Tescalcin promotes highly invasive papillary thyroid microcarcinoma by regulating FOS/ERK signaling pathway

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Abstract

Background

Part of papillary thyroid microcarcinoma (PTMC) has a high risk of tumor invasion and metastasis, which may occur in the regional lymph node metastasis or distant metastasis, severely threatening the life of patients. Invasion and metastasis are tightly involved in the proliferation, migration and invasion in cancer. This study aimed to investigate the role of tescalcin (TESC) in the proliferation, migration and invasion of PTMC.

Methods

The expressions of TESC in PTMC tissues and cells were detected by immunohistochemistry or qRT-PCR. Then, TPC-1 and BHT101 cells transfected with TESC-RNAi were used for the transcriptome sequencing. The proliferation, apoptosis, migration and invasion of TPC-1 and BHT101 cells were detected by CCK-8, colony formation, flow cytometric assay, transwell migration and scratch test. Moreover, TESC-RNAi transfected TPC-1 and BHT101 cells were subcutaneously injected into mice. Tumor volume and weight were calculated, and the positive rate of Ki-67 was determined by immunohistochemistry. Finally, the levels of c-Fos, ERK1/2 and p-ERK1/2 were determined by western blot.

Results

The expressions of TESC in PTMC tissues and cell lines were prominently enhanced. Transcriptome sequencing results showed that c-Fos was decreased in TPC-1 and BHT101 cells transfected with TESC-RNAi, which was associated with multiple different signaling pathways including the MAPK signaling pathway. Furthermore, TESC promoted the progress of PTMC by regulating the expression of c-Fos, which might be associated with the ERK signaling pathway.

Conclusions

TESC promoted the growth and metastasis of PTMC through regulating c-Fos/ERK1/2.

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Most cited references 32

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KEGG: integrating viruses and cellular organisms

Minoru Kanehisa, Miho Furumichi, Yoko Sato … (2020)

Abstract KEGG (https://www.kegg.jp/) is a manually curated resource integrating eighteen databases categorized into systems, genomic, chemical and health information. It also provides KEGG mapping tools, which enable understanding of cellular and organism-level functions from genome sequences and other molecular datasets. KEGG mapping is a predictive method of reconstructing molecular network systems from molecular building blocks based on the concept of functional orthologs. Since the introduction of the KEGG NETWORK database, various diseases have been associated with network variants, which are perturbed molecular networks caused by human gene variants, viruses, other pathogens and environmental factors. The network variation maps are created as aligned sets of related networks showing, for example, how different viruses inhibit or activate specific cellular signaling pathways. The KEGG pathway maps are now integrated with network variation maps in the NETWORK database, as well as with conserved functional units of KEGG modules and reaction modules in the MODULE database. The KO database for functional orthologs continues to be improved and virus KOs are being expanded for better understanding of virus-cell interactions and for enabling prediction of viral perturbations.

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ERK/MAPK signalling pathway and tumorigenesis

Yan-Jun Guo, Wei-Wei Pan, Sheng-Bing Liu … (2020)

Mitogen-activated protein kinase (MAPK) cascades are key signalling pathways that regulate a wide variety of cellular processes, including proliferation, differentiation, apoptosis and stress responses. The MAPK pathway includes three main kinases, MAPK kinase kinase, MAPK kinase and MAPK, which activate and phosphorylate downstream proteins. The extracellular signal-regulated kinases ERK1 and ERK2 are evolutionarily conserved, ubiquitous serine-threonine kinases that regulate cellular signalling under both normal and pathological conditions. ERK expression is critical for development and their hyperactivation plays a major role in cancer development and progression. The Ras/Raf/MAPK (MEK)/ERK pathway is the most important signalling cascade among all MAPK signal transduction pathways, and plays a crucial role in the survival and development of tumour cells. The present review discusses recent studies on Ras and ERK pathway members. With respect to processes downstream of ERK activation, the role of ERK in tumour proliferation, invasion and metastasis is highlighted, and the role of the ERK/MAPK signalling pathway in tumour extracellular matrix degradation and tumour angiogenesis is emphasised.

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Electrical and synaptic integration of glioma into neural circuits

Humsa S. Venkatesh, Wade Morishita, Anna C. Geraghty … (2019)

High-grade gliomas are lethal brain cancers whose progression is robustly regulated by neuronal activity. Activity-regulated growth factor release promotes glioma growth, but this alone is insufficient to explain the effect that activity exerts on glioma progression. Here, we use single-cell transcriptomics, electron microscopy, whole-cell patch-clamp electrophysiology and calcium imaging to demonstrate that neuron-glioma interactions include electrochemical communication through bona fide AMPA receptor-dependent neuron-glioma synapses. Neuronal activity also evokes non-synaptic activity-dependent potassium currents that are amplified through gap junction-mediated tumor interconnections forming an electrically-coupled network. Glioma membrane depolarization assessed with in vivo optogenetics promotes proliferation, while pharmacologically or genetically blocking electrochemical signaling inhibits glioma xenograft growth and extends mouse survival. Emphasizing positive feedback mechanisms by which gliomas increase neuronal excitability and thus activity-regulated glioma growth, human intraoperative electrocorticography demonstrates increased cortical excitability in glioma-infiltrated brain. Together, these findings indicate that synaptic and electrical integration in neural circuits promotes glioma progression.

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Author and article information

Contributors

Yanping Gong: gongyanping@wchscu.cn

Journal

Journal ID (nlm-ta): BMC Cancer

Journal ID (iso-abbrev): BMC Cancer

Title: BMC Cancer

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2407

Publication date (Electronic): 31 May 2022

Publication date PMC-release: 31 May 2022

Publication date Collection: 2022

Volume: 22

Electronic Location Identifier: 595

Affiliations

[1 ]GRID grid.13291.38, ISNI 0000 0001 0807 1581, Thyroid and Parathyroid Surgery Center, West China Hospital, , Sichuan University, ; No. 37 Guo Xue Xiang, Chengdu, 610041 Sichuan China

[2 ]GRID grid.13291.38, ISNI 0000 0001 0807 1581, West China School of Medicine, , Sichuan University, ; Chengdu, China

[3 ]GRID grid.13291.38, ISNI 0000 0001 0807 1581, Department of pathology, West China Hospital, , Sichuan University, ; Chengdu, China

Article

Publisher ID: 9643

DOI: 10.1186/s12885-022-09643-9

PMC ID: 9158259

PubMed ID: 35641944

SO-VID: 82e97044-5997-4dbd-8703-ca4b2288b3e2

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 6 September 2021

Date accepted : 5 May 2022

Custom metadata

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: tescalcin,papillary thyroid microcarcinoma,invasion,metastasis,fos,erk1/2

Data availability:

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: tescalcin, papillary thyroid microcarcinoma, invasion, metastasis, fos, erk1/2

Tescalcin promotes highly invasive papillary thyroid microcarcinoma by regulating FOS/ERK signaling pathway

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Abstract

Background

Methods

Results

Conclusions

Related collections

Karger: Oncology

Most cited references 32

KEGG: integrating viruses and cellular organisms

ERK/MAPK signalling pathway and tumorigenesis

Electrical and synaptic integration of glioma into neural circuits

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