A signature of circadian rhythm genes in driving anaplastic thyroid carcinoma malignant progression

Xu, Tong; Jin, Tiefeng; Lu, Xixuan; Pan, Zongfu; Tan, Zhuo; Zheng, Chuanming; Liu, Yujia; Hu, Xiaoping; Ba, Lisha; Ren, Hao; Chen, Jin‐Ming; Zhu, Chaozhuang; Ge, Minghua; Huang, Ping

doi:10.1016/j.cellsig.2022.110332

Cited by 11 publications

(18 citation statements)

References 46 publications

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“…The main results of the literature search are summarized in Table 1 . These indicated that each of the circadian clock genes mentioned in the Introduction was tested at least once in thyroid carcinoma between 2013 and 2022 ( Table 1 ) and the results of such testing were reported in nine selected publications, in the pioneer publication of Mannic et al (2013) [ 1 ] and eight following articles authored by Mond et al (2014) [ 2 ], Chitikova et al (2015) [ 3 ], Makhlouf et al (2016) [ 4 ], Gallo et al (2018) [ 5 ], Sadowski et al (2019) [ 6 ], Lou et al (2021) [ 7 ], Xu et al (2022) [ 8 ], and Mou et al (2022) [ 9 ] (article in Chinese with abstract in English). The authors of the nine selected publications interpreted the detected increase and decrease in expression of a gene compared to normal samples as its up- and downregulation, respectively.…”

Section: Resultsmentioning

confidence: 99%

“…The first results pointing to the alternation of expression of circadian clock genes in human malignant thyrocytes were published 10 years ago [ 1 ]. In the following years, further evidence for the association of these genes with thyroid cell oncogenic transformation was gradually accumulating [ 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

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A Review of Evidence for the Involvement of the Circadian Clock Genes into Malignant Transformation of Thyroid Tissue

Putilov

Budkevich

2023

Clocks & Sleep

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(1) Background: In 2013, the results of a pioneer study on abnormalities in the levels and circadian rhythmicity of expression of circadian clock genes in cancerous thyroid nodules was published. In the following years, new findings suggesting the involvement of circadian clockwork dysfunction into malignant transformation of thyroid tissue were gradually accumulating. This systematic review provides an update on existing evidence regarding the association of these genes with thyroid tumorigenesis. (2) Methods: Two bibliographic databases (Scopus and PubMed) were searched for articles from inception to 20 March 2023. The reference lists of previously published (nonsystematic) reviews were also hand-searched for additional relevant studies. (3) Results: Nine studies published between 2013 and 2022 were selected. In total, 9 of 12 tested genes were found to be either up- or downregulated. The list of such genes includes all families of core circadian clock genes that are the key components of three transcriptional–translational feedback loops of the circadian clock mechanism (BMAL1, CLOCK, NPAS2, RORα, REV-ERBα, PERs, CRYs, and DECs). (4) Conclusions: Examination of abnormalities in the levels and circadian rhythmicity of expression of circadian clock genes in thyroid tissue can help to reduce the rate of inadequate differential preoperative diagnosis for thyroid carcinoma.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Review of Evidence for the Involvement of the Circadian Clock Genes into Malignant Transformation of Thyroid Tissue

Putilov

Budkevich

2023

Clocks & Sleep

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“…In accordance with our findings, increased expression of NPAS2 has been suggested to indicate poor survival in lung cancer [ 24 , 25 ]. NPAS2 was overexpressed in anaplastic thyroid carcinoma and facilitated malignant progression [ 26 ]. The oncogenic properties of NPAS2 were associated with its role in promoting the Warburg effect [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Characterization of molecular subtypes based on chromatin regulators and identification of the role of NPAS2 in lung adenocarcinoma

