Identification of the Roles of Chromobox Family Members in Gastric Cancer: A Study Based on Multiple Datasets

Chen, Zhuoyuan; Sun, Shang-Xing; Zhu, Sixian; Bu, Jie

doi:10.1155/2020/5306509

Cited by 5 publications

(6 citation statements)

References 63 publications

(79 reference statements)

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“…The overexpression of HP1γ in pancreatic DAC promotes cell cycle transition-associated tumor progression [ 70 ]. HP1γ expression is higher in tumor tissues than paired normal tissues in kidney cancer [ 71 ], CRC [ 69 ], gastric cancer [ 72 ], and non-small cell lung cancer [ 73 ]. These unfavorable roles of HP1γ might be caused by its transcriptional activator function [ 74 , 75 ] collaborating with nuclear moonlighting metalloproteinases (MMP) [ 39 , 40 , 76 ] or RNA processing [ 77 ].…”

Section: Discussionmentioning

confidence: 99%

SCAND1 Reverses Epithelial-to-Mesenchymal Transition (EMT) and Suppresses Prostate Cancer Growth and Migration

Eguchi

Csizmadia

Kawai

et al. 2022

Cells

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Epithelial–mesenchymal transition (EMT) is a reversible cellular program that transiently places epithelial (E) cells into pseudo-mesenchymal (M) cell states. The malignant progression and resistance of many carcinomas depend on EMT activation, partial EMT, or hybrid E/M status in neoplastic cells. EMT is activated by tumor microenvironmental TGFβ signal and EMT-inducing transcription factors, such as ZEB1/2, in tumor cells. However, reverse EMT factors are less studied. We demonstrate that prostate epithelial transcription factor SCAND1 can reverse the cancer cell mesenchymal and hybrid E/M phenotypes to a more epithelial, less invasive status and inhibit their proliferation and migration in DU-145 prostate cancer cells. SCAND1 is a SCAN domain-containing protein and hetero-oligomerizes with SCAN-zinc finger transcription factors, such as MZF1, for accessing DNA and the transcriptional co-repression of target genes. We found that SCAND1 expression correlated with maintaining epithelial features, whereas the loss of SCAND1 was associated with mesenchymal phenotypes of tumor cells. SCAND1 and MZF1 were mutually inducible and coordinately included in chromatin with hetero-chromatin protein HP1γ. The overexpression of SCAND1 reversed hybrid E/M status into an epithelial phenotype with E-cadherin and β-catenin relocation. Consistently, the co-expression analysis in TCGA PanCancer Atlas revealed that SCAND1 and MZF1 expression was negatively correlated with EMT driver genes, including CTNNB1, ZEB1, ZEB2 and TGFBRs, in prostate adenocarcinoma specimens. In addition, SCAND1 overexpression suppressed tumor cell proliferation by reducing the MAP3K-MEK-ERK signaling pathway. Of note, in a mouse tumor xenograft model, SCAND1 overexpression significantly reduced Ki-67(+) and Vimentin(+) tumor cells and inhibited migration and lymph node metastasis of prostate cancer. Kaplan–Meier analysis showed high expression of SCAND1 and MZF1 to correlate with better prognoses in pancreatic cancer and head and neck cancers, although with poorer prognosis in kidney cancer. Overall, these data suggest that SCAND1 induces expression and coordinated heterochromatin-binding of MZF1 to reverse the hybrid E/M status into an epithelial phenotype and, inhibits tumor cell proliferation, migration, and metastasis, potentially by repressing the gene expression of EMT drivers and the MAP3K-MEK-ERK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

SCAND1 Reverses Epithelial-to-Mesenchymal Transition (EMT) and Suppresses Prostate Cancer Growth and Migration

Eguchi

Csizmadia

Kawai

et al. 2022

Cells

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“…High expression of CBX1 was related to poor differentiation of breast cancer and led to poor OS 22 . The expression of CBX1 was closely related to the staging of gastric cancer and lymph node metastasis 23 . In addition, CBX1 interacted with the transcription factor HMGA2, activates the Wnt/βCatenin signaling pathway and affected the prognosis of patients with liver cancer 24 .…”

Section: Discussionmentioning

confidence: 99%

Bioinformatic Analysis of Prognostic Value and Immune Cell Infiltration of Chromobox Family Proteins in Esophageal Cancer

Jiang

Pan

et al. 2021

Preprint

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BackgroundChromobox (CBX) family proteins (CBXs) are important components of epigenetic regulation complexes. Abnormal expression of CBXs is related to the occurrence and development of various cancers. However, the role and mechanism of CBXs in esophageal cancer (ESCA) need further research. MethodsThe mRNA expression of CBXs, clinicopathological parameters, prognostic values, genetic alteration, enrichment analysis, and immune cell infiltration were analyzed with several databases including Oncomine, UALCAN, Kaplan-Meier plotter, cBioPortal, DAVID, and TIMER2.0.ResultsThe expression level of CBX1/2/3/4/8 was significantly upregulated in ESCA while that of CBX7 was down-regulated. Besides, mRNA expressions of CBX1/2/3/4/5/7/8 were correlated with patients’ individual cancer stages and the nodal metastatic status. The mRNA expression of CBX3/4/7/8 was significantly correlated with the overall survival (OS) in ESCA. What is more, high mutation rate of CBXs (49%) was also observed in ESCA patients. Then, CBXs were related to the infiltration of a variety of immune cells.ConclusionsThis study may provide new ideas for the selection of prognostic biomarkers in the CBXs in ESCA.

