Evidence map›Paper›PMID 37056066›Full record

ArticleEndocrine, metabolic & immune disorders drug targets2024

A Specificity Protein 1 assists the Progression of the Papillary Thyroid Cell Line by Initiating

Jie Chen, Adheesh Bhandari, Suzita Hirachan, Shihui Lv, Sumnima Mainali, Chen Zheng, Rutian Hao

Abstract read
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In one paragraph

Article in Endocrine, metabolic & immune disorders drug targets, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 3 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Jie ChenDepartment of Operating Room, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Adheesh BhandariDepartment of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Suzita HirachanDepartment of General Surgery, Breast and Thyroid Unit, Tribhuvan University Teaching Hospital, Kathmandu, Nepal.
Shihui LvDepartment of Operating Room, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Sumnima MainaliDepartment of Obstetrics and Gynecology, Kulhudhuffushi Regional Hospital, Kulhudhuffushi, Maldives.
Chen ZhengDepartment of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Rutian HaoDepartment of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Wenzhou Medical University · CNTribhuvan University Teaching Hospital · NP

Funding

Natural Science Foundation of Zhejiang Province Grant no. LY20H160011Science and Technology Project of Wenzhou Grant no. Y20180855
6 · The paper itself

Abstract

aimsPapillary thyroid cancer (PTC) is one of the subtypes of thyroid cancer with increasing incidence worldwide, but the molecular mechanism is still unclear.

backgroundPapillary 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.

objectiveIn 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.

methodsThe 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.

resultsThe experiments in vitro showed that SP1 could promote cell proliferation, colony formation, migration, and invasion by regulating NECTIN4 in PTC cells.

conclusionIn 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.

Indexed as

Cell ProliferationNectinsSp1 Transcription FactorThyroid Cancer, PapillaryThyroid NeoplasmsCell Adhesion MoleculesCell Line, TumorCell MovementDisease ProgressionGene Expression Regulation, NeoplasticHumansCell Adhesion MoleculesNECTIN4 protein, humanNectinsSP1 protein, humanSp1 Transcription Factorcancer.NECTIN4papillary thyroid cancerproliferationSP1transcription factor

Identifiers

PMID37056066
OpenAlexW4365483358

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.