Expression of KITENIN, a KAI1/CD82 binding protein and metastasis enhancer, in bladder cancer cell lines: Relationship to KAI1/CD82 levels and invasive behaviour

Rowe, Alexandra; Jackson, Paul

doi:10.3892/or.16.6.1267

Cited by 7 publications

(7 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…KAI1 is a metastasis suppressor gene 39 , and KITENIN is a newly identified binding partner of the KAI1/CD82 metastasis suppressor 40 . KITENIN promotes tumorigenesis, invasiveness, and adhesion to fibronectin in mouse colon cells 41 .…”

Section: Discussionmentioning

confidence: 99%

The lichen secondary metabolite atranorin suppresses lung cancer cell motility and tumorigenesis

Zhou

Yang

Park

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Lichens are symbiotic organisms that produce various secondary metabolites. Here, different lichen extracts were examined to identify secondary metabolites with anti-migratory activity against human lung cancer cells. Everniastrum vexans had the most potent inhibitory activity, and atranorin was identified as an active subcomponent of this extract. Atranorin suppressed β-catenin-mediated TOPFLASH activity by inhibiting the nuclear import of β-catenin and downregulating β-catenin/LEF and c-jun/AP-1 downstream target genes such as CD44, cyclin-D1 and c-myc. Atranorin decreased KAI1 C-terminal interacting tetraspanin (KITENIN)-mediated AP-1 activity and the activity of the KITENIN 3′-untranslated region. The nuclear distribution of the AP-1 transcriptional factor, including c-jun and c-fos, was suppressed in atranorin-treated cells, and atranorin inhibited the activity of Rho GTPases including Rac1, Cdc42, and RhoA, whereas it had no effect on epithelial-mesenchymal transition markers. STAT-luciferase activity and nuclear STAT levels were decreased, whereas total STAT levels were moderately reduced. The human cell motility and lung cancer RT² Profiler PCR Arrays identified additional atranorin target genes. Atranorin significantly inhibited tumorigenesis in vitro and in vivo. Taken together, our results indicated that E. vexans and its subcomponent atranorin may inhibit lung cancer cell motility and tumorigenesis by affecting AP-1, Wnt, and STAT signaling and suppressing RhoGTPase activity.

show abstract

Section: Discussionmentioning

confidence: 99%

The lichen secondary metabolite atranorin suppresses lung cancer cell motility and tumorigenesis

Zhou

Yang

Park

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Taken together, these findings suggest that KITENIN might function to enhance metastasis, and that the role of KAI1/CD82 binding is to modulate this activity. It has been reported that expression of KITENIN is inversely correlated with that of KAI1 in CT‐26 mouse colon cancer cells8 and some bladder cancer cell lines 15. We have identified such an relationship between KITENIN and KAI1 in human head and neck cancer tissue 12…”

Section: Discussionmentioning

confidence: 54%

KAI1 COOH‐terminal interacting tetraspanin (KITENIN) expression in early and advanced laryngeal cancer

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Previous studies have also reported that the expression of KAI1 is correlated with the progression of several types of human cancer. It has been categorized as a metastatic suppressor in various types of human cancer, including cancer of the prostate (10,11), bladder (12,13), breast (14,15), colon (16,17), pancreas (18) and lungs (19,20). Previous studies have also reported that there is a significant association between downregulated expression of KAI1 and primary oral tumors, which are associated with lymph nodes (21–23).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of KAI1/CD82 suppresses in vitro cell growth, migration, invasion and xenograft growth in oral cancer

Chai

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

KAI1/CD82 is a metastatic suppressor gene in human prostate cancer and several other types of cancer in humans. The present study aimed to examine the role of the overexpression of KAI1 in the progression of oral cancer. Human KAI1/CD82 cDNA was transfected into OSCC-15 and 293T cell lines, and its effects on OSCC-15 cell proliferation, invasion and apoptosis were assessed by performing a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay, Matrigel invasion and Annexin V-FITC staining, respectively. In addition, a xenograft model was used to assess the effect of KAI1/CD82 on the in vivo growth of tumors. The overexpression of KAI1/CD82 inhibited the proliferation and invasion of OSCC-15 cells. It also enhanced the apoptotic rate of the OSCC-15 cells. Furthermore, the overexpression of KAI1/CD82 inhibited tumor growth in the xenograft model. The results demonstrated that the overexpression of KAI1/CD82 significantly inhibited the proliferation and invasion of human oral cancer cells, and inhibited tumor growth in the xenograft model. Therefore, KAI1/CD82 may be considered as a potential therapeutic target in oral cancer.

show abstract

Expression of KITENIN, a KAI1/CD82 binding protein and metastasis enhancer, in bladder cancer cell lines: Relationship to KAI1/CD82 levels and invasive behaviour

Cited by 7 publications

References 14 publications

The lichen secondary metabolite atranorin suppresses lung cancer cell motility and tumorigenesis

The lichen secondary metabolite atranorin suppresses lung cancer cell motility and tumorigenesis

KAI1 COOH‐terminal interacting tetraspanin (KITENIN) expression in early and advanced laryngeal cancer

Overexpression of KAI1/CD82 suppresses in vitro cell growth, migration, invasion and xenograft growth in oral cancer

Contact Info

Product

Resources

About