Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells

Q: What was the main objective of the study on ESM1 in papillary thyroid cancer?

To determine how ESM1 affects growth, migration, and invasion of papillary thyroid cancer cells and to clarify its potential role in PTC treatment.

Q: How was ESM1 expression measured in patient tissues?

ESM1 expression levels were detected in 53 PTC tumor samples and 59 matched adjacent normal tissue samples using immunohistochemical analysis.

Q: What effects did shRNA-mediated ESM1 knockdown have on PTC cells?

Knockdown reduced ESM1 mRNA and protein levels and significantly inhibited proliferation, migration, and invasion in TPC-1 and SW579 cells in vitro.

Sep 21, 2026

Upload by Ava Thompson

Objective-focused molecular study evaluates endothelial specific molecule-1 (ESM1) in papillary thyroid cancer (PTC), where its oncogenic contribution remains unclear. ESM1 levels are quantified in tumor and adjacent normal tissues, followed by shRNA-mediated knockdown in TPC-1 and SW579 cell lines. Cell proliferation, apoptosis, wound healing, and transwell assays assess growth, migration, and invasion. Results show higher ESM1 in PTC tissues, with knockdown significantly suppressing proliferation, migration, and invasion. ESM1 is proposed as a diagnostic and therapeutic target for PTC.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages16

Reading Time40 min

AccessFree to download

Abstract

Objective

Methods

Results

Conclusions

PLOS ONE OPEN ACCESS Citation: Xie L, He L, Zhang W, Wang H (2024) Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells. PLoS ONE 19(4): e0298631 . [https://](https://)[ ](https://)[doi.org/10.1371/journal.pone.0298631](doi.org/10.1371/journal.pone.0298631) Editor: Amirmohammad Khalaji, Tehran University of Medical Sciences, ISLAMIC REPUBLIC OF IRAN Received: October 17, 2023 Accepted: January 27, 2024 Published: April 16, 2024 Copyright: © 2024 Xie et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability Statement: All relevant data are within the paper and its Supporting Information files. Funding: The present study was funded by the Natural Science Foundation of China (grant nos. 81960320), Basic research project of Science and Technology Department of Yunnan Province (grant nos. 202101AT070148), Science and Technology Project of Sichuan Provincial Health Commission (23LCYJ023), and the Natural Science Foundation of Sichuan Province (grant nos. 2023NSFSC0635) . The funders had no role in study design, data RESEARCH ARTICLE Functional analysis of ESM1 by shRNAmediated knockdown of its expression in papillary thyroid cancer cells Lijun Xie1, Limeng He2, Wei Zhang2‡*, Hao Wang2‡* 1 Department of Nuclear Medicine, The First Affiliated Hospital of Kunming Medical University, Kunming, P. R. China, 2 Department of Nuclear Medicine, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, P. R. China ‡ HW and WZ are equal senior authorship to this work. * [zhangwscd@uestc.edu.cn](zhangwscd@uestc.edu.cn) (WZ); [18810566155@163.com](18810566155@163.com) (HW) Abstract Objective Endothelial specific molecule-1 (ESM1) is implicated as an oncogene in multiple human cancers. However, the function of ESM1 in papillary thyroid cancer (PTC) is not well understood. The current study aimed to investigate the effect of ESM1 on the growth, migration, and invasion of PTC to provide a novel perspective for PTC treatment. Methods The expression levels of ESM1 in PTC tissues form 53 tumor tissue samples and 59 matching adjacent normal tissue samples were detected by immunohistochemical analysis. Knockdown of ESM1 expression in TPC-1 and SW579 cell lines was established to investigate its role in PTC. Moreover, cell proliferation, apoptosis, wound healing, and transwell assays were conducted in vitro to assess cell proliferation, migration and invasion. Results The findings revealed that ESM1 expression was significantly higher in PTC tissues than that found in paraneoplastic tissues (P<0.0001) . Knockdown of ESM1 expression inhibited the proliferation, migration, and invasion of TPC-1 and SW579 cells in vitro. Compared with the control group, the mRNA and protein levels of ESM1 in PTC cells were significantly reduced following knockdown of its expression (P<0.01) . In addition, ESM1-knockdown cells indicated decreased proliferation and decreased migratory and invasive activities (P<0.01, P<0.01, P<0.001, respectively) . Conclusions ESM1 was identified as a major gene in the occurrence and progression of PTC, which could increase the proliferation, migration, and invasion of PTC cells. It may be a promising diagnostic and therapeutic target gene. collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist. Introduction Thyroid cancer, with an estimated 586,202 new cases worldwide in 2020 alone, stands as a significant public health concern [ 1] . Its incidence, particularly in affluent regions, has experienced a marked increase, attributed to improved detection methods and environmental facto

FAQs

What was the main objective of the study on ESM1 in papillary thyroid cancer?

To determine how ESM1 affects growth, migration, and invasion of papillary thyroid cancer cells and to clarify its potential role in PTC treatment.

How was ESM1 expression measured in patient tissues?

ESM1 expression levels were detected in 53 PTC tumor samples and 59 matched adjacent normal tissue samples using immunohistochemical analysis.

What effects did shRNA-mediated ESM1 knockdown have on PTC cells?

Knockdown reduced ESM1 mRNA and protein levels and significantly inhibited proliferation, migration, and invasion in TPC-1 and SW579 cells in vitro.

Sep 21, 2026

Upload by Ava Thompson