CENP-H regulates the cell growth of human hepatocellular carcinoma cells through the mitochondrial apoptotic pathway

Lu, Guifang; Hou, Helei; Lu, Xinlan; Ke, Xia; Wang, Xin; Zhang, Dan; Zhao, Yan; Zhang, Jun; Ren, Mudan; He, Shuixiang

doi:10.3892/or.2017.5602

Cited by 17 publications

(13 citation statements)

References 27 publications

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“…Centromere protein A (CENPA) is one of the first identified kinetochore components in humans and is involved in several human malignancies 11–14. It has been found that several centromere proteins were upregulated in HCC and associated with HCC malignant progression 11,15,16. Centromere protein K (CENPK) is important for proper kinetochore function and mitotic progression 17.…”

Section: Introductionmentioning

confidence: 99%

<p>Downregulation of CENPK suppresses hepatocellular carcinoma malignant progression through regulating YAP1</p>

Wang¹,

Li²,

Chen³

et al. 2019

OTT

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BackgroundSeveral studies have found that centromere protein K (CENPK) is overexpressed in several tumour types and promotes tumor progression. However, there has been little research on the role of CENPK in the progression of hepatocellular carcinoma (HCC).Materials and methodsThe expression of CENPK in HCC tissues was quantified by Western blot and quantitative real-time PCR. Cells were transfected with lentiviral plasmids containing shRNA sequences targeting CENPK and YAP1 to silence the expression of CENPK and YAP1. Cell Counting Kit-8 assay, colony formation assay, wound healing assay, and transwell invasion assay were performed to evaluate cell growth, migration, and invasion of HCC cells. Tumorigenicity assay was used to detect the effect of CENPK on the growth of HCC cells. Western blot assay was performed to investigate the expression of epithelial–mesenchymal transition (EMT) markers and YAP1.ResultsCompared to that in adjacent non-tumor tissues, CENPK was aberrantly upregulated in HCC tumor tissues. Furthermore, CENPK knockdown significantly inhibited proliferation, migration, invasion, and EMT progression in HCC cells. Mechanistically, we identified that YAP1 was responsible for the tumor-suppressive effects of CENPK knockdown in the HCC cells. The inhibitory effects of CENPK silencing on cell proliferation, migration, invasion, and EMT were partially reversed by the restoration of YAP1 expression.ConclusionOur results suggested that the CENPK–YAP1–EMT axis plays a critical role in regulating HCC malignant progression, indicating the role of this axis as a potential therapeutic target for HCC.

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Section: Introductionmentioning

confidence: 99%

<p>Downregulation of CENPK suppresses hepatocellular carcinoma malignant progression through regulating YAP1</p>

Wang¹,

Li²,

Chen³

et al. 2019

OTT

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“…Centromere protein H (CENP-H) is a component of the kinetochore and plays an essential role in mitotic processes ( Lu et al, 2017 ), accurate chromosome segregation ( Zhu et al, 2015 ) as well as appropriate kinetochore assembly ( Zhao et al, 2012 ). Many studies have shown that CENPH is closely associated with human cancers, including colorectal cancer ( Wu et al, 2017 ), renal cell carcinoma ( Wu et al, 2015 ), non-small cell lung cancer ( Liao et al, 2009 ) as well as breast cancer ( Walian, Hang & Mao, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of NUF2 and FAM83D as potential biomarkers in triple-negative breast cancer

