High PLK4 expression promotes tumor progression and induces epithelial‑mesenchymal transition by regulating the Wnt/β‑catenin signaling pathway in colorectal cancer Corrigendum in /10.3892/ijo.2021.5213

Liao, Zhibin; Zhang, Hongwei; Fan, Ping; Huang, Qibo; Dong, Kai; Qi, Yongqiang; Song, Jia; Chen, Lin; Liang, Huifang; Chen, Xiaoping; Zhang, Zhanguo; Zhang, Bixiang

doi:10.3892/ijo.2018.4659

Cited by 45 publications

(12 citation statements)

References 35 publications

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“…In addition, PLK4 is found in various tumor types and has a close connection with cancer patients' outcomes [ 45 , 46 ]. For example, via regulating the Wnt/ β -catenin axis, the elevated PLK4 accelerates colorectal cancer progression and induces epithelial-mesenchymal transition [ 47 ], which is similar to our findings, while conversely, PLK4 downregulation suppresses cell apoptosis, and underexpressed PLK4 is linked to unfavorable prognosis of hepatocellular carcinoma [ 48 ]. Therefore, the role of PLK4 in COAD warrants further study.…”

Section: Discussionsupporting

confidence: 86%

Identification of 9 Gene Signatures by WGCNA to Predict Prognosis for Colon Adenocarcinoma

Yang

Peng

et al. 2022

Computational Intelligence and Neuroscience

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Background. A risk assessment model for prognostic prediction of colon adenocarcinoma (COAD) was established based on weighted gene co-expression network analysis (WGCNA). Methods. From the Cancer Genome Atlas (TCGA) database, RNA-seq data and clinical data of COAD patients were retrieved. After screening of differentially expressed genes (DEGs), WGCNA was performed to identify gene modules and screen those associated with COAD progression. Then, via protein-protein interaction (PPI) network construction of module genes, hub genes were obtained, which were then subjected to the least absolute shrinkage and selection operator (LASSO) and Cox regression to build a hub gene-based prognostic scoring model. The receiver operating characteristic curve (ROC curve) was plotted for the optimal cutoff (OCO) of the risk score, based on which, patients were assigned to high or low-risk groups. Areas under the ROC curve (AUCs) were calculated, and model performance was visualized using Kaplan–Meier (KM) survival curves and verified in the external dataset GSE29621. Finally, the model’s independent prognostic value was evaluated by univariate and multivariate Cox regression analyses, and a nomogram was built. Results. Totally 2840 DEGs were screened from COAD dataset of TCGA, including 1401 upregulated ones and 1439 downregulated ones, which were divided into 10 modules by WGCNA. The eigenvalue of the black module was found to have a high correlation with COAD progression. PPI interaction networks were constructed for genes in the black module, and 34 hub genes were obtained by using the MCODE plug-in. A LASSO-Cox regression approach was utilized to analyze the hub genes, and a prognostic risk score model based on the signatures of 9 genes (CHEK1, DEPDC1B, FANCI, MCM10, NCAPG, PARPBP, PLK4, RAD51AP1, and RFC4) was constructed. KM analysis identified shorter overall lower survival in the high-risk group. The model was verified to have favorable predictive ability through training set and validation set. The nomogram, composed of tumor node metastasis (TNM) staging and risk score, was of good predictability. Conclusions. The COAD prognostic risk model constructed upon the signatures of 9 genes (CHEK1, DEPDC1B, FANCI, MCM10, NCAPG, PARPBP, PLK4, RAD51AP1, and RFC4) can effectively predict the survival status of COAD patients.

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Section: Discussionsupporting

confidence: 86%

Identification of 9 Gene Signatures by WGCNA to Predict Prognosis for Colon Adenocarcinoma

Yang

Peng

et al. 2022

Computational Intelligence and Neuroscience

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“…Centrosomal localization of all PLK isoforms have been reported in humans [ 80 ]. PLK4 is the keystone centrosomal duplication protein and increased expression of PLK4 has been reported in cancers originating from different tissues and organs including colon, stomach, breast, prostate, and brain [ 8 , 81 , 82 , 83 , 84 , 85 ]. By contrast, decreased PLK4 expression is observed in hepatocellular carcinoma [ 86 ] and hematological malignancies [ 87 ].…”

