The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition

<p dir="ltr">The phosphatidylinositol 3‐kinase/Protein Kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signalling pathway is pivotal in various cancers, including T‐cell acute lymphoblastic leukaemia (T‐ALL), a particularly aggressive type of leukaemia. This study investigates...

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محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Shilpa Kuttikrishnan (3520079) (author)
مؤلفون آخرون: Abdul W. Ansari (14557391) (author), Muhammad Suleman (3829027) (author), Fareed Ahmad (134672) (author), Kirti S. Prabhu (4246144) (author), Tamam El‐Elimat (17714580) (author), Feras Q. Alali (2691907) (author), Ammira S. Al Shabeeb Akil (22155844) (author), Ajaz A. Bhat (12984701) (author), Maysaloun Merhi (4246147) (author), Said Dermime (79420) (author), Martin Steinhoff (5340194) (author), Shahab Uddin (154400) (author)
منشور في: 2024
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author Shilpa Kuttikrishnan (3520079)
author2 Abdul W. Ansari (14557391)
Muhammad Suleman (3829027)
Fareed Ahmad (134672)
Kirti S. Prabhu (4246144)
Tamam El‐Elimat (17714580)
Feras Q. Alali (2691907)
Ammira S. Al Shabeeb Akil (22155844)
Ajaz A. Bhat (12984701)
Maysaloun Merhi (4246147)
Said Dermime (79420)
Martin Steinhoff (5340194)
Shahab Uddin (154400)
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author_facet Shilpa Kuttikrishnan (3520079)
Abdul W. Ansari (14557391)
Muhammad Suleman (3829027)
Fareed Ahmad (134672)
Kirti S. Prabhu (4246144)
Tamam El‐Elimat (17714580)
Feras Q. Alali (2691907)
Ammira S. Al Shabeeb Akil (22155844)
Ajaz A. Bhat (12984701)
Maysaloun Merhi (4246147)
Said Dermime (79420)
Martin Steinhoff (5340194)
Shahab Uddin (154400)
author_role author
dc.creator.none.fl_str_mv Shilpa Kuttikrishnan (3520079)
Abdul W. Ansari (14557391)
Muhammad Suleman (3829027)
Fareed Ahmad (134672)
Kirti S. Prabhu (4246144)
Tamam El‐Elimat (17714580)
Feras Q. Alali (2691907)
Ammira S. Al Shabeeb Akil (22155844)
Ajaz A. Bhat (12984701)
Maysaloun Merhi (4246147)
Said Dermime (79420)
Martin Steinhoff (5340194)
Shahab Uddin (154400)
dc.date.none.fl_str_mv 2024-11-14T09:00:00Z
dc.identifier.none.fl_str_mv 10.1111/cpr.13773
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/The_apoptotic_and_anti_proliferative_effects_of_Neosetophomone_B_in_T_cell_acute_lymphoblastic_leukaemia_via_PI3K_AKT_mTOR_pathway_inhibition/30024295
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biomedical and clinical sciences
Oncology and carcinogenesis
Pharmacology and pharmaceutical sciences
Molecular docking
Selective cytotoxicity
Natural product
Targeted therapy
CD3+ T cells
dc.title.none.fl_str_mv The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p dir="ltr">The phosphatidylinositol 3‐kinase/Protein Kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signalling pathway is pivotal in various cancers, including T‐cell acute lymphoblastic leukaemia (T‐ALL), a particularly aggressive type of leukaemia. This study investigates the effects of Neosetophomone B (NSP‐B), a meroterpenoid fungal metabolite, on T‐ALL cell lines, focusing on its anti‐cancer mechanisms and therapeutic potential. NSP‐B significantly inhibited the proliferation of T‐ALL cells by inducing G0/G1 cell cycle arrest and promoting caspase‐dependent apoptosis. Additionally, NSP‐B led to the dephosphorylation and subsequent inactivation of the PI3K/AKT/mTOR signalling pathway, a critical pathway in cell survival and growth. Molecular docking studies revealed a strong binding affinity of NSP‐B to the active site of AKT, primarily involving key residues crucial for its activity. Interestingly, NSP‐B treatment also induced apoptosis and significantly reduced proliferation in phytohemagglutinin‐activated primary human CD3+ T cells, accompanied by a G0/G1 cell cycle arrest. Importantly, NSP‐B did not affect normal primary T cells, indicating a degree of selectivity in its action, targeting only T‐ALL cells and activated T cells. In conclusion, our findings highlight the potential of NSP‐B as a novel therapeutic agent for T‐ALL, specifically targeting the aberrantly activated PI3K/AKT/mTOR pathway and being selective in action. These results provide a strong basis for further investigation into NSP‐B's anti‐cancer properties and potential application in T‐ALL clinical therapies.</p><h2>Other Information</h2><p dir="ltr">Published in: Cell Proliferation<br>License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1111/cpr.13773" target="_blank">https://dx.doi.org/10.1111/cpr.13773</a></p><p dir="ltr">Other Institutions affiliated with: Hamad Bin Khalifa University, College of Health and Life Sciences, Weill Cornell Medicine-Qatar</p>
