GINS2 affects cell proliferation, apoptosis, migration and invasion in thyroid cancer via regulating MAPK signaling pathway

He, Saifei; Zhang, Miao; Ye, Ying; Song, Yanan; Ma, Xing; Wang, Guoyu; Zhuang, Juhua; Xia, Weiya; Zhao, Bin

doi:10.3892/mmr.2021.11885

Cited by 6 publications

(7 citation statements)

References 39 publications

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“…Accumulated evidence reports that the MAPK pathway is activated in TC and is involved in tumor immune escape 24,25,41 . Through KEGG pathway enrichment analysis, it was found that DEGs were primarily enriched in the MAPK pathway.…”

Section: Discussionmentioning

confidence: 97%

“…Accumulated evidence reports that the MAPK pathway is activated in TC and is involved in tumor immune escape. 24,25,41 Through KEGG pathway enrichment analysis, it was found that DEGs were primarily enriched in the MAPK pathway. Among these DEGs, KIT was not only located upstream of the MAPK pathway but also had the largest differential change multiple in the chip.…”

Section: Discussionmentioning

confidence: 99%

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Mechanism of immune escape mediated by receptor tyrosine kinase KIT in thyroid cancer

Luo

et al. 2023

Immunity Inflam & Disease

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Objective Thyroid cancer (TC) is one of the fastest‐growing malignant tumors. This study sought to explore the mechanism of immune escape mediated by receptor tyrosine kinase (KIT) in TC. Methods The expression microarray of TC was acquired through the GEO database, and the difference analysis and Kyoto encyclopedia of genes and genomes pathway enrichment analysis were carried out. KIT levels in TC cell lines (K1/SW579/BCPAP) and human normal thyroid cells were detected using reverse transcription quantitative polymerase chain reaction and western blot analysis. TC cells were transfected with overexpressed (oe)‐KIT and CD8+ T cells were cocultured with SW579 cells. Subsequently, cell proliferation, migration, and invasion abilities, CD8+ T cell proliferation, cytokine levels (interferon‐γ [IFN‐γ]/tumor necrosis factor‐α [TNF‐α]) were determined using colony formation assay, Transwell assays, flow cytometry, and enzyme‐linked immunosorbent assay. The phosphorylation of MAPK pathway‐related protein (ERK) was measured by western blot analysis. After transfection with oe‐KIT, cells were treated with anisomycin (an activator of the MAPK pathway), and the protein levels of p‐ERK/ERK and programmed death‐ligand 1 (PD‐L1) were detected. Results Differentially expressed genes (N = 2472) were obtained from the GEO database. KIT was reduced in TC samples and lower in tumor cells than those in normal cells. Overexpression of KIT inhibited immune escape of TC cells. Specifically, the proliferation, migration, and invasion abilities of TC cells were lowered, the proliferation level of CD8+ T cells was elevated, and IFN‐γ and TNF‐α levels were increased. KIT inhibited the activation of the MAPK pathway in TC cells and downregulated PD‐L1. Conclusion KIT suppressed immune escape of TC by blocking the activation of the MAPK pathway and downregulating PD‐L1.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Mechanism of immune escape mediated by receptor tyrosine kinase KIT in thyroid cancer

Luo

et al. 2023

Immunity Inflam & Disease

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“…The results show that GINS2 expression is increased in most tumors compared to normal tissues and correlates with various clinicopathological features. It has been demonstrated that GINS2 is expressed at higher levels in tumor tissue than in adjacent normal tissue, such as in CC[ 3 ], gastric adenocarcinoma[ 6 ], glioma[ 7 ], NSCLC[ 8 , 9 ], pancreatic cancer[ 10 , 11 ], and thyroid cancer (TC)[ 12 , 13 ]. Specifically, analysis of potential correlations between GINS2 expression levels and clinicopathological features has indicated that high GINS2 expression levels are closely associated with tumor size[ 6 , 10 ], tumor nodal metastasis (TNM) stage[ 6 , 8 ], pathological grade[ 7 ] and vascular permeation[ 10 ].…”

