Targeting TNF-related apoptosis-inducing ligand (TRAIL) receptor by natural products as a potential therapeutic approach for cancer therapy

Xiaoyun Dai; Jingwen Zhang; Frank Arfuso; Arunachalam Chinnathambi; M. E. Zayed; Sulaiman Ali Alharbi; Alan Prem Kumar; Kwang Seok Ahn; Gautam Sethi

doi:10.1177/1535370215579167

Targeting TNF-related apoptosis-inducing ligand (TRAIL) receptor by natural products as a potential therapeutic approach for cancer therapy

Xiaoyun Dai, Jingwen Zhang, Frank Arfuso, Arunachalam Chinnathambi, M. E. Zayed, Sulaiman Ali Alharbi, Alan Prem Kumar, Kwang Seok Ahn, Gautam Sethi

Research output: Contribution to journal › Article › peer-review

163 Citations (Scopus)

Abstract

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to selectively induce apoptotic cell death in various tumor cells by engaging its death-inducing receptors (TRAIL-R1 and TRAIL-R2). This property has led to the development of a number of TRAIL–receptor agonists such as the soluble recombinant TRAIL and agonistic antibodies, which have shown promising anticancer activity in preclinical studies. However, besides activating caspase-dependent apoptosis in several cancer cells, TRAIL may also activate nonapoptotic signal transduction pathways such as nuclear factor-kappa B, mitogen-activated protein kinases, AKT, and signal transducers and activators of transcription 3, which may contribute to TRAIL resistance that is being now frequently encountered in various cancers. TRAIL resistance can be overcome by the application of efficient TRAIL-sensitizing pharmacological agents. Natural compounds have shown a great potential in sensitizing cells to TRAIL treatment through suppression of distinct survival pathways. In this review, we have summarized both apoptotic and nonapoptotic pathways activated by TRAIL, as well as recent advances in developing TRAIL–receptor agonists for cancer therapy. We also briefly discuss combination therapies that have shown great potential in overcoming TRAIL resistance in various tumors.

Original language	English
Pages (from-to)	760-773
Number of pages	14
Journal	Experimental Biology and Medicine
Volume	240
Issue number	6
DOIs	https://doi.org/10.1177/1535370215579167
Publication status	Published - 12 Jun 2015
Externally published	Yes

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title = "Targeting TNF-related apoptosis-inducing ligand (TRAIL) receptor by natural products as a potential therapeutic approach for cancer therapy",

abstract = "Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to selectively induce apoptotic cell death in various tumor cells by engaging its death-inducing receptors (TRAIL-R1 and TRAIL-R2). This property has led to the development of a number of TRAIL–receptor agonists such as the soluble recombinant TRAIL and agonistic antibodies, which have shown promising anticancer activity in preclinical studies. However, besides activating caspase-dependent apoptosis in several cancer cells, TRAIL may also activate nonapoptotic signal transduction pathways such as nuclear factor-kappa B, mitogen-activated protein kinases, AKT, and signal transducers and activators of transcription 3, which may contribute to TRAIL resistance that is being now frequently encountered in various cancers. TRAIL resistance can be overcome by the application of efficient TRAIL-sensitizing pharmacological agents. Natural compounds have shown a great potential in sensitizing cells to TRAIL treatment through suppression of distinct survival pathways. In this review, we have summarized both apoptotic and nonapoptotic pathways activated by TRAIL, as well as recent advances in developing TRAIL–receptor agonists for cancer therapy. We also briefly discuss combination therapies that have shown great potential in overcoming TRAIL resistance in various tumors.",

keywords = "apoptosis, cancer, natural products, NF-κB, TRAIL",

author = "Xiaoyun Dai and Jingwen Zhang and Frank Arfuso and Arunachalam Chinnathambi and Zayed, {M. E.} and Alharbi, {Sulaiman Ali} and Kumar, {Alan Prem} and Ahn, {Kwang Seok} and Gautam Sethi",

note = "Funding Information: This work was supported by NUHS Bench to Bedside to Product grant to GS. The Deanship of Scientific Research, College of Science Research Centre, King Saud University, Kingdom of Saudi Arabia also supported the work. KSA was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korean Ministry of Education, Science and Technology (MoEST) (No. 2011-0006220). APK was supported by grants from the Singapore Ministry of Education Tier 2 [MOE2012-T2-2-139], NUHS Bench-to-Bedside-To-Product [R-184-000-243-515] and Cancer Science Institute of Singapore, Experimental Therapeutics I Program [R-713-001-011-271]. Publisher Copyright: {\textcopyright} 2015 by the Society for Experimental Biology and Medicine",

year = "2015",

month = jun,

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doi = "10.1177/1535370215579167",

language = "English",

volume = "240",

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journal = "Experimental Biology and Medicine",

