Thalidomide potentiates etoposide-induced apoptosis in murine neuroblastoma through suppression of NF-κB activation

Hiramatsu, Tomomasa; Yoshizawa, Jyoji; Miyaguni, Kazuaki; Sugihara, Tetsuro; Harada, Atsushi; Kaji, Sayuri; Uchida, Goki; Kanamori, Daisuke; Baba, Yuji; Ashizuka, Shuichi; Ohki, Takao

doi:10.1007/s00383-018-4234-4

Cited by 9 publications

(3 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 40 Thalidomide could suppress TNF-dependent NF-κB activation, 41 and thus thalidomide inhibits etoposide-induced NF-κB activation and enhances etoposide-induced tumor cells apoptosis and inhibition of tumor cells proliferation when thalidomide combined with etoposide in vitro and in vivo. 42 The combination of etoposide and thalidomide slowed tumor growth and increased mouse survival in vivo. 42 …”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

<p>Effective Treatment with PD-1 Antibody, Chidamide, Etoposide, and Thalidomide (PCET) for Relapsed/Refractory Natural Killer/T-Cell Lymphoma: A Report of Three Cases</p>

Du¹,

Zhang²,

Li³

et al. 2020

OTT

View full text Add to dashboard Cite

Extranodal natural killer (NK)/T-cell lymphoma, nasal type (ENKTL) is a specific subtype of peripheral T cell lymphoma (PTCL) with a poor prognosis. To date, there exist no standard therapeutic regimens for relapsed/refractory (R/R) ENKTL. More potent treatment strategies are urgently needed to improve the survival of these patients with R/R ENKTL. Herein, we present three R/R ENKTL patients who failed prior therapies (L-asparaginase containing chemotherapy, radiotherapy or biological-cell therapy, etc.) benefited from the combination regimen comprised of anti-programmed-death-1 (PD-1) antibody toripalimab, chidamide, etoposide, and thalidomide. They received the treatment regimen continuously until the disease progression occurs. As of data collection, two patients achieved complete remission (CR) after 4, 6 cycles of treatment, respectively, and another patient was evaluated as partial remission (PR) after 2 cycles. Treatment-related adverse events (AEs) mainly presented grade 2~3 leukocytopenia and anemia, which were controllable. It follows that PD-1 antibody, chidamide, etoposide, and thalidomide (PCET) regimen may be a promising choice for patients with R/R ENKTL and warrants further investigation.

show abstract

Section: Discussionmentioning

confidence: 99%

“… 42 The combination of etoposide and thalidomide slowed tumor growth and increased mouse survival in vivo. 42 …”

Section: Discussionmentioning

confidence: 99%

<p>Effective Treatment with PD-1 Antibody, Chidamide, Etoposide, and Thalidomide (PCET) for Relapsed/Refractory Natural Killer/T-Cell Lymphoma: A Report of Three Cases</p>

Du¹,

Zhang²,

Li³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…NF-κB upregulates the expression of the oncogene miR-130b, which acts directly on USP13, decreasing its expression and thereby regulating the proliferation, invasion and migration of tumor cells. Therefore, it is a potential target for cancer therapeutics ( 82 , 83 ). miR-130b/miR-301b binds to USP13 via the 3′-UTR.…”

Section: Role Of Usp13 In Tumorsmentioning

confidence: 99%

Roles of ubiquitin‑specific protease 13 in normal physiology and tumors (Review)

Tao,

Xu,

Shen

et al. 2023

Oncol Lett

View full text Add to dashboard Cite

Ubiquitin-specific protease 13 (USP13) is one of the most important deubiquitinases involved in various diseases. As deubiquitinases are components of the deubiquitination process, a significant post-translational modification, they are potential treatment targets for different diseases. With recent technological developments, the structure of USP13 and its pathological and physiological functions have been investigated. However, USP13 expression and function differ in various diseases, especially in tumors, and the associated mechanisms are complex and remain to be fully investigated. The present review summarized the recent discoveries and the current understanding of the USP13 function in tumors. Contents 1. Introduction 2. Domain architectures of USP13 3. USP13 in normal physiology 4. Regulation of USP13 signaling 5. Role of USP13 in tumors 6. Conclusions

show abstract

A Targeted Nanosystem for Detection of Inflammatory Diseases via Fluorescent/Optoacoustic Imaging and Therapy via Modulating Nrf2/NF‐κB Pathways

Ouyang

Sun

Pan

et al. 2021

Small

View full text Add to dashboard Cite

Inflammatory diseases are sometimes devastating and notoriously difficult to treat. Precisely modulating inflammatory signaling pathways is a promising approach for treating inflammatory diseases. Herein, a multifunctional nanosystem is developed for active targeting, activatable imaging and on‐demand therapy against inflammatory diseases through modulating inflammatory pathways. A chromophore‐drug dyad (QBS‐FIS) is synthesized by linking a chromophore and a Nrf2 (nuclear factor E2‐related factor) activator fisetin through boronate bond which serves as fluorescence quencher and ROS (reactive oxygen species)‐responsive linker. QBS‐FIS molecules form nanoparticles in water and are coated with macrophage cell membrane to ensure active targeting toward inflammation site. To further improve therapeutic efficacy, a NF‐kB (nuclear‐factor kappa‐light‐chain‐enhancer of activated B cells) inhibitor thalidomide is co‐encapsulated to afford the nanosystem (QBS‐FIS&Thd@MM). Upon administration into mice, the nanosystem migrates to inflammatory site and pathological ROS therein cleaves the boronate bonds, thereby activating the chromophore for imaging liver/kidney inflammatory diseases for disease diagnosis and recovery evaluation via fluorescence and optoacoustic imaging as well as releasing the active drugs for treating acute liver inflammation through activating Nrf2 pathway and inhibiting NF‐kB pathway. The 3D multispectral optoacoustic tomography imaging is applied to precisely locate the inflammatory foci in a spatiotemporal manner.

show abstract

Thalidomide potentiates etoposide-induced apoptosis in murine neuroblastoma through suppression of NF-κB activation

Abstract: Thalidomide potentiates etoposide-induced apoptosis in murine neuroblastoma by suppressing NF-κB.

Cited by 9 publications

References 45 publications

<p>Effective Treatment with PD-1 Antibody, Chidamide, Etoposide, and Thalidomide (PCET) for Relapsed/Refractory Natural Killer/T-Cell Lymphoma: A Report of Three Cases</p>

<p>Effective Treatment with PD-1 Antibody, Chidamide, Etoposide, and Thalidomide (PCET) for Relapsed/Refractory Natural Killer/T-Cell Lymphoma: A Report of Three Cases</p>

Roles of ubiquitin‑specific protease 13 in normal physiology and tumors (Review)

A Targeted Nanosystem for Detection of Inflammatory Diseases via Fluorescent/Optoacoustic Imaging and Therapy via Modulating Nrf2/NF‐κB Pathways

Contact Info

Product

Resources

About