Abstract
T-cell lymphomas are lymphoid malignancies with aggressive clinical course and poor prognosis. Increasing evidences suggest that deregulation of signal transducer and activator of transcription-3 (STAT3) and suppressor of cytokine signaling 3 (SOCS3) is associated with the pathogenesis of T-cell lymphomas. The hedgehog (Hh)/glioma-associated oncogene-1 (GLI1) pathway, aberrantly activated in a number of tumors, has also been extensively studied. We found that protein expressions of GL11, p-STAT3, STAT3, and SOCS3 were up-regulated in T-cell lymphoma tissues and cell lines. Moreover, the protein expressions of p-STAT3 and SOCS3 were positively correlated with GLI1 in T-cell lymphomas. GLI1 inhibitor GANT61 and lentivirus-mediated siGLI1 exhibited inhibitory effects in the three T-cell lines (Jurkat, Karpass299 and Myla3676 cells). The protein expressions of p-STAT3 and SOCS3 were decreased accompanied with the inhibition of GLI1. These findings indicated that GANT61 is a promising agent against T-cell lymphoma and the antitumor activity might be partly mediated by down-regulating p-STAT3 and SOCS3.
Highlights
T-cell lymphomas are a heterogeneous group of lymphoid malignancies committed to the T-cell lineage
We found that protein expressions of GL11, p-signal transducer and activator of transcription-3 (STAT3), STAT3, and suppressor of cytokine signaling 3 (SOCS3) were up-regulated in T-cell lymphoma tissues and cell lines
The protein expressions of p-STAT3 and SOCS3 were decreased accompanied with the inhibition of GLI1
Summary
T-cell lymphomas are a heterogeneous group of lymphoid malignancies committed to the T-cell lineage. Compared with B-cell lymphomas, T- cell are more aggressive with poorer prognosis [1]. The etiology remains to be elucidated, and no uniformed therapeutic strategies have been achieved. Accumulating lines of evidence suggests that the improper activation of signal transduction pathways (e.g. PI3K/AKT, Hedgehog, STAT3) are critical events in pathologies of T-cell lymphomas [2, 3]. The intermediates in these pathways contributing to the tumorgenesis are attractive therapeutic targets. This study mainly focuses on the Hh/GLI1 and STAT3/SOCS3 pathways in T-cell lymphomas
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