc0b9fa6710&pid=1-s2.0-S0014480024000285-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Epithelial-mesenchymal transition associated markers in sarcomatoid transformation of clear cell renal cell carcinoma\",\"authors\":\"Tanja Čugura, Emanuela Boštjančič, Sara Uhan, Nina Hauptman, Jera Jeruc\",\"doi\":\"10.1016/j.yexmp.2024.104909\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Epithelial-mesenchymal transition (EMT) plays a pivotal role in the development and progression of many cancers. Partial EMT (pEMT) could represent a critical step in tumor migration and dissemination. Sarcomatoid renal cell carcinoma (sRCC) is an aggressive form of renal cell carcinoma (RCC) composed of a carcinomatous (sRCC-Ca) and sarcomatous (sRCC-Sa) component. The role of (p)EMT in the progression of RCC to sRCC remains unclear. The aim of this study was to investigate the involvement of (p)EMT in RCC and sRCC. Tissue samples from 10 patients with clear cell RCC (ccRCC) and 10 patients with sRCC were selected. The expression of main EMT markers (<em>miR-200</em> family, <em>miR-205</em>, <em>SNAI1/2, TWIST1/2, ZEB1/2</em>, <em>CDH1/2, VIM</em>) was analyzed by qPCR in ccRCC, sRCC-Ca, and sRCC-Sa and compared to non-neoplastic tissue and between both groups. Expression of E-cadherin, N-cadherin, vimentin and ZEB2 was analyzed using immunohistochemistry. <em>miR-200c</em> was downregulated in sRCC-Ca compared to ccRCC, while <em>miR-200a</em> was downregulated in sRCC-Sa compared to ccRCC. <em>CDH1</em> was downregulated in sRCC-Sa when compared to any other group. <em>ZEB2</em> was downregulated in ccRCC and sRCC compared to corresponding non-neoplastic kidney. A positive correlation was observed between <em>CDH1</em> expression and <em>miR-200a/b/c</em>. Our results suggest that full EMT is not present in sRCC. 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Epithelial-mesenchymal transition associated markers in sarcomatoid transformation of clear cell renal cell carcinoma
Epithelial-mesenchymal transition (EMT) plays a pivotal role in the development and progression of many cancers. Partial EMT (pEMT) could represent a critical step in tumor migration and dissemination. Sarcomatoid renal cell carcinoma (sRCC) is an aggressive form of renal cell carcinoma (RCC) composed of a carcinomatous (sRCC-Ca) and sarcomatous (sRCC-Sa) component. The role of (p)EMT in the progression of RCC to sRCC remains unclear. The aim of this study was to investigate the involvement of (p)EMT in RCC and sRCC. Tissue samples from 10 patients with clear cell RCC (ccRCC) and 10 patients with sRCC were selected. The expression of main EMT markers (miR-200 family, miR-205, SNAI1/2, TWIST1/2, ZEB1/2, CDH1/2, VIM) was analyzed by qPCR in ccRCC, sRCC-Ca, and sRCC-Sa and compared to non-neoplastic tissue and between both groups. Expression of E-cadherin, N-cadherin, vimentin and ZEB2 was analyzed using immunohistochemistry. miR-200c was downregulated in sRCC-Ca compared to ccRCC, while miR-200a was downregulated in sRCC-Sa compared to ccRCC. CDH1 was downregulated in sRCC-Sa when compared to any other group. ZEB2 was downregulated in ccRCC and sRCC compared to corresponding non-neoplastic kidney. A positive correlation was observed between CDH1 expression and miR-200a/b/c. Our results suggest that full EMT is not present in sRCC. Instead, discreet molecular differences exist between ccRCC, sRCC-Ca, and sRCC-Sa, possibly representing distinct intermediary states undergoing pEMT.
期刊介绍：
Under new editorial leadership, Experimental and Molecular Pathology presents original articles on disease processes in relation to structural and biochemical alterations in mammalian tissues and fluids and on the application of newer techniques of molecular biology to problems of pathology in humans and other animals. The journal also publishes selected interpretive synthesis reviews by bench level investigators working at the "cutting edge" of contemporary research in pathology. In addition, special thematic issues present original research reports that unravel some of Nature''s most jealously guarded secrets on the pathologic basis of disease.
Research Areas include: Stem cells; Neoangiogenesis; Molecular diagnostics; Polymerase chain reaction; In situ hybridization; DNA sequencing; Cell receptors; Carcinogenesis; Pathobiology of neoplasia; Complex infectious diseases; Transplantation; Cytokines; Flow cytomeric analysis; Inflammation; Cellular injury; Immunology and hypersensitivity; Athersclerosis.
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