Nuclear protein 1 (NUPR1) is a transcription cofactor that senses stressful
conditions and modulates cellular response by promoting or inhibiting
apoptosis. NUPR1 is usually highly expressed in tumor cells where it enables
them to adapt and resist environmental stress or chemotherapeutic compounds.
NUPR1 can be involved in cell proliferation. Data about the involvement of
NUPR1 in the proliferation and apoptosis of lymphocytes are scarce.
Therefore, in this study we focused on the role of NUPR1 in lymphocyte
physiology and found that NUPR1 might be involved in the initiation of their
proliferation. Lymphocytes were isolated from the cervical lymph nodes of
C57BL/6 mice. NUPR1 expression subsided 24 h after the induction of
proliferation by a mitogen. Also, stressful conditions after cell isolation
led to increased NUPR1 mRNA and protein expression in vitro that coincided
with cell apoptosis. Similarly, apoptosis induction by staurosporine, a
broad-range protein kinase inhibitor, led to increased NUPR1 expression. In
addition, NUPR1 inhibition by smallinterfering RNA prevented the
staurosporine-induced apoptosis (judging from decreased caspase activity) in
the whole cell population of cervical lymph nodes. However, NUPR1 absence was
irrelevant to the induction of apoptosis in CD3+ T lymphocytes, suggesting
that NUPR1 is probably a mediator of apoptosis in other immune cell
populations within the lymph node, such as B lymphocytes. In conclusion, our
results suggest that NUPR1 is important for the initiation of lymphocyte cell
division and for the apoptotic process of non-T cells during stressful
conditions.
The Role of Ultrasonography for Differentiating and Management of Malignant Cervical Lymph Nodes