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T1 - Targeting TNF-related apoptosis-inducing ligand (TRAIL) receptor by natural products as a potential therapeutic approach for cancer therapy

AU - Dai, Xiaoyun

AU - Zhang, Jingwen

AU - Arfuso, Frank

AU - Chinnathambi, Arunachalam

AU - Zayed, M. E.

AU - Alharbi, Sulaiman Ali

AU - Kumar, Alan Prem

AU - Ahn, Kwang Seok

AU - Sethi, Gautam

N1 - Funding Information: This work was supported by NUHS Bench to Bedside to Product grant to GS. The Deanship of Scientific Research, College of Science Research Centre, King Saud University, Kingdom of Saudi Arabia also supported the work. KSA was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korean Ministry of Education, Science and Technology (MoEST) (No. 2011-0006220). APK was supported by grants from the Singapore Ministry of Education Tier 2 [MOE2012-T2-2-139], NUHS Bench-to-Bedside-To-Product [R-184-000-243-515] and Cancer Science Institute of Singapore, Experimental Therapeutics I Program [R-713-001-011-271]. Publisher Copyright: © 2015 by the Society for Experimental Biology and Medicine

PY - 2015/6/12

Y1 - 2015/6/12

N2 - Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to selectively induce apoptotic cell death in various tumor cells by engaging its death-inducing receptors (TRAIL-R1 and TRAIL-R2). This property has led to the development of a number of TRAIL–receptor agonists such as the soluble recombinant TRAIL and agonistic antibodies, which have shown promising anticancer activity in preclinical studies. However, besides activating caspase-dependent apoptosis in several cancer cells, TRAIL may also activate nonapoptotic signal transduction pathways such as nuclear factor-kappa B, mitogen-activated protein kinases, AKT, and signal transducers and activators of transcription 3, which may contribute to TRAIL resistance that is being now frequently encountered in various cancers. TRAIL resistance can be overcome by the application of efficient TRAIL-sensitizing pharmacological agents. Natural compounds have shown a great potential in sensitizing cells to TRAIL treatment through suppression of distinct survival pathways. In this review, we have summarized both apoptotic and nonapoptotic pathways activated by TRAIL, as well as recent advances in developing TRAIL–receptor agonists for cancer therapy. We also briefly discuss combination therapies that have shown great potential in overcoming TRAIL resistance in various tumors.

AB - Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to selectively induce apoptotic cell death in various tumor cells by engaging its death-inducing receptors (TRAIL-R1 and TRAIL-R2). This property has led to the development of a number of TRAIL–receptor agonists such as the soluble recombinant TRAIL and agonistic antibodies, which have shown promising anticancer activity in preclinical studies. However, besides activating caspase-dependent apoptosis in several cancer cells, TRAIL may also activate nonapoptotic signal transduction pathways such as nuclear factor-kappa B, mitogen-activated protein kinases, AKT, and signal transducers and activators of transcription 3, which may contribute to TRAIL resistance that is being now frequently encountered in various cancers. TRAIL resistance can be overcome by the application of efficient TRAIL-sensitizing pharmacological agents. Natural compounds have shown a great potential in sensitizing cells to TRAIL treatment through suppression of distinct survival pathways. In this review, we have summarized both apoptotic and nonapoptotic pathways activated by TRAIL, as well as recent advances in developing TRAIL–receptor agonists for cancer therapy. We also briefly discuss combination therapies that have shown great potential in overcoming TRAIL resistance in various tumors.

KW - apoptosis

KW - cancer

KW - natural products

KW - NF-κB

KW - TRAIL

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U2 - 10.1177/1535370215579167

DO - 10.1177/1535370215579167

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AN - SCOPUS:84930795938

SN - 1535-3702

VL - 240

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EP - 773

JO - Experimental Biology and Medicine

JF - Experimental Biology and Medicine

IS - 6

ER -

Targeting TNF-related apoptosis-inducing ligand (TRAIL) receptor by natural products as a potential therapeutic approach for cancer therapy

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