METTL14-mediated m6A modification upregulated SOCS3 expression alleviates thyroid cancer progression by regulating the JAK2/STAT3 pathway

Thyroid cancer (TC) is the most common malignant tumor of the head and neck. As a common epigenetic modification in mRNAs, N6-methyladenosine (m6A) modification plays critical roles in biological process of cancers. However, m6A methyltransferase methyltransferase-like 14 (METTL14)-mediated m6A modi...

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Main Authors: Ming Zhou, Yaqi Zhang, Qiong Zhang, Yanchu Tong
Format: Article
Language:English
Published: Elsevier 2024-12-01
Series:Molecular and Cellular Probes
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Online Access:http://www.sciencedirect.com/science/article/pii/S0890850824000392
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author Ming Zhou
Yaqi Zhang
Qiong Zhang
Yanchu Tong
author_facet Ming Zhou
Yaqi Zhang
Qiong Zhang
Yanchu Tong
author_sort Ming Zhou
collection DOAJ
description Thyroid cancer (TC) is the most common malignant tumor of the head and neck. As a common epigenetic modification in mRNAs, N6-methyladenosine (m6A) modification plays critical roles in biological process of cancers. However, m6A methyltransferase methyltransferase-like 14 (METTL14)-mediated m6A modification and its potential regulatory mechanisms in TC are not fully elucidated. In our study, we observed that METTL14 was decreased in TC tissues and cells. And upregulation of METTL14 induced apoptotic cell death and hampered cell proliferation, epithelial mesenchymal transition (EMT) and tumor growth in vitro and in vivo. Mechanistically, METTL14 increased the expression of suppressor of cytokine signaling 3 (SOCS3) through m6A methylation modification, and knockdown of SOCS3 reversed the inhibitory effect of overexpressing METTL14 on TC tumorigenesis. In addition, METTL14-mediated m6A modification of SOCS3 inactivated the janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway, and in the METTL14-overexpressing TC cells, silencing SOCS3-induced upregulation of cell proliferation, EMT and suppression of apoptosis was reversed by JAK2/STAT3 inhibitor AG490 and WP1066. Together, we indicated that METTL14/m6A/SOCS3/JAK2/STAT3 axis play an important role in the progression of TC.
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spelling doaj-art-23fc2af8d82c4ffdb4c89aa60f858f8d2024-12-17T04:58:48ZengElsevierMolecular and Cellular Probes0890-85082024-12-0178101987METTL14-mediated m6A modification upregulated SOCS3 expression alleviates thyroid cancer progression by regulating the JAK2/STAT3 pathwayMing Zhou0Yaqi Zhang1Qiong Zhang2Yanchu Tong3Department of Thyroid Vascular Surgery, Jingzhou Central Hospital, Jingzhou Hospital Affiliated to Yangtze University, Jingzhou, 434000, China; Corresponding author. Department of Thyroid Vascular Surgery, Jingzhou Central Hospital, Jingzhou Hospital Affiliated to Yangtze University, No. 26, Chuyuan Avenue, Jingzhou District, Jingzhou, Hubei, 434000, China.Department of Oncology, Huanggang Central Hospital, Huanggang, 438000, ChinaDepartment of Dermatology, Jingzhou Central Hospital, Jingzhou Hospital Affiliated to Yangtze University, Jingzhou, 434000, ChinaDepartment of Thyroid Vascular Surgery, Jingzhou Central Hospital, Jingzhou Hospital Affiliated to Yangtze University, Jingzhou, 434000, ChinaThyroid cancer (TC) is the most common malignant tumor of the head and neck. As a common epigenetic modification in mRNAs, N6-methyladenosine (m6A) modification plays critical roles in biological process of cancers. However, m6A methyltransferase methyltransferase-like 14 (METTL14)-mediated m6A modification and its potential regulatory mechanisms in TC are not fully elucidated. In our study, we observed that METTL14 was decreased in TC tissues and cells. And upregulation of METTL14 induced apoptotic cell death and hampered cell proliferation, epithelial mesenchymal transition (EMT) and tumor growth in vitro and in vivo. Mechanistically, METTL14 increased the expression of suppressor of cytokine signaling 3 (SOCS3) through m6A methylation modification, and knockdown of SOCS3 reversed the inhibitory effect of overexpressing METTL14 on TC tumorigenesis. In addition, METTL14-mediated m6A modification of SOCS3 inactivated the janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway, and in the METTL14-overexpressing TC cells, silencing SOCS3-induced upregulation of cell proliferation, EMT and suppression of apoptosis was reversed by JAK2/STAT3 inhibitor AG490 and WP1066. Together, we indicated that METTL14/m6A/SOCS3/JAK2/STAT3 axis play an important role in the progression of TC.http://www.sciencedirect.com/science/article/pii/S0890850824000392Thyroid cancerMethyltransferase-like 14 (METTL14)N6-methyladenosine (m6A)Suppressor of cytokine signaling 3 (SOCS3)
spellingShingle Ming Zhou
Yaqi Zhang
Qiong Zhang
Yanchu Tong
METTL14-mediated m6A modification upregulated SOCS3 expression alleviates thyroid cancer progression by regulating the JAK2/STAT3 pathway
Molecular and Cellular Probes
Thyroid cancer
Methyltransferase-like 14 (METTL14)
N6-methyladenosine (m6A)
Suppressor of cytokine signaling 3 (SOCS3)
title METTL14-mediated m6A modification upregulated SOCS3 expression alleviates thyroid cancer progression by regulating the JAK2/STAT3 pathway
title_full METTL14-mediated m6A modification upregulated SOCS3 expression alleviates thyroid cancer progression by regulating the JAK2/STAT3 pathway
title_fullStr METTL14-mediated m6A modification upregulated SOCS3 expression alleviates thyroid cancer progression by regulating the JAK2/STAT3 pathway
title_full_unstemmed METTL14-mediated m6A modification upregulated SOCS3 expression alleviates thyroid cancer progression by regulating the JAK2/STAT3 pathway
title_short METTL14-mediated m6A modification upregulated SOCS3 expression alleviates thyroid cancer progression by regulating the JAK2/STAT3 pathway
title_sort mettl14 mediated m6a modification upregulated socs3 expression alleviates thyroid cancer progression by regulating the jak2 stat3 pathway
topic Thyroid cancer
Methyltransferase-like 14 (METTL14)
N6-methyladenosine (m6A)
Suppressor of cytokine signaling 3 (SOCS3)
url http://www.sciencedirect.com/science/article/pii/S0890850824000392
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