Broad targeting of resistance to apoptosis in cancer

Ramzi M. Mohammad; Irfana Muqbil; Leroy Lowe; Clement Yedjou; Hsue Yin Hsu; Liang Tzung Lin; Markus David Siegelin; Carmela Fimognari; Nagi B. Kumar; Q. Ping Dou; Huanjie Yang; Abbas K. Samadi; Gian Luigi Russo; Carmela Spagnuolo; Swapan K. Ray; Mrinmay Chakrabarti; James D. Morre; Helen M. Coley; Kanya Honoki; Hiromasa Fujii; Alexandros G. Georgakilas; Amedeo Amedei; Elena Niccolai; Amr Amin; S. Salman Ashraf; William G. Helferich; Xujuan Yang; Chandra S. Boosani; Gunjan Guha; Dipita Bhakta; Maria Rosa Ciriolo; Katia Aquilano; Sophie Chen; Sulma I. Mohammed; W. Nicol Keith; Alan Bilsland; Dorota Halicka; Somaira Nowsheen; Asfar S. Azmi

doi:10.1016/j.semcancer.2015.03.001

Broad targeting of resistance to apoptosis in cancer

Ramzi M. Mohammad, Irfana Muqbil, Leroy Lowe, Clement Yedjou, Hsue Yin Hsu, Liang Tzung Lin, Markus David Siegelin, Carmela Fimognari, Nagi B. Kumar, Q. Ping Dou, Huanjie Yang, Abbas K. Samadi, Gian Luigi Russo, Carmela Spagnuolo, Swapan K. Ray, Mrinmay Chakrabarti, James D. Morre, Helen M. Coley, Kanya Honoki, Hiromasa FujiiAlexandros G. Georgakilas, Amedeo Amedei, Elena Niccolai, Amr Amin, S. Salman Ashraf, William G. Helferich, Xujuan Yang, Chandra S. Boosani, Gunjan Guha, Dipita Bhakta, Maria Rosa Ciriolo, Katia Aquilano, Sophie Chen, Sulma I. Mohammed, W. Nicol Keith, Alan Bilsland, Dorota Halicka, Somaira Nowsheen, Asfar S. Azmi

Research output: Contribution to journal › Review article › peer-review

614 Citations (Scopus)

Abstract

Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer.

Original language	English
Pages (from-to)	S78-S103
Number of pages	26
Journal	Seminars in Cancer Biology
Volume	35
DOIs	https://doi.org/10.1016/j.semcancer.2015.03.001
Publication status	Published - Dec 1 2015

Keywords

Apoptosis
Apoptosis evasion
Autophagy
Necrosis
Nuclear transporters, natural chemopreventive agents

ASJC Scopus subject areas

Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.semcancer.2015.03.001

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Mohammad, R. M., Muqbil, I., Lowe, L., Yedjou, C., Hsu, H. Y., Lin, L. T., Siegelin, M. D., Fimognari, C., Kumar, N. B., Dou, Q. P., Yang, H., Samadi, A. K., Russo, G. L., Spagnuolo, C., Ray, S. K., Chakrabarti, M., Morre, J. D., Coley, H. M., Honoki, K., ... Azmi, A. S. (2015). Broad targeting of resistance to apoptosis in cancer. Seminars in Cancer Biology, 35, S78-S103. https://doi.org/10.1016/j.semcancer.2015.03.001

Mohammad, RM, Muqbil, I, Lowe, L, Yedjou, C, Hsu, HY, Lin, LT, Siegelin, MD, Fimognari, C, Kumar, NB, Dou, QP, Yang, H, Samadi, AK, Russo, GL, Spagnuolo, C, Ray, SK, Chakrabarti, M, Morre, JD, Coley, HM, Honoki, K, Fujii, H, Georgakilas, AG, Amedei, A, Niccolai, E, Amin, A, Ashraf, SS, Helferich, WG, Yang, X, Boosani, CS, Guha, G, Bhakta, D, Ciriolo, MR, Aquilano, K, Chen, S, Mohammed, SI, Keith, WN, Bilsland, A, Halicka, D, Nowsheen, S & Azmi, AS 2015, 'Broad targeting of resistance to apoptosis in cancer', Seminars in Cancer Biology, vol. 35, pp. S78-S103. https://doi.org/10.1016/j.semcancer.2015.03.001

