CBX3 promotes tumor proliferation by regulating G1/S phase via p21 downregulation and associates with poor prognosis in tongue squamous cell carcinoma

Zhang, Hua Yong; Chen, Wei Chao; Xiao, Fu; Su, Xuan; Yang, Ankui

doi:10.1016/j.gene.2018.02.043

Cited by 38 publications

(28 citation statements)

References 21 publications

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“…Further study demonstrated that CBX3 can suppress the transcription of CDK6 and p21, the negative cell cycle regulators, and promote proliferation of colorectal cancer cells [ 13 ]. Similar observation was obtained in tongue squamous cell carcinoma, in which overexpression of CBX3 inhibited p21 and promoted G1/S cell cycle transition [ 14 ]. In addition, CBX3 was found overexpressed in breast cancer and non-small cell lung cancer tissues, and its expression may predict the poor prognosis of patients with these cancers [ 15 , 16 ].…”

Section: Introductionsupporting

confidence: 82%

Overexpression of CBX3 in Pancreatic Adenocarcinoma Promotes Cell Cycle Transition-Associated Tumor Progression

Chen

Cheng

et al. 2018

IJMS

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Background: Previous studies showed that Chromobox protein homolog 3 (CBX3) was overexpressed in several types of human cancers, however its pattern and role in pancreatic adenocarcinoma (PAAD) has not yet been understood. The aim of this study was to identify the expression and function of CBX3 in PAAD. Methods: Data of transcriptomic and protein expression of CBX3 in PAAD were collected from different databases and analyzed. The in vitro and in vivo role of CBX3 in PAAD was examined. Results: CBX3 was overexpressed in human PAAD tissues, which was associated with poor prognosis of overall and disease-free survival of the patients. Overexpression of CBX3 induced the in vitro proliferation, anchorage-free growth, migration and invasion of the PAAD cells, and led to in vivo growth of orthotoptic PAAD tumors in mice. GO and KEGG pathway analysis, as well as experimental observation showed that CBX3 may be associated with cell cycle transition of PAAD cells, and cyclin-dependent kinase 1 (CDK1) and proliferating cell nuclear antigen (PCNA) may mediate the tumor-promoting action of CBX3. CDK1 knockdown attenuated the cell cycle transition, proliferation and invasion of CBX3-overexpressing PAAD cells. Conclusion: Our findings suggest the tumor-promoting role of CBX3 in PAAD to be targeted by novel therapeutic strategies.

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Section: Introductionsupporting

confidence: 82%

Overexpression of CBX3 in Pancreatic Adenocarcinoma Promotes Cell Cycle Transition-Associated Tumor Progression

Chen

Cheng

et al. 2018

IJMS

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“…Elevated expression of CBX3 was found in prostate cancer [14] , breast cancer [15] , lung cancer and colorectal cancer [16] . Overexpression of CBX3 was correlated with poor prognosis in tongue squamous cell carcinoma [17] , non-small cell lung cancer [18] and prostate cancer [14] . Increased CBX5 expression was reported in prostate cancer [19] , [20] and breast cancer [15] .…”

Section: Discussionmentioning

confidence: 98%

CBX1 Indicates Poor Outcomes and Exerts Oncogenic Activity in Hepatocellular Carcinoma

Yang

Pan

Qing

et al. 2018

Translational Oncology

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Dysregulation of chromobox proteins contributes to the progression of human diseases. CBX1 has been implicated in epigenetic control of chromatin structure and gene expression, but its role in human cancers remains largely unknown. Here we show that CBX1 exhibits oncogenic activities in hepatocellular carcinoma (HCC) and indicates poor outcomes. The expression of CBX1 was noticeably increased, at both mRNA and protein levels, in HCC tissues and cell lines, compared with the nontumorous ones. High CBX1 expression was significantly associated with larger tumor size, poor tumor differentiation and tumor vascular invasion. Patients with elevated expression of CBX1 were frequently accompanied with unfavorable overall and disease-free survivals in two independent cohorts consisting of 648 HCC cases. The prognostic value of CBX1 was further confirmed by stratified survival analyses. Multivariate cox regression model suggested CBX1 as an independent factor for overall survival (hazard ratio = 1.735, 95% confident interval: 1.342–2.244, P < .001). In vitro data demonstrated that CBX1 overexpression promoted cell proliferation and migration, whereas the knockdown of CBX1 resulted in the opposite phenotypes. Mechanistically, CBX1 interacted with transcription factor HMGA2 to activate the Wnt/β-Catenin signaling pathway. Suppression of β-Catenin by siRNA or specific inhibitor XAV-939 markedly attenuated CBX1-mediated cell growth. Collectively, our findings indicate that CBX1 functions as an oncogene and may serve as a potential prognostic biomarker in HCC.

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“…p21 is one of the most important cyclin-dependent kinases and regulates cell cycle transition from the G 1 to the S phase (28). A previous study by Zhang et al (29) demonstrated that downregulation of p21 was closely associated with poor prognosis in patients with TSCC. Collectively, this indicates that the inhibitory effect of lncRNA PCAT-1 knockdown in TSCC is, at least in part associated with the induction of p21 expression.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of long non‑coding RNA prostate cancer‑associated transcript 1 inhibits the proliferation and metastasis of tongue squamous cell carcinoma cells by upregulating p21

Yan

Zhao²,

et al. 2020

Oncol Lett

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Long non-coding RNA (lncRNA) prostate cancer-associated transcript 1 (PCAT-1) is a long non-coding RNA involved in the development of various cancer types. Tongue squamous cell carcinoma (TSCC) is the most frequently diagnosed type of oral cancer worldwide. The present study aimed to explore the role of lncRNA PCAT-1 in TSCC, and to provide a preliminary assessment of the downstream pathways involved. The expression levels of lncRNA PCAT-1 in TSCC specimens were first assessed. Subsequently, lncRNA PCAT-1 was knocked down in TSCC cell lines and the resulting effect on the proliferation and apoptosis, as well as the metastatic and invasive potential of TSCC cells was investigated. To assess the downstream signaling resulting from lncRNA PCAT-1 inhibition, the expression of p21 was also detected. The results indicated that lncRNA PCAT-1 was upregulated in clinical TSCC compared with peri-tumor tissues. Inhibition of lncRNA PCAT-1 resulted in reduced proliferation and apoptosis of TSCC cells, in addition to the suppression of migration and invasion. Furthermore, the expression of p21 was induced following lncRNA PCAT-1 inhibition. Collectively, the present study demonstrated an oncogenic role for lncRNA PCAT-1 in TSCC; inhibition of lncRNA PCAT-1 reduced the growth, metastasis and invasion of TSCC, at least in part via the induction of p21 signaling.

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CBX3 promotes tumor proliferation by regulating G1/S phase via p21 downregulation and associates with poor prognosis in tongue squamous cell carcinoma

Cited by 38 publications

References 21 publications

Overexpression of CBX3 in Pancreatic Adenocarcinoma Promotes Cell Cycle Transition-Associated Tumor Progression

Overexpression of CBX3 in Pancreatic Adenocarcinoma Promotes Cell Cycle Transition-Associated Tumor Progression

CBX1 Indicates Poor Outcomes and Exerts Oncogenic Activity in Hepatocellular Carcinoma

Knockdown of long non‑coding RNA prostate cancer‑associated transcript 1 inhibits the proliferation and metastasis of tongue squamous cell carcinoma cells by upregulating p21

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