KOREASCHOLAR

SOCS3, a suppressor of cytokine signaling 3, is known as a negative regulator of various cytokines and a tumor suppressor gene in human tumors. This study aimed to investigate the role of SOCS3 in oral squamous cell carcinoma (OSCC) and its impact on epithelial-mesenchymal transition (EMT) in OSCC cells. Although SOCS3 is recognized as a negative regulator of various cytokines and a tumor suppressor gene in human tumors, its specific effects on OSCC remain poorly understood.
For the assessment of SOCS3 expression in OSCC, the UALCAN website and TCGA data were used to evaluate its expression in head and neck cancer. Additionally, immunohistochemical staining was conducted to determine the SOCS3 expression specifically in OSCC. The findings indicated a significant decrease in SOCS3 expression in tumor tissue compared to that in normal tissues.
To investigate the enhancement of SOCS3 expression in OSCC cancer cell lines, IL6 treatment was administered to MC3 cells. However, no significant differences were observed in cell viability, wound healing assay, and invasion assay. Conversely, the transfection of SOCS3 siRNA into OSCC cells led to a notable increase in cell viability and statistically significant increases in wound healing and invasion assays. These results suggest that SOCS3 plays a crucial role in cell viability and EMT in OSCC, thereby contributing to oral carcinogenesis. Further research is necessary to elucidate the precise role of SOCS3 in OSCC.

Abstract
Ⅰ. INTRODUCTION
Ⅱ. PATIENTS and METHODS
    1. Bioinformatics analysis
    2. SOCS3 immunohistochemical (IHC) staining
    3. Evaluation of immunohistochemical staining
    4. Cell culture
    5. Western blotting
    6. Il-6 treatment
    7. SOCS3 siRNA transfection
    8. Cell viability assay
    9. Wound healing assay
    10. Invasion assay
    11. Statistical analysis
Ⅲ. RESULTS
    1. Demographic and clinicopathological data
    2. The effect of IL6 treatment on the induction ofincreased SOCS3 expression in MC3 cells
    3. The effect of SOCS3 knockdown by SOCS3siRNA transfection in SAS and YD15 cells
Ⅳ. DISCUSSION
Ⅴ. CONCLUSION
ACKNOWLEDGMENTS
CONFLICT OF INTEREST
REFERENCES

• 유미현(부산대학교 치의학전문대학원 구강병리학교실, 부산대학교 치의생명과학 교육연구팀, 치의생명과학연구소) | Mi Heon Ryu (Department of Oral Pathology, School of Dentistry, Education and Research Team for Life Science on Dentistry, Dental and Life Science Institute, Pusan National University)
• 장민아(부산대학교 치의생명과학연구소) | Min-A Jang (Dental and Life Science Institute, Pusan National University)
• 한혜연(진주보건대학교 치위생과) | Hye-Yeon Han (Department of Dental Hygiene, Jinju Health College)
• 김욱규(부산대학교 치의학전문대학원 구강악안면외과학교실, 치의생명과학연구소) | Uk-Kyu Kim (Department of Oral and Maxillofacial Surgery, School of Dentistry, Pusan National Univer) Corresponding Author