Doxycycline is an NF-κB inhibitor that induces apoptotic cell death in malignant T-cells

Department

Research

Document Type

Article

Publication Title

Oncotarget

Abstract

Cutaneous T-cell Lymphoma (CTCL) is a rare non-Hodgkin's lymphoma that can affect the skin, blood, and lymph nodes, and can metastasize at late stages. Novel therapies that target all affected disease compartments and provide longer lasting responses while being safe are needed. One potential therapeutic target is NF-κB, a regulator of immune responses and an important participant in carcinogenesis and cancer progression. As a transcription factor, NF-κB targets genes that promote cell proliferation and survival. Constitutive or aberrant activation of NF-κB is encountered in many types of cancer, including CTCL.Recently, while analyzing gene-expression profiles of a variety of small molecule compounds that target NF-κB, we discovered the tetracycline family of antibiotics, including doxycycline, to be potent inhibitors of the NF-κB pathway. Doxycycline is well-tolerated, safe, and inexpensive; and is commonly used as an antibiotic and anti-inflammatory for the treatment a multitude of medical conditions.In our current study, we show that doxycycline induces apoptosis in a dose dependent manner in multiple different cell lines from patients with the two most common subtypes of CTCL, Mycosis Fungoides (MF) and Sézary Syndrome (SS). Similar results were found using primary CD4+ T cells from a patient with SS. Doxycycline inhibits TNF induced NF-κB activation and reduces expression of NF-κB dependent anti-apoptotic proteins, such as BCL2α. Furthermore, we have identified that doxycycline induces apoptosis through reactive oxygen species.

First Page

75954

Last Page

75967

DOI

10.18632/oncotarget.12488

Volume

7

Issue

46

Publication Date

11-15-2016

Medical Subject Headings

Aged; Apoptosis (drug effects); Caspase 8 (metabolism); Cell Line, Tumor; Doxycycline (pharmacology); Female; Humans; Lymphoma, T-Cell, Cutaneous (metabolism, pathology); Male; NF-kappa B (antagonists & inhibitors); Phosphorylation; Reactive Oxygen Species (metabolism); Sezary Syndrome (metabolism); Signal Transduction (drug effects); T-Lymphocytes (drug effects, metabolism, pathology); Tumor Necrosis Factor-alpha (pharmacology); Young Adult

PubMed ID

27732942

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