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Updated: May 3, 2026

Isolation and Expansion of Cytotoxic Cytokine-induced Killer T Cells for Cancer Treatment
Published on: January 24, 2020
Targeting chronic lymphocytic leukemia using CIGB-300, a clinical-stage CK2-specific cell-permeable peptide inhibitor
Leila R Martins1, Yasser Perera, Paulo Lúcio
1Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.
Abstract:
Chronic lymphocytic leukemia (CLL) remains an incurable malignancy, urging for the identification of new molecular targets for therapeutic intervention. CLL cells rely on overexpression and hyperactivation of the ubiquitous serine/threonine protein kinase CK2 for their viability in vitro. CIGB-300 is a cell-permeable selective CK2 inhibitor peptide undergoing clinical trials for several cancers. Here, we show that CIGB-300 promotes activation of the tumor suppressor PTEN and abrogates PI3K-mediated downstream signaling in CLL cells. In accordance, CIGB-300 decreases the viability and proliferation of CLL cell lines, promotes apoptosis of primary leukemia cells and displays antitumor efficacy in a xenograft mouse model of human CLL. Our studies provide pre-clinical support for the testing and possible inclusion of CK2 inhibitors in the clinical arsenal against CLL.
Insights
The protein kinase CK2 inhibitor CIGB-300 shows promise for treating chronic lymphocytic leukemia (CLL). This study demonstrates CIGB-300
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Chronic lymphocytic leukemia (CLL) is an incurable blood cancer.
- CLL cells depend on the overactive protein kinase CK2 for survival.
- CK2 inhibitors are potential therapeutic agents for various cancers.
Purpose of the Study:
- To investigate the efficacy of CIGB-300, a selective CK2 inhibitor, against CLL.
- To explore the molecular mechanisms of CIGB-300 in CLL cells.
Main Methods:
- Treatment of CLL cell lines and primary cells with CIGB-300.
- Analysis of PTEN activation and PI3K signaling pathway.
- Assessment of cell viability, proliferation, and apoptosis.
- Evaluation of antitumor efficacy in a human CLL xenograft mouse model.
Main Results:
- CIGB-300 activated the tumor suppressor PTEN in CLL cells.
- CIGB-300 inhibited PI3K-mediated downstream signaling.
- CIGB-300 reduced CLL cell viability and proliferation.
- CIGB-300 induced apoptosis in primary CLL cells and showed antitumor effects in vivo.
Conclusions:
- CIGB-300 demonstrates significant preclinical efficacy against CLL.
- Targeting CK2 with inhibitors like CIGB-300 is a viable strategy for CLL treatment.
- Further clinical investigation of CK2 inhibitors for CLL is warranted.
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