Zhai

Yang

Liu

et al. 2020

PeerJ

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Background Breast cancer is a heterogeneous disease. Compared with other subtypes of breast cancer, triple-negative breast cancer (TNBC) is easy to metastasize and has a short survival time, less choice of treatment options. Here, we aimed to identify the potential biomarkers to TNBC diagnosis and prognosis. Material/Methods Three independent data sets (GSE45827, GSE38959, GSE65194) were downloaded from the Gene Expression Omnibus (GEO). The R software packages were used to integrate the gene profiles and identify differentially expressed genes (DEGs). A variety of bioinformatics tools were used to explore the hub genes, including the DAVID database, STRING database and Cytoscape software. Reverse transcription quantitative PCR (RT-qPCR) was used to verify the hub genes in 14 pairs of TNBC paired tissues. Results In this study, we screened out 161 DEGs between 222 non-TNBC and 126 TNBC samples, of which 105 genes were up-regulated and 56 were down-regulated. These DEGs were enriched for 27 GO terms and two pathways. GO analysis enriched mainly in “cell division”, “chromosome, centromeric region” and “microtubule motor activity”. KEGG pathway analysis enriched mostly in “Cell cycle” and “Oocyte meiosis”. PPI network was constructed and then 10 top hub genes were screened. According to the analysis results of the Kaplan-Meier survival curve, the expression levels of only NUF2, FAM83D and CENPH were associated with the recurrence-free survival in TNBC samples (P < 0.05). RT-qPCR confirmed that the expression levels of NUF2 and FAM83D in TNBC tissues were indeed up-regulated significantly. Conclusions The comprehensive analysis showed that NUF2 and FAM83D could be used as potential biomarkers for diagnosis and prognosis of TNBC.

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“…Centromere protein H (CENP-H) is a component of the kinetochore and plays an essential role in mitotic processes (Lu et al 2017), accurate chromosome segregation (Zhu et al 2015) as well as appropriate kinetochore assembly (Zhao et al 2012). Many studies have shown that CENPH is closely associated with human cancers, including colorectal cancer (Wu et al 2017), renal cell carcinoma (Wu et al 2015), non-small cell lung cancer (Liao et al 2009) as well as breast cancer (Walian et al 2016).…”

Section: Manuscript To Be Reviewedmentioning

confidence: 99%

Peer Review #2 of "Identification of NUF2 and FAM83D as potential biomarkers in triple-negative breast cancer (v0.2)"

2020

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Background. Breast cancer is a heterogeneous disease. Compared with other subtypes of breast cancer, triple-negative breast cancer (TNBC) is easy to metastasize and has a short survival time, less choice of treatment options. Here, we aimed to identify the potential biomarkers to TNBC diagnosis and prognosis. Material/Methods. Three independent data sets (GSE45827, GSE38959, GSE65194) were downloaded from the Gene Expression Omnibus (GEO). The R software packages were used to integrate the gene profiles and identify differentially expressed genes (DEGs). A variety of bioinformatics tools were used to explore the hub genes, including the DAVID database, STRING database and Cytoscape software. Reverse transcription quantitative PCR (RT-qPCR) was used to verify the hub genes in 14 pairs of TNBC paired tissues. Results. In this study, we screened out 161 DEGs between 222 non-TNBC and 126 TNBC samples, of which 105 genes were up-regulated and 56 were down-regulated. These DEGs were enriched for 27 GO terms and 2 pathways. GO analysis enriched mainly in "cell division", "chromosome, centromeric region" and "microtubule motor activity". KEGG pathway analysis enriched mostly in "Cell cycle" and "Oocyte meiosis". PPI network was constructed and then 10 top hub genes were screened. According to the analysis results of the Kaplan-M eier survival curve, the expression levels of only NUF2, FAM83D and CENPH were associated with the recurrence-free survival in TNBC samples (P<0.05). RT-qPCR confirmed that the expression levels of NUF2 and FAM83D in TNBC tissues were indeed up-regulated significantly. Conclusions. The comprehensive analysis showed that NUF2 and FAM83D could be used as potential biomarkers for diagnosis and prognosis of TNBC.

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CENP-H regulates the cell growth of human hepatocellular carcinoma cells through the mitochondrial apoptotic pathway

Cited by 17 publications

References 27 publications

<p>Downregulation of CENPK suppresses hepatocellular carcinoma malignant progression through regulating YAP1</p>

<p>Downregulation of CENPK suppresses hepatocellular carcinoma malignant progression through regulating YAP1</p>

Identification of NUF2 and FAM83D as potential biomarkers in triple-negative breast cancer

Peer Review #2 of "Identification of NUF2 and FAM83D as potential biomarkers in triple-negative breast cancer (v0.2)"

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