et al. 2023

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Background Chromatin regulators (CRs) are critical epigenetic modifiers and have been reported to play critical roles during the progression of various tumors, but their role in lung adenocarcinoma (LUAD) has not been comprehensively studied. Methods Differential expression and univariate Cox regression analyses were conducted to identify the prognostic CRs. Consensus clustering was applied to classify the subtypes of LUAD based on prognostic CRs. LASSO-multivariate Cox regression method was used for construction of a prognostic signature and development of chromatin regulator-related gene index (CRGI). The capacity of CRGI to distinguish survival was evaluated via Kaplan–Meier method in multiple datasets. Relationship between CRGI and tumor microenvironment (TME) was evaluated. Additionally, clinical variables and CRGI were incorporated to create a nomogram. The role of the prognostic gene NPAS2 in LUAD was elucidated via clinical samples validation and a series of in vitro and in vivo experiments. Results Two subtypes of LUAD were classified based on 46 prognostic CRs via consensus clustering which had significantly different survival and TME. A prognostic signature consisting of six CRs (MOCS, PBK, CBX3, A1CF, NPAS2, and CTCFL) was developed and proved to be an effective survival predictor in multiple independent datasets. The prognostic signature was also demonstrated to be an indicator of TME and sensitivity to immunotherapy and chemotherapy. The nomogram was suggested to be a simple tool that can predict survival accurately. Clinical samples show that NPAS2 is highly expressed in LUAD tissues, and in vitro and in vivo experiments demonstrated that inhibition of NPAS2 impeded malignant progression of LUAD cells. Conclusions Our study comprehensively unveiled the functions of CRs in LUAD, developed a classifier to predict survival and response to treatments, and suggested that NPAS2 promoted LUAD progression for the first time.

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“…Transwell assays and wound healing assays were performed as previously described. 34 For transwell assays, cells treated with siRNA or BAY‐1816032 were plated in the upper transwell chamber in the presence (invasion) or absence (migration) of Matrigel® (Cat. 356234, BD Bioscience, USA).…”

Section: Methodsmentioning

confidence: 99%

BUB1/KIF14 complex promotes anaplastic thyroid carcinoma progression by inducing chromosome instability

Jin,

Ding,

Chen

et al. 2024

J Cellular Molecular Medi

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Chromosome instability (CIN) is a common contributor driving the formation and progression of anaplastic thyroid cancer (ATC), but its mechanism remains unclear. The BUB1 mitotic checkpoint serine/threonine kinase (BUB1) is responsible for the alignment of mitotic chromosomes, which has not been thoroughly studied in ATC. Our research demonstrated that BUB1 was remarkably upregulated and closely related to worse progression‐free survival. Knockdown of BUB1 attenuated cell viability, invasion, migration and induced cell cycle arrests, whereas overexpression of BUB1 promoted the cell cycle progression of papillary thyroid cancer cells. BUB1 knockdown remarkably repressed tumour growth and tumour formation of nude mice with ATC xenografts and suppressed tumour metastasis in a zebrafish xenograft model. Inhibition of BUB1 by its inhibitor BAY‐1816032 also exhibited considerable anti‐tumour activity. Further studies showed that enforced expression of BUB1 evoked CIN in ATC cells. BUB1 induced CIN through phosphorylation of KIF14 at serine1292 (Ser1292). Overexpression of the KIF14ΔSer1292 mutant was unable to facilitate the aggressiveness of ATC cells when compared with that of the wild type. Collectively, these findings demonstrate that the BUB1/KIF14 complex drives the aggressiveness of ATC by inducing CIN.

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A signature of circadian rhythm genes in driving anaplastic thyroid carcinoma malignant progression

Cited by 11 publications

References 46 publications

A Review of Evidence for the Involvement of the Circadian Clock Genes into Malignant Transformation of Thyroid Tissue

A Review of Evidence for the Involvement of the Circadian Clock Genes into Malignant Transformation of Thyroid Tissue

Characterization of molecular subtypes based on chromatin regulators and identification of the role of NPAS2 in lung adenocarcinoma

BUB1/KIF14 complex promotes anaplastic thyroid carcinoma progression by inducing chromosome instability

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