Page 51 - D. Cancer biology
P. 51
SPON2 Enhanced by Notch Signaling Marks Aggressive Tumor Growth in
Gastric Cancer
Hyeon-Gu Kang, Jun-Ho Jang and Seok-Jun Kim
Department of Integrative Biological Sciences, BK21 FOUR Educational Research Group for Age-associated Disorder Control Technology,
College of Natural Sciences, Chosun University
BACKGROUND AIM
SPON2 is involved in cancer progression and metastasis We investigate the role of SPON2 and related signaling
of many tumors; however, its role and underlying pathway in gastric cancer progression and metastasis.
mechanism in gastric cancer are still obscure. We
identified SPON2 regulated through Notch signaling as
potential target gene to inhibit gastric cancer progression.
RESULTS
Figure 2. SPON2 downregulation decreases cell
Figure 1. SPON2 upregulates in patients with gastric proliferation, migration, and invasion abilities in gastric
cancer and is associated with poor prognosis cancer cells.
Figure 3. Effect of SPON2 inhibition on tumor growth in Figure 4. SPON2 expression is regulated by Notch
xenografted mice. signaling pathway.
SPON2 expression levels were found to be upregulated in gastric cancer cell lines and patient tissues compared to normal
gastric epithelial cells and normal controls. Furthermore, SPON2 silencing was observed to decrease cell proliferation and
motility and reduce tumor growth in xenograft mice. Subsequently, we focused on regulatory mechanism of SPON2 in gastric
cancer. We confirmed how Notch signaling pathway regulate SPON2 expression using Notch signaling-related transcription
factor interaction and reporter gene assay. Our study demonstrated that Notch signaling-mediated SPON2 upregulation is
associated with aggressive progression of gastric cancer.
CONCLUSION REFERENCES ACKNOWLEDGEMENTS
Kang et al., SPON2 Is Upregulated This study was supported by the
through Notch Signaling Pathway and Chosun University in 2020. Also helped
Promotes Tumor Progression in by lab members.
Gastric Cancer. Cancers 2020, 12(6),
1439. Contact information
kang84562@nate.com
010-5539-3058

