Related Experiment Video

Updated: Apr 21, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

14.0K

Exportin 1 Inhibitor Combined With Venetoclax Induces Apoptosis in Myelodysplastic Syndrome by Mitochondria-Induced

Xiaohan Liu1,2,3, Lei Huang1,2,3, Junzhu Wang1,2,3

  • 1Department of Hematology, Tianjin Medical University General Hospital, Tianjin, China.

Journal of Clinical Laboratory Analysis
|April 20, 2026
PubMed
Abstract

Insights

Exportin 1 (XPO1) inhibition shows promise for treating myelodysplastic syndromes (MDS). Combining XPO1 inhibitor Selinexor with Venetoclax effectively targets MDS cells, offering a potential new therapy for this blood cancer.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Myelodysplastic syndromes (MDS) are clonal hematopoietic malignancies with limited treatment options.
  • Resistance to current therapies, like hypomethylating agents, is a significant clinical challenge.
  • The role of Exportin 1 (XPO1) in MDS pathogenesis and its therapeutic potential are unexplored.

Purpose of the Study:

  • To investigate the role of XPO1 in MDS development.
  • To evaluate the efficacy of the XPO1 inhibitor Selinexor in MDS cells.
  • To assess the synergistic effect of Selinexor with Venetoclax in MDS.

Main Methods:

  • Analysis of XPO1 expression in MDS patients and healthy controls.
  • Assessment of Selinexor's effects on MDS cell proliferation and apoptosis using CCK-8, EdU, and flow cytometry.
  • Evaluation of the combination therapy of Selinexor and Venetoclax.

Main Results:

  • XPO1 plays a role in MDS pathogenesis.
  • Selinexor inhibited MDS cell proliferation and induced apoptosis by blocking p53 nuclear export.
  • Selinexor synergized with Venetoclax, increasing ROS levels and activating mitochondrial apoptosis pathways.

Conclusions:

  • XPO1 inhibition is a promising therapeutic strategy for MDS.
  • Combination therapy with Selinexor and Venetoclax demonstrates significant potential for MDS treatment.
  • Targeting XPO1 represents a novel therapeutic avenue for MDS.
Keywords:
Bcl‐2MDSVenetoclaxXPO1apoptosis

More Related Videos

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

11.7K

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
9.4K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.5K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
6.4K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
17.3K
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
9
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
5.1K