Title:A Specificity Protein 1 assists the Progression of the Papillary Thyroid Cell
Line by Initiating NECTIN4
Volume: 24
Issue: 7
Author(s): Jie Chen, Adheesh Bhandari, Suzita Hirachan*, Shihui Lv, Sumnima Mainali, Chen Zheng*Rutian Hao*
Affiliation:
- Department of General Surgery, Breast and Thyroid Unit, Tribhuvan University Teaching Hospital, Kathmandu, Nepal
- Department of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University,
Wenzhou, 325000, Zhejiang, China
- Department of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University,
Wenzhou, 325000, Zhejiang, China
Keywords:
NECTIN4, SP1, papillary thyroid cancer, transcription factor, proliferation, cancer.
Abstract:
Aims: Papillary thyroid cancer (PTC) is one of the subtypes of thyroid cancer with increasing
incidence worldwide, but the molecular mechanism is still unclear.
Background: Papillary thyroid cancer (PTC) is one of the subtypes of thyroid cancer with increasing
incidence worldwide, but the molecular mechanism is still unclear. Studies have indicated that
nectin cell adhesion molecule 4 (NECTIN4) was an oncogene and played an important role in the
development and progression of PTC. Meanwhile, specificity protein 1 (SP1) expresses many important
oncogenes and tumor suppressor genes. However, the relationship between NECTIN4 and
SP1 in regulating PTC growth is unclear.
Objective: In the present study, reverse transcription PCR was utilized to detect the mRNA expression
of NECTIN4 and SP1 in thyroid cancer cell lines and normal thyroid cell lines. Chromatin
immunoprecipitation assays and luciferase reporter assays were used to study whether SP1 could
bind to the promoter region of NECTIN4 and activate its transcription. The biological functions of
SP1 correlated with NECTIN4 were also performed in TPC-1 and KTC1 cell lines.
Methods: The study revealed that the mRNA expression level of SP1 and NECTIN-4 showed a
positive correlation and were upregulated in PTC cell lines. Moreover, the results of ChIP and luciferase
reporter assays showed that SP1 could bind to the NECTIN4 promoter regions and activate
the transcriptional level of NECTIN4.
Results: The experiments in vitro showed that SP1 could promote cell proliferation, colony formation,
migration, and invasion by regulating NECTIN4 in PTC cells.
Conclusion: In conclusion, our study, for the first time, demonstrated that SP1 could control the
transcriptional regulation of NECTIN4 and accelerate the growth of PTC, which may provide a
new potential therapeutic target for PTC patients.