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Related Concept Videos

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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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...
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Inhibition of Ephrin B2 Reverse Signaling Abolishes Multiple Myeloma Pathogenesis.

Joshua P Sasine1,2,3,4, Natalia Y Kozlova1,2, Lisa Valicente1,2

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|January 17, 2024
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Summary

Ephrin B2 (EFNB2) signaling in bone marrow endothelial cells promotes multiple myeloma growth and treatment resistance. Targeting EFNB2 offers a new therapeutic strategy to improve patient outcomes in multiple myeloma.

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Area of Science:

  • Hematology
  • Cancer Biology
  • Molecular Oncology

Background:

  • Bone marrow endothelial cells (BM EC) play a crucial role in multiple myeloma (MM) pathogenesis.
  • Understanding the molecular mechanisms of EC-MM interaction is vital for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the role of receptor tyrosine kinases (RTKs) and their ligands in MM progression.
  • To identify potential therapeutic targets for MM treatment by analyzing EC-MM interactions.

Main Methods:

  • Transcriptomic analysis of human ECs supporting MM growth.
  • Gene silencing (siRNA) of EPHB1/EPHB4 in ECs and EFNB2 in MM cells.
  • In vitro co-culture and in vivo xenograft models using immune-deficient mice.
  • Administration of EFNB2-targeted single-chain variable fragment (scFv).
  • Analysis of STAT5 activation and chemotherapy sensitivity.

Main Results:

  • Overexpression of EPHB1 and EPHB4 in MM-supportive ECs and EFNB2 in MM cells.
  • Silencing EPHB1/EPHB4 in ECs or EFNB2 in MM cells suppressed MM growth, proliferation, and survival.
  • Loss of EFNB2 abrogated MM engraftment in mice and increased sensitivity to chemotherapy.
  • Targeted inhibition of EFNB2 suppressed MM growth in vivo.
  • EFNB2 overexpression in MM cells conferred resistance to chemotherapy via STAT5 activation.
  • Increased EFNB2 expression in MM patients correlated with adverse-risk disease and poorer survival.

Conclusions:

  • Ephrin B2 (EFNB2) reverse signaling, mediated by endothelial cells, is a key driver of multiple myeloma progression and treatment resistance.
  • Targeting EFNB2 represents a promising therapeutic strategy for improving outcomes in multiple myeloma patients.