Section: Expression Profiles Of Gins2 In Cancersmentioning

confidence: 99%

“…In most tumors, elevated levels of GINS2 expression can increase malignant features such as tumor cell proliferation[ 3 - 7 ], migration[ 8 , 13 , 14 ], invasion[ 8 , 13 ], epithelial-mesenchymal transition (EMT)[ 8 , 10 ], anti-apoptosis effects[ 12 - 16 ] and cell cycle arrest[ 7 , 9 , 11 , 12 ], as shown in Figure 2 , which are related to the many mechanisms GINS2 is involved in, as shown in Figure 3 and Table 2 .…”

Section: Molecular Pathways Involved In Gins2mentioning

confidence: 99%

“…Ye et al [ 12 ] found that GINS2 plays a role in TC cell proliferation and apoptosis by regulating the expression of CITED2 and LOXL2 in TC cells. He et al [ 13 ] reported that GINS2 plays a vital role in the survival, migration and invasion of TC cells and regulates the MAPK signaling pathway. GINS2 may be a potential biomarker for TC diagnosis or prognosis and a drug target for treatment.…”

Section: Molecular Pathways Involved In Gins2mentioning

confidence: 99%

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Go-Ichi-Ni-San 2: A potential biomarker and therapeutic target in human cancers

Shan¹,

Zheng²,

Chen³

2022

World J Gastrointest Oncol

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Cancer incidence and mortality are increasing globally, leading to its rising status as a leading cause of death. The Go-Ichi-Ni-San (GINS) complex plays a crucial role in DNA replication and the cell cycle. The GINS complex consists of four subunits encoded by the GINS1, GINS2, GINS3, and GINS4 genes. Recent findings have shown that GINS2 expression is upregulated in many diseases, particularly tumors. For example, increased GINS2 expression has been found in cervical cancer, gastric adenocarcinoma, glioma, non-small cell lung cancer, and pancreatic cancer. It correlates with the clinicopathological characteristics of the tumors. In addition, high GINS2 expression plays a pro-carcinogenic role in tumor development by promoting tumor cell proliferation and migration, inhibiting tumor cell apoptosis, and blocking the cell cycle. This review describes the upregulation of GINS2 expression in most human tumors and the pathway of GINS2 in tumor development. GINS2 may serve as a new marker for tumor diagnosis and a new biological target for therapy.

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Isoglutaminyl Cyclase Overexpression Enhances KYSE30 Cancer Cell Proliferation and Migration via the MAPK Signaling Pathway

Chen,

Yu,

Cui

et al. 2024

J. Proteome Res.

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To understand how upregulated isoglutaminyl cyclase (isoQC) is involved in the initiation of diseases such as cancer, we developed a human KYSE30 carcinoma cell model in which isoQC was stably overexpressed. GO and KEGG analysis of the DEGs (228) and DEPs (254) respectively implicated isoQC on the proliferation invasion and metastasis of cells and suggested that isoQC might participate in the regulation of MAPK, RAS, circadian rhythm, and related pathways. At the functional level, isoQCoverexpressing KYSE30 cells showed enhanced proliferation, migration, and invasion capacity. Next, we decided to study the precise effect of isoQC overexpression on JNK, p-JNK, AKT, p-AKT, ERK, p-ERK, and PER2, as RNA levels of these proteins are significantly correlated with signal levels indicated in RNA-Seq analysis, and these candidates are the top correlated DEPs enriched in RT-qPCR analysis. We saw that only p-ERK expression was inhibited, while PER2 was increased. These phenotypes were inhibited upon exposure to PER2 inhibitor KL044, which allowed for the restoration of p-ERK levels. These data support upregulated isoQC being able to promote cancer cell proliferation and migration in vitro, likely by helping to regulate the MAPK and RAS signaling pathways, and the circadian protein PER2 might be a potential mediator.

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GINS2 affects cell proliferation, apoptosis, migration and invasion in thyroid cancer via regulating MAPK signaling pathway

Cited by 6 publications

References 39 publications

Mechanism of immune escape mediated by receptor tyrosine kinase KIT in thyroid cancer

Mechanism of immune escape mediated by receptor tyrosine kinase KIT in thyroid cancer

Go-Ichi-Ni-San 2: A potential biomarker and therapeutic target in human cancers

Isoglutaminyl Cyclase Overexpression Enhances KYSE30 Cancer Cell Proliferation and Migration via the MAPK Signaling Pathway

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