Evidence map›Paper›PMID 34464977›Full record

ArticleBlood advances2021

IAP and HDAC inhibitors interact synergistically in myeloma cells through noncanonical NF-κB- and caspase-8-dependent mechanisms.

Liang Zhou, Yu Zhang, Mark B Meads, Yun Dai, Yanxia Ning, Xiaoyan Hu, Lin Li, Kanika Sharma, Jewel Nkwocha, Rebecca Parker and 14 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

24 authors at 3 institutions in 2 countries.

Liang ZhouDivision of Hematology/Oncology, Department of Medicine, and.ORCID 0000-0001-5457-7532
Yu ZhangDivision of Hematology/Oncology, Department of Medicine, and.
Mark B MeadsDepartment of Hematology, Moffitt Cancer Center, Tampa, FL.
Yun DaiCancer Center, First Hospital of Jilin University, Changchun, China.
Yanxia NingDivision of Hematology/Oncology, Department of Medicine, and.
Xiaoyan HuDivision of Hematology/Oncology, Department of Medicine, and.
Lin LiDivision of Hematology/Oncology, Department of Medicine, and.
Kanika SharmaDivision of Hematology/Oncology, Department of Medicine, and.
Jewel NkwochaDivision of Hematology/Oncology, Department of Medicine, and.
Rebecca ParkerDivision of Hematology/Oncology, Department of Medicine, and.ORCID 0000-0003-3647-1616
Danny BuiDivision of Hematology/Oncology, Department of Medicine, and.
Jacquelyn McCarterDivision of Hematology/Oncology, Department of Medicine, and.
Lora KramerDivision of Hematology/Oncology, Department of Medicine, and.
Cullen PurcellDepartment of Biology, Virginia Commonwealth University, Richmond, VA.
Praneeth R SudalaguntaDepartment of Cancer Physiology and.ORCID 0000-0003-1283-9332
Rafael R CanevaroloDepartment of Cancer Physiology and.ORCID 0000-0002-8722-8512
Maria D Coelho Siqueira SilvaDepartment of Cancer Physiology and.
Gabriel De AvilaDepartment of Hematology, Moffitt Cancer Center, Tampa, FL.
Raghunandan Reddy AlugubelliDepartment of Collaborative Data Services, Moffitt Cancer Center, Tampa, FL; and.
Ariosto S SilvaDepartment of Cancer Physiology and.
Maciej KmeiciakMassey Cancer Center, Virginia Commonwealth University, Richmond, VA.
Andrea Ferreira-GonzalezDivision of Molecular Diagnostics, Department of Pathology, Virginia Commonwealth University, Richmond, VA.
Kenneth H ShainDepartment of Hematology, Moffitt Cancer Center, Tampa, FL.
Steven GrantDivision of Hematology/Oncology, Department of Medicine, and.
Virginia Commonwealth University · USMoffitt Cancer Center · USJilin University · CN

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI John L. Cleveland · 1998 to 2026
$93.5M
Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Renato Martins · 1985 to 2026
$51.0M
"Research Supplement to Promote Diversity in Health-Related Research", as part of Moffitt PS-OC, "Cancer as a Complex adaptive System"U54CA193489 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDERSON, ALEXANDER ROBERTSON ALLAN, GATENBY, ROBERT A · 2015 to 2020
$12.5M
Targeting Multiple Myeloma with Smac-mimetics and HDAC InhibitorsR01CA205607 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GRANT, STEVEN · 2016 to 2020
$1.6M
NCI NIH HHS P30 CA016059NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA205607NCI NIH HHS U54 CA193489
6 · The paper itself

Abstract

Interactions between the inhibitor of apoptosis protein antagonist LCL161 and the histone deacetylase inhibitor panobinostat (LBH589) were examined in human multiple myeloma (MM) cells. LCL161 and panobinostat interacted synergistically to induce apoptosis in diverse MM cell lines, including those resistant to bortezomib (PS-R). Similar interactions were observed with other histone deacetylase inhibitors (MS-275) or inhibitors of apoptosis protein antagonists (birinapant). These events were associated with downregulation of the noncanonical (but not the canonical) NF-κB pathway and activation of the extrinsic, caspase-8-related apoptotic cascade. Coexposure of MM cells to LCL161/LBH589 induced TRAF3 upregulation and led to TRAF2 and NIK downregulation, diminished expression of BCL-XL, and induction of γH2A.X. Ectopic expression of TRAF2, NIK, or BCL-XL, or short hairpin RNA TRAF3 knock-down, significantly reduced LCL161/LBH589 lethality, as did ectopic expression of dominant-negative FADD. Stromal/microenvironmental factors failed to diminish LCL161/LBH589-induced cell death. The LCL161/LBH589 regimen significantly increased cell killing in primary CD138+ cells (N = 31) and was particularly effective in diminishing the primitive progenitor cell-enriched CD138-/19+/20+/27+ population (N = 23) but was nontoxic to normal CD34+ cells. Finally, combined LCL161/LBH589 treatment significantly increased survival compared with single-agent treatment in an immunocompetent 5TGM1 murine MM model. Together, these findings argue that LCL161 interacts synergistically with LBH589 in MM cells through a process involving inactivation of the noncanonical NF-κB pathway and activation of the extrinsic apoptotic pathway, upregulation of TRAF3, and downregulation of TRAF2/BCL-XL. Notably, this regimen overcomes various forms of resistance, is active against primary MM cells, and displays significant in vivo activity. This strategy warrants further consideration in MM.

Indexed as

Histone Deacetylase InhibitorsMultiple MyelomaAnimalsCaspase 8Cell Line, TumorHumansMiceNF-kappa BCaspase 8Histone Deacetylase InhibitorsNF-kappa B

Identifiers

PMID34464977
PMCPMC8679669
OpenAlexW3197321548

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.