eu_rights_str_mv openAccess
id Manara2_061a31d12508c75f94ce1817b0aab6f7
identifier_str_mv 10.1111/cpr.13773
network_acronym_str Manara2
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oai_identifier_str oai:figshare.com:article/30024295
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spelling The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibitionShilpa Kuttikrishnan (3520079)Abdul W. Ansari (14557391)Muhammad Suleman (3829027)Fareed Ahmad (134672)Kirti S. Prabhu (4246144)Tamam El‐Elimat (17714580)Feras Q. Alali (2691907)Ammira S. Al Shabeeb Akil (22155844)Ajaz A. Bhat (12984701)Maysaloun Merhi (4246147)Said Dermime (79420)Martin Steinhoff (5340194)Shahab Uddin (154400)Biomedical and clinical sciencesOncology and carcinogenesisPharmacology and pharmaceutical sciencesMolecular dockingSelective cytotoxicityNatural productTargeted therapyCD3+ T cells<p dir="ltr">The phosphatidylinositol 3‐kinase/Protein Kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signalling pathway is pivotal in various cancers, including T‐cell acute lymphoblastic leukaemia (T‐ALL), a particularly aggressive type of leukaemia. This study investigates the effects of Neosetophomone B (NSP‐B), a meroterpenoid fungal metabolite, on T‐ALL cell lines, focusing on its anti‐cancer mechanisms and therapeutic potential. NSP‐B significantly inhibited the proliferation of T‐ALL cells by inducing G0/G1 cell cycle arrest and promoting caspase‐dependent apoptosis. Additionally, NSP‐B led to the dephosphorylation and subsequent inactivation of the PI3K/AKT/mTOR signalling pathway, a critical pathway in cell survival and growth. Molecular docking studies revealed a strong binding affinity of NSP‐B to the active site of AKT, primarily involving key residues crucial for its activity. Interestingly, NSP‐B treatment also induced apoptosis and significantly reduced proliferation in phytohemagglutinin‐activated primary human CD3+ T cells, accompanied by a G0/G1 cell cycle arrest. Importantly, NSP‐B did not affect normal primary T cells, indicating a degree of selectivity in its action, targeting only T‐ALL cells and activated T cells. In conclusion, our findings highlight the potential of NSP‐B as a novel therapeutic agent for T‐ALL, specifically targeting the aberrantly activated PI3K/AKT/mTOR pathway and being selective in action. These results provide a strong basis for further investigation into NSP‐B's anti‐cancer properties and potential application in T‐ALL clinical therapies.</p><h2>Other Information</h2><p dir="ltr">Published in: Cell Proliferation<br>License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1111/cpr.13773" target="_blank">https://dx.doi.org/10.1111/cpr.13773</a></p><p dir="ltr">Other Institutions affiliated with: Hamad Bin Khalifa University, College of Health and Life Sciences, Weill Cornell Medicine-Qatar</p>2024-11-14T09:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1111/cpr.13773https://figshare.com/articles/journal_contribution/The_apoptotic_and_anti_proliferative_effects_of_Neosetophomone_B_in_T_cell_acute_lymphoblastic_leukaemia_via_PI3K_AKT_mTOR_pathway_inhibition/30024295CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/300242952024-11-14T09:00:00Z
spellingShingle The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition
Shilpa Kuttikrishnan (3520079)
Biomedical and clinical sciences
Oncology and carcinogenesis
Pharmacology and pharmaceutical sciences
Molecular docking
Selective cytotoxicity
Natural product
Targeted therapy
CD3+ T cells
status_str publishedVersion
title The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition
title_full The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition
title_fullStr The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition
title_full_unstemmed The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition
title_short The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition
title_sort The apoptotic and anti‐proliferative effects of Neosetophomone B in T‐cell acute lymphoblastic leukaemia via PI3K/AKT/mTOR pathway inhibition
topic Biomedical and clinical sciences
Oncology and carcinogenesis
Pharmacology and pharmaceutical sciences
Molecular docking
Selective cytotoxicity
Natural product
Targeted therapy
CD3+ T cells