ArticleBMC endocrine disorders2025
Targeting syndecan-2 inhibits papillary thyroid cancer invasiveness and de-differentiation.
Article in BMC endocrine disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Precision Thyroid Oncology: A Review of Multi-Omics Biomarkers and Spatiotemporal Technologies.International journal of general medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundThe high incidence of recurrence and metastatic disease remain the major issues for papillary thyroid cancer (PTC) patients. Previous studies have demonstrated that Syndecan-2 (SDC2) plays a key role in multiple cancers progression. However, the potential role of SDC2 in PTC progression and recurrence remains unclear.
methodsFirst, we performed bioinformatics analysis and western-blotting analysis to explore the potential prognostic value of SDC2 in PTC. Then we applied transient siRNA knockdown and plasmid overexpression to alter SDC2 expression level in PTC cell line B-CPAP and KTC-1. After that, we carried out scratch wound healing assay, transwell assay and cell counting kits-8 (CCK8) assay to explore the cell migration, invasiveness and viability. We also explored expressions of mesenchymal and epithelial markers, multiple thyroids differentiating markers and hedgehog signaling members to address the potential underlying mechanisms.
resultsFirstly, we found a significant negative correlation of SDC2 expression with advanced disease characters in PTC. Then bioinformatic analysis indicated the SDC2 expression was closely related to multiple key pathways and thyroid differentiation markers. Targeting SDC2 expression significantly influenced the growth and invasion of PTC cells according to series of assays. Western-blotting results of α-SMA and ZO-1 also indicated the altered EMT process. Furthermore, attenuated SDC2 expression also leads to the PTC de-differentiation, which could be due to hedgehog signaling alteration.
conclusionsOur findings suggest that SDC2 would be a promising therapy target for advanced radioiodine refractory thyroid cancer, but the role in PTC progression is complicated and requires further exploration.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.