Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment

Targeting specific biological processes through innovative therapeutic techniques is necessary to enhance patient outcomes, as breast cancer is still a major global health concern. With a particular emphasis on the impact of arginase-induced autophagy, we examined the complex interactions among auto...

وصف كامل

محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Zeineddine, Mira (author)
التنسيق: masterThesis
منشور في: 2023
الموضوعات:
الوصول للمادة أونلاين:http://hdl.handle.net/10725/15808
https://doi.org/10.26756/th.2023.667
http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.php
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author Zeineddine, Mira
author_facet Zeineddine, Mira
author_role author
dc.creator.none.fl_str_mv Zeineddine, Mira
dc.date.none.fl_str_mv 2023
2023-12-08
2024-06-27T10:22:16Z
2024-06-27T10:22:16Z
dc.identifier.none.fl_str_mv http://hdl.handle.net/10725/15808
https://doi.org/10.26756/th.2023.667
http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.php
dc.language.none.fl_str_mv en
dc.publisher.none.fl_str_mv Lebanese American University
dc.rights.*.fl_str_mv info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Lebanese American University--Dissertations
Dissertations, Academic
Breast--Cancer--Treatment--Case studies
Autophagic vacuoles--Therapeutic use
Arginine--Therapeutic use
Rho GTPases
dc.title.none.fl_str_mv Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment
Unraveling its Impact on Breast Cancer Metastasis and Autophagic Regulation
dc.type.none.fl_str_mv Thesis
info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/masterThesis
description Targeting specific biological processes through innovative therapeutic techniques is necessary to enhance patient outcomes, as breast cancer is still a major global health concern. With a particular emphasis on the impact of arginase-induced autophagy, we examined the complex interactions among autophagy, Rho GTPases, and cell migration in breast cancer cells in this work. Our results identify a unique regulatory axis whereby arginine deprivation induces strong autophagic responses in breast cancer cells, which, because of disturbed autophagy flux, accumulate autophagosomes. Additionally, during arginine starvation, we noticed a remarkable downregulation of RhoA activation, which corresponded with inhibited cell motility. Chloroquine-induced autophagy suppression was notably ineffective in restoring cell migration, underscoring the importance of Rho GTPase signaling pathways, particularly RhoA, in controlling the motility of breast cancer cells. Furthermore, independent of autophagy, our research revealed that the PI3K/mTOR pathways are important regulators of cell migration. The significance of PI3K in breast cancer cell motility was highlighted by the efficient prevention of cell migration achieved by the pharmacological intervention of wortmannin, a powerful PI3K inhibitor. Notably, our study shows that deciphering the context-dependent functions of signaling pathways is essential to understanding the intricacies of cancer cell behavior. Through the process of unraveling the complex relationships among autophagy, Rho GTPases, and cell migration, we have been able to highlight points of vulnerability in cancer cells. By focusing on these pathways, it may be possible to develop highly specialized therapies and customized treatment regimens, which would completely alter the way that breast cancer is treated. Moreover, our study results lay the groundwork for the creation of innovative combination treatments that specifically target different facets of cancer cell behavior, offering patients with breast cancer better prognoses and increased therapeutic efficacy.
eu_rights_str_mv openAccess
format masterThesis
id LAURepo_bba21edadad86f4a4f37073fa65a7d8f
language_invalid_str_mv en
network_acronym_str LAURepo
network_name_str Lebanese American University repository
oai_identifier_str oai:laur.lau.edu.lb:10725/15808
publishDate 2023
publisher.none.fl_str_mv Lebanese American University
repository.mail.fl_str_mv
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spelling Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase TreatmentUnraveling its Impact on Breast Cancer Metastasis and Autophagic RegulationZeineddine, MiraLebanese American University--DissertationsDissertations, AcademicBreast--Cancer--Treatment--Case studiesAutophagic vacuoles--Therapeutic useArginine--Therapeutic useRho GTPasesTargeting specific biological processes through innovative therapeutic techniques is necessary to enhance patient outcomes, as breast cancer is still a major global health concern. With a particular emphasis on the impact of arginase-induced autophagy, we examined the complex interactions among autophagy, Rho GTPases, and cell migration in breast cancer cells in this work. Our results identify a unique regulatory axis whereby arginine deprivation induces strong autophagic responses in breast cancer cells, which, because of disturbed autophagy flux, accumulate autophagosomes. Additionally, during arginine starvation, we noticed a remarkable downregulation of RhoA activation, which corresponded with inhibited cell motility. Chloroquine-induced autophagy suppression was notably ineffective in restoring cell migration, underscoring the importance of Rho GTPase signaling pathways, particularly RhoA, in controlling the motility of breast cancer cells. Furthermore, independent of autophagy, our research revealed that the PI3K/mTOR pathways are important regulators of cell migration. The significance of PI3K in breast cancer cell motility was highlighted by the efficient prevention of cell migration achieved by the pharmacological intervention of wortmannin, a powerful PI3K inhibitor. Notably, our study shows that deciphering the context-dependent functions of signaling pathways is essential to understanding the intricacies of cancer cell behavior. Through the process of unraveling the complex relationships among autophagy, Rho GTPases, and cell migration, we have been able to highlight points of vulnerability in cancer cells. By focusing on these pathways, it may be possible to develop highly specialized therapies and customized treatment regimens, which would completely alter the way that breast cancer is treated. Moreover, our study results lay the groundwork for the creation of innovative combination treatments that specifically target different facets of cancer cell behavior, offering patients with breast cancer better prognoses and increased therapeutic efficacy.1 online resource (xiv, 60 leaves) : ill. (some col.)Includes bibliographical references (leaves 55-60).Lebanese American University2024-06-27T10:22:16Z2024-06-27T10:22:16Z20232023-12-08Thesisinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesishttp://hdl.handle.net/10725/15808https://doi.org/10.26756/th.2023.667http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.phpeninfo:eu-repo/semantics/openAccessoai:laur.lau.edu.lb:10725/158082024-06-27T10:22:16Z
spellingShingle Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment
Zeineddine, Mira
Lebanese American University--Dissertations
Dissertations, Academic
Breast--Cancer--Treatment--Case studies
Autophagic vacuoles--Therapeutic use
Arginine--Therapeutic use
Rho GTPases
status_str publishedVersion
title Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment
title_full Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment
title_fullStr Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment
title_full_unstemmed Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment
title_short Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment
title_sort Decoding the Therapeutic Potential of [HuArgI (Co)-PEG5000] Arginase Treatment
topic Lebanese American University--Dissertations
Dissertations, Academic
Breast--Cancer--Treatment--Case studies
Autophagic vacuoles--Therapeutic use
Arginine--Therapeutic use
Rho GTPases
url http://hdl.handle.net/10725/15808
https://doi.org/10.26756/th.2023.667
http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.php