Synergistic Enhancement of Chemotherapy-Induced Cell Death and Antitumor Efficacy against Tumoral T-Cell Lymphoblasts by IMMUNEPOTENT CRP.
Ana Luisa Rivera-LazarínKenny Misael Calvillo-RodríguezMizael Izaguirre-RodríguezJosé Manuel Vázquez-GuillénAna Carolina Martínez-TorresCristina Rodríguez-PadillaPublished in: International journal of molecular sciences (2024)
T-cell malignancies, including T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL), present significant challenges to treatment due to their aggressive nature and chemoresistance. Chemotherapies remain a mainstay for their management, but the aggressiveness of these cancers and their associated toxicities pose limitations. Immunepotent CRP (ICRP), a bovine dialyzable leukocyte extract, has shown promise in inducing cytotoxicity against various cancer types, including hematological cancers. In this study, we investigated the combined effect of ICRP with a panel of chemotherapies on cell line models of T-ALL and T-LBL (CEM and L5178Y-R cells, respectively) and its impact on immune system cells (peripheral blood mononuclear cells, splenic and bone marrow cells). Our findings demonstrate that combining ICRP with chemotherapies enhances cytotoxicity against tumoral T-cell lymphoblasts. ICRP + Cyclophosphamide (CTX) cytotoxicity is induced through a caspase-, reactive oxygen species (ROS)-, and calcium-dependent mechanism involving the loss of mitochondrial membrane potential, an increase in ROS production, and caspase activation. Low doses of ICRP in combination with CTX spare non-tumoral immune cells, overcome the bone marrow-induced resistance to CTX cell death, and improves the CTX antitumor effect in vivo in syngeneic Balb/c mice challenged with L5178Y-R. This led to a reduction in tumor volume and a decrease in Ki-67 proliferation marker expression and the granulocyte/lymphocyte ratio. These results set the basis for further research into the clinical application of ICRP in combination with chemotherapeutic regimens for improving outcomes in T-cell malignancies.
Keyphrases
- cell death
- cell cycle arrest
- induced apoptosis
- bone marrow
- reactive oxygen species
- oxidative stress
- acute lymphoblastic leukemia
- signaling pathway
- klebsiella pneumoniae
- endoplasmic reticulum stress
- mesenchymal stem cells
- diabetic rats
- high glucose
- low dose
- peripheral blood
- poor prognosis
- type diabetes
- escherichia coli
- squamous cell carcinoma
- radiation therapy
- high dose
- multidrug resistant
- machine learning
- diffuse large b cell lymphoma
- skeletal muscle
- papillary thyroid
- endothelial cells
- adipose tissue
- binding protein
- lymph node metastasis
- childhood cancer
- human health
- lymph node
- single molecule
- rectal cancer