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“…Compared with normal tissues or paracancerous tissues, the expression of all or some of the CBX1/2/3/4/5/8 members is upregulated in most cancer tissues, including glioma (67-69), tongue squamous cell carcinoma (TSCC) (70), head and neck squamous cell carcinoma (HNSCC) (71), breast cancer (BC) (15,(72)(73)(74)(75)(76)(77)(78)(79)(80), non-small cell lung cancer (NSCLC) (81)(82)(83)(84)(85), esophageal cancer (EC) (86)(87)(88)(89)(90), gastric cancer (GC) (91)(92)(93)(94)(95)(96)(97)(98), pancreatic adenocarcinoma (PAAD) (99,100), colorectal cancer (CRC) (101-104), urinary bladder cancer (UBC) (105), sarcoma (106) and osteosarcoma (107,108). As a tumor suppressor, CBX7 is expressed at low levels in most tumors, such as glioma, HNSCC (71), EC (87,88), GC (93)(94)(95)(96)(97)(98), PAAD (109), CRC (103,104), clear cell renal cell carcinoma (ccRCC) …”

Section: Expression Of Cbxs In Cancers and The Relationship Between C...mentioning

confidence: 99%

“…CBX4 is of prognostic value in BC (76,80), LUAD (85), EC (86)(87)(88), GC (92,94,95,98), HCC (11) and ccRCC (110). In addition, patients with BC (80), LUAD (84), GC (94)(95)(96)(97)(98), CRC (103), sarcoma (106), SKCM (113) with upregulated CBX5 and HNSCC (71) and ccRCC (110) with downregulated CBX5 have poor prognosis. CBX6 may be either a poor prognostic factor or a favorable prognostic factor, depending on the type of cancer (67,77,94,(96)(97)(98)(99)103,110,117,122).…”

Section: Othersmentioning

confidence: 99%

“…In addition, patients with BC (80), LUAD (84), GC (94)(95)(96)(97)(98), CRC (103), sarcoma (106), SKCM (113) with upregulated CBX5 and HNSCC (71) and ccRCC (110) with downregulated CBX5 have poor prognosis. CBX6 may be either a poor prognostic factor or a favorable prognostic factor, depending on the type of cancer (67,77,94,(96)(97)(98)(99)103,110,117,122). CBX7 acts as a tumor suppressor in glioma (68), BC (15,77), LUAD (83,84,125), HCC (114,119), PAAD (99,109), ccRCC (110), CCA (112), sarcoma (106) and SKCM (113).…”

Section: Othersmentioning

confidence: 99%

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Chromobox proteins in cancer: Multifaceted functions and strategies for modulation (Review)

et al. 2023

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Chromobox (CBX) proteins are important epigenetic regulatory proteins and are widely involved in biological processes, such as embryonic development, the maintenance of stem cell characteristics and the regulation of cell proliferation and apoptosis. Disorder and dysfunction of CBXs in cancer usually lead to the blockade or ectoptic activation of developmental pathways, promoting the occurrence, development and progression of cancer. In the present review, the characteristics and functions of CBXs were first introduced. Subsequently, the expression of CBXs in cancers and the relationship between CBXs and clinical characteristics (mainly cancer grade, stage, metastasis and relapse) and prognosis were discussed. Finally, it was described how CBXs regulate cell proliferation and self-renewal, apoptosis and the acquisition of malignant phenotypes, such as invasion, migration and chemoresistance, through mechanisms involving epigenetic modification, nuclear translocation, noncoding RNA interactions, transcriptional regulation, posttranslational modifications, protein-protein interactions, signal transduction and metabolic reprogramming. The study also focused on cancer therapies targeting CBXs. The present review provides new insight and a comprehensive basis for follow-up research on CBXs and cancer. Contents1. Introduction 2. Constituent members of CBXs 3. Characteristics and functions of PcG family CBXs 4. Characteristics and functions of HP1 family CBXs 5. Expression of CBXs in cancers and the relationship between CBXs and clinical characteristics and prognosis 6. CBXs regulate biological tumor processes through epigenetic modification, nuclear translocation, ncRNA interactions, transcriptional regulation, PTMs, proteinprotein interactions, signal transduction and metabolic reprogramming 7. Cancer therapies targeting CBXs 8. Conclusion and prospects

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Identification of the Roles of Chromobox Family Members in Gastric Cancer: A Study Based on Multiple Datasets

Cited by 5 publications

References 63 publications

SCAND1 Reverses Epithelial-to-Mesenchymal Transition (EMT) and Suppresses Prostate Cancer Growth and Migration

SCAND1 Reverses Epithelial-to-Mesenchymal Transition (EMT) and Suppresses Prostate Cancer Growth and Migration

Bioinformatic Analysis of Prognostic Value and Immune Cell Infiltration of Chromobox Family Proteins in Esophageal Cancer

Chromobox proteins in cancer: Multifaceted functions and strategies for modulation (Review)

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