Section: Centrosome Amplification In Tumors and The Causesmentioning

confidence: 99%

Keep Calm and Carry on with Extra Centrosomes

Kalkan

Özcan

Quintyne

et al. 2022

Cancers

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Aberrations in the centrosome number and structure can readily be detected at all stages of tumor progression and are considered hallmarks of cancer. Centrosome anomalies are closely linked to chromosome instability and, therefore, are proposed to be one of the driving events of tumor formation and progression. This concept, first posited by Boveri over 100 years ago, has been an area of interest to cancer researchers. We have now begun to understand the processes by which these numerical and structural anomalies may lead to cancer, and vice-versa: how key events that occur during carcinogenesis could lead to amplification of centrosomes. Despite the proliferative advantages that having extra centrosomes may confer, their presence can also lead to loss of essential genetic material as a result of segregational errors and cancer cells must deal with these deadly consequences. Here, we review recent advances in the current literature describing the mechanisms by which cancer cells amplify their centrosomes and the methods they employ to tolerate the presence of these anomalies, focusing particularly on centrosomal clustering.

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“… 10 The PLK4 enzyme is expressed at low levels in proliferating tissues and has pleiotropic functions in processes related to mitotic progression, including cytokinesis, cell mobility, and DNA damage repair. 11 , 12 Increasing evidence indicates that PLK4 is aberrantly expressed in patient‐derived tumor samples, including colorectal cancer, 13 , 14 breast cancer, 15 , 16 bladder cancer, 17 and melanoma, 18 but is also expressed at low levels in proliferative tissues. 19 , 20 , 21 However, its expression level differs among cancers and proliferative tissues.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of PLK4 expression induces apoptosis and G0/G1‐phase cell cycle arrest in keloid fibroblasts

Huang

Liu

et al. 2022

Cell Proliferation

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Objectives: Keloids are benign fibroproliferative tumors that display many cancer-like characteristics, such as progressive uncontrolled growth, lack of spontaneous regression, and extremely high rates of recurrence. Polo-like kinase 4 (PLK4) was recently identified as a master regulator of centriole replication, and its aberrant expression is closely associated with tumorigenesis. This study aimed to investigate the expression and biological role of PLK4 in the pathogenesis of keloids. Materials and Methods:We evaluated the expression of PLK4 in keloids and adjacent normal skin tissue samples. Then, we established PLK4 knockdown and overexpression cell lines in keloid fibroblasts (KFs) and normal skin fibroblasts (NFs), respectively, to investigate the roles of PLK4 in the regulation of proliferation, migration, invasion, apoptosis, and cell cycle in KFs. Centrinone B (Cen-B), a highly selective PLK4 inhibitor, was used to inhibit PLK4 activity in KFs to evaluate the therapeutic effect on KFs.Results: We discovered that PLK4 was overexpressed in keloid dermal samples and KFs compared with adjacent normal skin samples and NFs derived from the same patients. High PLK4 expression was positively associated with the proliferation, migration, and invasion of KFs. Furthermore, knockdown of PLK4 expression or inhibition of PLK4 activity by Cen-B suppressed KF growth, induced KF apoptosis via the caspase-9/3 pathway, and induced cell cycle arrest at the G0/G1 phase in vitro.Conclusions: These findings demonstrate that PLK4 is a critical regulator of KF proliferation, migration, and invasion, and thus, Cen-B is a promising candidate drug for keloid treatment. | INTRODUCTIONKeloids are benign fibroproliferative reticular dermal tumors of unknown etiopathogenesis that can occur following any dermal injury, leading to an exophytic protuberant outgrowth that invades the adjacent normal skin beyond the original wound boundary. [1][2][3] Keloids are uniquely characterized by their aggressiveness, persistence, and progressive perilesional expansile behaviors. Due to their continued growth and lack of spontaneous regression, patients usually experience intense pain and pruritus, especially for keloid contractures located near the joints, which may lead to serious dysfunction and thus affect patients' physiological and psychological health.

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High PLK4 expression promotes tumor progression and induces epithelial‑mesenchymal transition by regulating the Wnt/β‑catenin signaling pathway in colorectal cancer Corrigendum in /10.3892/ijo.2021.5213

Cited by 45 publications

References 35 publications

Identification of 9 Gene Signatures by WGCNA to Predict Prognosis for Colon Adenocarcinoma

Identification of 9 Gene Signatures by WGCNA to Predict Prognosis for Colon Adenocarcinoma

Keep Calm and Carry on with Extra Centrosomes

Downregulation of PLK4 expression induces apoptosis and G0/G1‐phase cell cycle arrest in keloid fibroblasts

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