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Strain and Extracellular Tenascin-C in the Progression of Early Lung Adenocarcinoma to Invasive Disease.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Strain and Extracellular Tenascin-C in the Progression of Early Lung Adenocarcinoma to Invasive Disease./
作者:	Zitnay, Rebecca Suzanne Goldstein.
面頁冊數:	1 online resource (160 pages)
附註:	Source: Dissertations Abstracts International, Volume: 85-02, Section: B.
Contained By:	Dissertations Abstracts International85-02B.
標題:	Biomedical engineering. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30425482click for full text (PQDT)
ISBN:	9798380128797

Strain and Extracellular Tenascin-C in the Progression of Early Lung Adenocarcinoma to Invasive Disease.
Zitnay, Rebecca Suzanne Goldstein.

Strain and Extracellular Tenascin-C in the Progression of Early Lung Adenocarcinoma to Invasive Disease. - 1 online resource (160 pages)

Source: Dissertations Abstracts International, Volume: 85-02, Section: B.

Thesis (Ph.D.)--The University of Utah, 2023.

Includes bibliographical references

Genetic transformation and extracellular matrix alterations drive tumor cell invasion and metastasis. In lung cancer, the most common cause of cancer-related death, tumor invasion and subsequent metastasis destroy the native lung tissue and cause morbidity and mortality. While the role of the tumor microenvironment in tumor progression has been recognized, the contributions of the lung extracellular matrix and tissue mechanics to invasive tumor behavior in lung cancer are poorly understood. This research aimed to investigate lung adenocarcinoma (LUAD) related changes to the composition and physical properties of the tumor extracellular matrix (ECM) to illuminate factors that may contribute to tumor invasion and progression.The glycoprotein tenascin-C (TNC) is an indicator of poor prognosis in LUAD and has been linked to invasion and metastasis in many solid tumors. Furthermore, TNC expression is related to high tissue strain. Observations of TNC at the periphery of early tumors and in mouse models of LUAD and in clinical LUAD tumors led to the hypotheses that 1) mechanical changes associated with tumor development in the lung contribute to tumor progression and 2) accumulation of TNC in early LUAD promotes tumor progression.Computational simulations revealed that tumors could amplify strain and implicated ECM remodeling as a mechanism of tumor progression. Immunohistochemistry and in situ hybridization experiments showed that TNC was associated with stroma and was produced by fibroblasts in the earliest tumors. In clinical samples of LUAD, TNC was additionally produced by tumor cells. Bioinformatic analysis, LUAD 2D and 3D tissue culture experiments, and in vivo experiments demonstrated that TNC correlated with pro-tumorigenic signaling, promoted cell migration, and enhanced tumor growth.The results of our computational model are the first to suggest the role of mechanics in the development of tracks of ECM associated with tumor progression and invasion. Additionally, this dissertation provides evidence of TNC accumulation in LUAD earlier than previously described. Our results suggest TNC can promote tumor invasion and growth. Together, these findings implicate lung tissue remodeling as a contributor to tumor progression and inform future investigation into strain and TNC-mediated signaling as potential therapeutic targets for LUAD.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2023

Mode of access: World Wide Web

ISBN: 9798380128797Subjects--Topical Terms:

535387
Biomedical engineering.
Subjects--Index Terms:

Extracellular matrixIndex Terms--Genre/Form:

542853
Electronic books.

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