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title = "Broad targeting of resistance to apoptosis in cancer",

abstract = "Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer.",

keywords = "Apoptosis, Apoptosis evasion, Autophagy, Necrosis, Nuclear transporters, natural chemopreventive agents",

author = "Mohammad, {Ramzi M.} and Irfana Muqbil and Leroy Lowe and Clement Yedjou and Hsu, {Hsue Yin} and Lin, {Liang Tzung} and Siegelin, {Markus David} and Carmela Fimognari and Kumar, {Nagi B.} and Dou, {Q. Ping} and Huanjie Yang and Samadi, {Abbas K.} and Russo, {Gian Luigi} and Carmela Spagnuolo and Ray, {Swapan K.} and Mrinmay Chakrabarti and Morre, {James D.} and Coley, {Helen M.} and Kanya Honoki and Hiromasa Fujii and Georgakilas, {Alexandros G.} and Amedeo Amedei and Elena Niccolai and Amr Amin and Ashraf, {S. Salman} and Helferich, {William G.} and Xujuan Yang and Boosani, {Chandra S.} and Gunjan Guha and Dipita Bhakta and Ciriolo, {Maria Rosa} and Katia Aquilano and Sophie Chen and Mohammed, {Sulma I.} and Keith, {W. Nicol} and Alan Bilsland and Dorota Halicka and Somaira Nowsheen and Azmi, {Asfar S.}",

note = "Publisher Copyright: {\textcopyright} 2015 Elsevier Ltd.",

year = "2015",

month = dec,

day = "1",

doi = "10.1016/j.semcancer.2015.03.001",

language = "English",

volume = "35",

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T1 - Broad targeting of resistance to apoptosis in cancer

AU - Mohammad, Ramzi M.

AU - Muqbil, Irfana

AU - Lowe, Leroy

AU - Yedjou, Clement

AU - Hsu, Hsue Yin

AU - Lin, Liang Tzung

AU - Siegelin, Markus David

AU - Fimognari, Carmela

AU - Kumar, Nagi B.

AU - Dou, Q. Ping

AU - Yang, Huanjie

AU - Samadi, Abbas K.

AU - Russo, Gian Luigi

AU - Spagnuolo, Carmela

AU - Ray, Swapan K.

AU - Chakrabarti, Mrinmay

AU - Morre, James D.

AU - Coley, Helen M.

AU - Honoki, Kanya

AU - Fujii, Hiromasa

AU - Georgakilas, Alexandros G.

AU - Amedei, Amedeo

AU - Niccolai, Elena

AU - Amin, Amr

AU - Ashraf, S. Salman

AU - Helferich, William G.

AU - Yang, Xujuan

AU - Boosani, Chandra S.

AU - Guha, Gunjan

AU - Bhakta, Dipita

AU - Ciriolo, Maria Rosa

AU - Aquilano, Katia

AU - Chen, Sophie

AU - Mohammed, Sulma I.

AU - Keith, W. Nicol

AU - Bilsland, Alan

AU - Halicka, Dorota

AU - Nowsheen, Somaira

AU - Azmi, Asfar S.

PY - 2015/12/1

Y1 - 2015/12/1

N2 - Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer.

AB - Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer.

KW - Apoptosis

KW - Apoptosis evasion

KW - Autophagy

KW - Necrosis

KW - Nuclear transporters, natural chemopreventive agents

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U2 - 10.1016/j.semcancer.2015.03.001

DO - 10.1016/j.semcancer.2015.03.001

M3 - Review article

C2 - 25936818

AN - SCOPUS:84928539179

SN - 1044-579X

VL - 35

SP - S78-S103

JO - Seminars in Cancer Biology

JF - Seminars in Cancer Biology

ER -

Broad targeting of resistance to apoptosis in cancer

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

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