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Table 1 Table summarizes main basic studies assessing the role of proteasome inhibitors in NPC tissue samples, cell lines, xenografts and murine models

From: Current approach and novel perspectives in nasopharyngeal carcinoma: the role of targeting proteasome dysregulation as a molecular landmark in nasopharyngeal cancer

Study Cell lines Patient Samples / animal studies Treatment Endpoints or objectives Outcomes/Results
Li et al. [36] CNE1, CNE-LMP1+ MG-132 Study of LMP1 regulating the expression of MDM2 MDM2 expression is upregulated by LMP1 through a post-ubiquitination mechanism.
Hau et al. [38] HONE1, HONE1-EBV, CNE2-EBV C666–1, NP460-hTERT MG-132 Examination of LMP1 protein levels in different EBV-infected cell lines - LMP1 protein is rapidly degraded via proteasome-mediated proteolysis.
- Binding of Id1 to LMP1 suppressed polyubiquitination of LMP1 and may be involved in stabilization of LMP1 in EBV-infected nasopharyngeal epithelial cells.
-Proteasome inhibitor could effectively stabilize LMP1 protein in EBV-infected cells
- Id1 could interact and stabilize LMP1 by suppressing LMP1 polyubiquitination.
Gainullin et al. [39] CNE1, CNE2, TWO3, HONE1 9 NPC tissues
10 normal epithelial tissues from chronic nasopharyngitis patients
MG-132 Role of LMP2A in the accumulation of cofilin in NPC. - LMP2A was found to interfere with cofilin degradation in NPC cells by accelerating the proteasomal degradation of Cbl and Syk.
- Interference with cofilin degradation may enhance the metastatic potential of NPC cells
Zhou et al. [40] HONE1/Akata, HK1/Akata, C666–1, CNE1/Akata, CNE1 (EBV-) 43 NPC tissues
BALB/c nude mice
Anti-cancer effect of triptolide and mechanism of EBNA1 in NPC cells Low dose of triptolide reduce the half-life of EBNA1 and significantly decreased EBNA1 expression by promoting the process of proteasome ubiquitin pathway.
Zhang et al. [22] CNE1, CNE2, HNE1, HONE1, HK1, SUNE1, C666–1,
NPEC2-Tert, NPEC5-Tert
Primary NPC cell lines
Interplay between EBV gB and host proteins - FBXO2 ubiquitinates and degrades glycosylated gB.
- Identification of SCFFBXO2 as an E3 ubiquitin ligase targeting EBV envelope protein gB.
Meng et al. [41] CNE1, CNE2 (S18, S26), SUNE-1 (5–8) 50 NPC tissues MG132 Molecular mechanisms of NPC metastasis - S100A14 promoted the ubiquitin-proteasome-mediated degradation ofIRAK1 to suppress NPC cellular migration.
- Lower S100A14 expression was significantly correlated with shorter patient OS and DMFS.
Pan et al. [42] CNE1, CNE2, HONE1, C666.1 45 NPC tissues
30 control
Functional relationship between Jab1 and p27 protein expression - Jab1-mediated p27 degradation in a proteasome-dependent manner.
- Overexpression of Jab1 correlated with poor survival in NPC patients.
Liu et al. [43] HONE1
Effect of curcumin on the proliferation, cycle arrest, and apoptosis of EBV+ NPC cells Curcumin induced EBNA1 degradation via the proteasome-ubiquitin pathway
Friboulet et al. [44] C666–1
13 NPC biopsies
C15 and C17 (EBV+ in nude mice) NPC xenografts
Functions of c-IAP2 in NPC cells - RMT 5265 induces the proteasome-mediated degradation of c-IAP2, resulting from the enhanced polyubiquitination of c-IAP2
Hui et al. [45] HONE1, HK1-EBV, HONE1-EBV, HA, C666–1 Female BALB/c nude (nu/nu) mice Bortezomib, SAHA (Vorinostat) Mechanisms of apoptosis and effects on lytic cycle activation of EBV - Combination of bortezomib and SAHA synergistically induce killing of a panel of NPC cell lines and suppresses the growth of NPC xenografts in nude mice.
- Bortezomib inhibits SAHA’s induction of EBV replication and abrogates production of infectious viral particles in NPC cells.
Xu C. et al. [46] NP69, CNE2, Hone1, C666–1   MG132 Mechanisms by which EBV elude immune responses - LMP1 inhibits Sendai virus mediated type I interferon production and downregulates RIG-I signaling pathway by promotion RIG-I degradation dependent on proteasome.
- EBV employs a unique strategy to evade RIG-I mediated immune responses.
Jiang et al. [44] CNE2, CNE1   Bortezomib (PS-341) Mechanism by which immune evasion affects the response to treatment of NPC. - Bortezomib downregulates IFNγ-induced IDO expression via inhibition of JAK/STAT1 signaling pathway.
- Bortezomib can promote IkB-α phosphorylation-ubiquitination to release NF-kB from IkB-α.