PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathway

IntroductionIn thyroid carcinoma (TC), follicular thyroid carcinoma (FTC) represents the second most prevalent pathological type following papillary thyroid carcinoma. Notably, FTC exhibits a more aggressive clinical course and a higher propensity for distant metastasis. However, the underlying mech...

Full description

Saved in:
Bibliographic Details
Main Authors: Haobo Wang, Fangjian Shang, Yifang Wang, Bo Pang, Longfei Kang, Chuanmin Zhou, Dongyun Li, Zhongxin Li, Xia Jiang, Bo Liu, Zengren Zhao
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-01-01
Series:Frontiers in Oncology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fonc.2025.1502391/full
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832582872371822592
author Haobo Wang
Fangjian Shang
Yifang Wang
Bo Pang
Bo Pang
Longfei Kang
Longfei Kang
Chuanmin Zhou
Chuanmin Zhou
Dongyun Li
Dongyun Li
Zhongxin Li
Zhongxin Li
Xia Jiang
Xia Jiang
Bo Liu
Zengren Zhao
author_facet Haobo Wang
Fangjian Shang
Yifang Wang
Bo Pang
Bo Pang
Longfei Kang
Longfei Kang
Chuanmin Zhou
Chuanmin Zhou
Dongyun Li
Dongyun Li
Zhongxin Li
Zhongxin Li
Xia Jiang
Xia Jiang
Bo Liu
Zengren Zhao
author_sort Haobo Wang
collection DOAJ
description IntroductionIn thyroid carcinoma (TC), follicular thyroid carcinoma (FTC) represents the second most prevalent pathological type following papillary thyroid carcinoma. Notably, FTC exhibits a more aggressive clinical course and a higher propensity for distant metastasis. However, the underlying mechanisms governing the progression of FTC remain poorly understood. PMAIP1 is a gene implicated in various cancers and biological processes. Investigating the role and mechanism of PMAIP1 in FTC is crucial for enhancing our understanding of FTC and informing clinical treatment strategies. MethodsThis study examined the expression level of PMAIP1 in FTC through comprehensive analysis of databases, tumor tissues, and cell lines. Following the establishment of a stably transfected plasmid in cell lines, a series of functional assays and subcutaneous xenograft experiment were conducted to investigate the role of PMAIP1 in FTC. Additionally, transcriptome sequencing was employed to identify potential signaling pathways associated with PMAIP1. Mechanistic studies involved a series of rescue experiments to elucidate the regulatory mechanisms of PMAIP1 in FTC. ResultsPMAIP1 was found to be highly expressed in FTC, and its knockdown significantly inhibited the proliferation and metastasis of FTC cells both in vivo and in vitro. The results of transcriptome sequencing analysis indicated that PMAIP1 may influence the progression of FTC via the Wnt signaling pathway. Subsequent investigations revealed a direct correlation between PMAIP1 expression levels and those of Wnt3 and FOSL1 in FTC. A series of rescue experiments further substantiated the regulatory role of PMAIP1 on Wnt3/FOSL1 in FTC. DiscussionIn conclusion, our research demonstrated that PMAIP1 emerges as a novel pro-cancer factor in FTC, and its knockdown significantly inhibited the proliferation and metastasis of FTC both in vivo and in vitro. Mechanistically, PMAIP1 regulated FOSL1 by modulating the Wnt signaling pathway, thereby promoting FTC progression. Targeting PMAIP1 may present a promising therapeutic strategy for FTC.
format Article
id doaj-art-7323e15ebb8541409d2a3180b5bce2d9
institution Kabale University
issn 2234-943X
language English
publishDate 2025-01-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Oncology
spelling doaj-art-7323e15ebb8541409d2a3180b5bce2d92025-01-29T06:46:11ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2025-01-011510.3389/fonc.2025.15023911502391PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathwayHaobo Wang0Fangjian Shang1Yifang Wang2Bo Pang3Bo Pang4Longfei Kang5Longfei Kang6Chuanmin Zhou7Chuanmin Zhou8Dongyun Li9Dongyun Li10Zhongxin Li11Zhongxin Li12Xia Jiang13Xia Jiang14Bo Liu15Zengren Zhao16Department of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaGastrointestinal Disease Diagnosis and Treatment Center, Hebei Key Laboratory of Colorectal Cancer Precision Diagnosis and Treatment, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaGastrointestinal Disease Diagnosis and Treatment Center, Hebei Key Laboratory of Colorectal Cancer Precision Diagnosis and Treatment, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaGastrointestinal Disease Diagnosis and Treatment Center, Hebei Key Laboratory of Colorectal Cancer Precision Diagnosis and Treatment, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaGastrointestinal Disease Diagnosis and Treatment Center, Hebei Key Laboratory of Colorectal Cancer Precision Diagnosis and Treatment, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaGastrointestinal