Evidence map›Paper›PMID 42755572›Full record

ArticleFrontiers in oncology2026

SYTL5 drives malignant progression in differentiated thyroid carcinoma: unveiling its regulatory mechanisms.

Xiaohui Zhu, Xia Pan, Dongmei Jiang, Hengfeng Cui, Haiyan Wu, Yuying Wang, Xia Li

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Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Xiaohui Zhu *Department of Endocrinology, Yancheng Third People's Hospital, Yancheng, China.
Xia Pan *Department of Endocrinology, Yancheng Third People's Hospital, Yancheng, China.
Dongmei JiangDepartment of Endocrinology, Yancheng Third People's Hospital, Yancheng, China.
Hengfeng CuiAffiliated Hospital 6 of Nantong University, Yancheng, China.
Haiyan WuAffiliated Hospital 6 of Nantong University, Yancheng, China.
Yuying WangDepartment of Endocrinology, Yancheng Third People's Hospital, Yancheng, China.
Xia LiAffiliated Hospital 6 of Nantong University, Yancheng, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To investigate the expression of SYTL5 in differentiated thyroid carcinoma (DTC) and elucidate its clinical significance and underlying molecular mechanisms. Methods: SYTL5 expression in 107 paired DTC and adjacent normal tissues was evaluated by immunohistochemistry, qRT-PCR, and Western blot. Associations with clinicopathological variables were assessed using chi-square or Fisher's exact tests with Benjamini-Hochberg false discovery rate adjustment, and the distant metastasis subgroup was summarized descriptively because only one M1 case was available. Stable SYTL5 knockdown or overexpression DTC cell lines were established using RNA interference and lentiviral transfection. Cell proliferation, apoptosis, invasion, and migration were assessed using EdU staining, flow cytometry, and Transwell assays. A nude mouse subcutaneous xenograft model was constructed to evaluate tumor growth Results: SYTL5 expression was significantly upregulated in DTC tissues and was positively associated with lymph node metastasis after false discovery rate adjustment. SYTL5 silencing inhibited DTC cell proliferation, invasion, and migration while modestly increasing apoptosis, whereas SYTL5 overexpression exerted opposite effects. Mechanistically, SYTL5 knockdown was associated with reduced TGFBR2 and phosphorylated Smad3 expression without affecting total Smad3 levels, both Conclusion: SYTL5 is associated with DTC progression and lymph node metastasis and functionally supports malignant phenotypes in DTC models. The data support a ZNF384-SYTL5-TGFBR2/Smad3 regulatory axis, while direct regulation of TGFBR2 by SYTL5 and the contribution of Smad2 or non-canonical pathways require further study. SYTL5 may represent a candidate therapeutic target for DTC.

Indexed as

cell proliferationoncogeneSYTL5 proteinthyroid carcinomaZNF384 protein

Identifiers

PMID42755572
PMCPMC13581719

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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.