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Knockdown of SUMO-activating enzyme subunit 2 (SAE2) suppresses cancer malignancy
and enhances chemotherapy sensitivity in small cell lung cancer
#MMPMID26063074
Liu X
; Xu Y
; Pang Z
; Guo F
; Qin Q
; Yin T
; Sang Y
; Feng C
; Li X
; Jiang L
; Shu P
; Wang Y
J Hematol Oncol
2015[Jun]; 8
(?): 67
PMID26063074
show ga
BACKGROUND: SUMO-activating enzyme subunit 2 (SAE2) is the sole E1-activating
enzyme required for numerous important protein SUMOylation, abnormal of which is
associated with carcinogenesis. SAE2 inactivation was recently reported to be a
therapeutic strategy in cancers with Myc overexpression. However, the roles of
SAE2 in small cell lung cancer (SCLC) are largely unknown. METHODS: Stably SAE2
knockdown in H446 cells were established with a lentiviral system. Cell
viability, cell cycle, and apoptosis were analyzed using MTT assay and flow
cytometric assay. Expression of SAE2 mRNA and protein were detected by qPCR,
western blotting, and immunohistochemical staining. Cell invasion and migration
assay were determined by transwell chamber assay. H446 cells with or without SAE2
knockdown, nude mice models were established to observe tumorigenesis. RESULTS:
SAE2 was highly expressed in SCLC and significantly correlated with tumorigenesis
in vivo. Cancer cells with RNAi-mediated reduction of SAE2 expression exhibited
growth retardation and apoptosis increasing. Furthermore, down-regulation of SAE2
expression inhibited migration and invasion, simultaneously increased the
sensitivity of H446 to etoposide and cisplatin. CONCLUSIONS: SAE2 plays an
important role in tumor growth, metastasis, and chemotherapy sensitivity of H446
and is a potential clinical biomarker and therapeutic target in SCLC with high
c-Myc expression.
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