Disease Diagnosis and Treatment Center, Hebei Key Laboratory of Colorectal Cancer Precision Diagnosis and Treatment, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaGastrointestinal Disease Diagnosis and Treatment Center, Hebei Key Laboratory of Colorectal Cancer Precision Diagnosis and Treatment, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaDepartment of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, ChinaIntroductionIn thyroid carcinoma (TC), follicular thyroid carcinoma (FTC) represents the second most prevalent pathological type following papillary thyroid carcinoma. Notably, FTC exhibits a more aggressive clinical course and a higher propensity for distant metastasis. However, the underlying mechanisms governing the progression of FTC remain poorly understood. PMAIP1 is a gene implicated in various cancers and biological processes. Investigating the role and mechanism of PMAIP1 in FTC is crucial for enhancing our understanding of FTC and informing clinical treatment strategies. MethodsThis study examined the expression level of PMAIP1 in FTC through comprehensive analysis of databases, tumor tissues, and cell lines. Following the establishment of a stably transfected plasmid in cell lines, a series of functional assays and subcutaneous xenograft experiment were conducted to investigate the role of PMAIP1 in FTC. Additionally, transcriptome sequencing was employed to identify potential signaling pathways associated with PMAIP1. Mechanistic studies involved a series of rescue experiments to elucidate the regulatory mechanisms of PMAIP1 in FTC. ResultsPMAIP1 was found to be highly expressed in FTC, and its knockdown significantly inhibited the proliferation and metastasis of FTC cells both in vivo and in vitro. The results of transcriptome sequencing analysis indicated that PMAIP1 may influence the progression of FTC via the Wnt signaling pathway. Subsequent investigations revealed a direct correlation between PMAIP1 expression levels and those of Wnt3 and FOSL1 in FTC. A series of rescue experiments further substantiated the regulatory role of PMAIP1 on Wnt3/FOSL1 in FTC. DiscussionIn conclusion, our research demonstrated that PMAIP1 emerges as a novel pro-cancer factor in FTC, and its knockdown significantly inhibited the proliferation and metastasis of FTC both in vivo and in vitro. Mechanistically, PMAIP1 regulated FOSL1 by modulating the Wnt signaling pathway, thereby promoting FTC progression. Targeting PMAIP1 may present a promising therapeutic strategy for FTC.https://www.frontiersin.org/articles/10.3389/fonc.2025.1502391/fullfollicular thyroid carcinomaPMAIP1Wnt3FOSL1progression
spellingShingle Haobo Wang
Fangjian Shang
Yifang Wang
Bo Pang
Bo Pang
Longfei Kang
Longfei Kang
Chuanmin Zhou
Chuanmin Zhou
Dongyun Li
Dongyun Li
Zhongxin Li
Zhongxin Li
Xia Jiang
Xia Jiang
Bo Liu
Zengren Zhao
PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathway
Frontiers in Oncology
follicular thyroid carcinoma
PMAIP1
Wnt3
FOSL1
progression
title PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathway
title_full PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathway
title_fullStr PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathway
title_full_unstemmed PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathway
title_short PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathway
title_sort pmaip1 regulates the progression of follicular thyroid carcinoma through the wnt3 fosl1 pathway
topic follicular thyroid carcinoma
PMAIP1
Wnt3
FOSL1
progression
url https://www.frontiersin.org/articles/10.3389/fonc.2025.1502391/full
work_keys_str_mv AT haobowang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT fangjianshang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT yifangwang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT bopang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT bopang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT longfeikang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT longfeikang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT chuanminzhou pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT chuanminzhou pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT dongyunli pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT dongyunli pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT zhongxinli pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT zhongxinli pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT xiajiang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT xiajiang pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT boliu pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway
AT zengrenzhao pmaip1regulatestheprogressionoffollicularthyroidcarcinomathroughthewnt3fosl1pathway