KSHV LANA and EBV LMP1 induce the expression of UCH-L1 following viral transformation.

[primary effusion lymphoma]

Ubiquitin C-terminal Hydrolase L 1 (UCH-L 1 ) has oncogenic properties and is highly expressed during malignancies . We recently documented that Epstein-Barr virus (EBV ) infection induces uch-l 1 expression . Here we show that Kaposi 's Sarcoma -associated herpesvirus (KSHV ) infection induced UCH-L 1 expression , via cooperation of KSHV Latency-Associated Nuclear Antigen (LANA ) and RBP-J κ and activation of the uch-l 1 promoter . UCH-L 1 expression was also increased in Primary Effusion Lymphoma (PEL ) cells co -infected with KSHV and EBV compared with PEL cells infected only with KSHV , suggesting EBV augments the effect of LANA on uch-l 1 . EBV latent membrane protein 1 (LMP 1 ) is one of the few EBV products expressed in PEL cells . Results showed that LMP 1 was sufficient to induce uch-l 1 expression , and co -expression of LMP 1 and LANA had an additive effect on uch-l 1 expression . These results indicate that viral latency products of both human γ-herpesviruses contribute to uch-l 1 expression , which may contribute to the progression of lymphoid malignancies .

Diseases
Validation

Diseases presenting "lymphoma" symptom

adrenal incidentaloma

alpha-thalassemia

carcinoma of the gallbladder

cushing syndrome

dedifferentiated liposarcoma

erdheim-chester disease

erythropoietic protoporphyria

esophageal adenocarcinoma

esophageal carcinoma

familial hypocalciuric hypercalcemia

focal myositis

hirschsprung disease

hodgkin lymphoma, classical

kabuki syndrome

liposarcoma

locked-in syndrome

monosomy 21

oculocutaneous albinism

primary effusion lymphoma

severe combined immunodeficiency

systemic capillary leak syndrome

waldenström macroglobulinemia

wiskott-aldrich syndrome

This symptom has already been validated