Upregulation of CENP-H in tongue cancer correlates with poor prognosis and progression

Liao, Wen Ting; Yu, Chenchen; Wu, Dong; Zhang, Ling; Xu, Li; Weng, Gui Xiang; Zeng, Mu Sheng; Song, Li; Li, Jin Song

doi:10.1186/1756-9966-28-74

Cited by 22 publications

(22 citation statements)

References 32 publications

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“…Compared with the control cells, the population doubling time was shorter and the colony formation ability was decreased in Tca8113/CENP-H RNAi cells, which highlighted the compromised viability caused by the downregulation of CENP-H (18). Consistent with these studies (12,17,18), our MTT and colony formation data also revealed that shRNA-mediated CENP-H knockdown caused Hep3B proliferation inhibition. Similarly to the in vitro experiments, Lv3-CENP-H1 cells exhibited decreased tumorigenicity in nude mice in vivo.…”

Section: Discussionsupporting

confidence: 78%

“…Orthaus et al (17) reported that depletion of CENP-H resulted in the decreased number of living cells and increased cell death in human HEp-2 cells by RNAi knockdown of CENP-H. Compared with the control cells, the population doubling time was shorter and the colony formation ability was decreased in Tca8113/CENP-H RNAi cells, which highlighted the compromised viability caused by the downregulation of CENP-H (18). Consistent with these studies (12,17,18), our MTT and colony formation data also revealed that shRNA-mediated CENP-H knockdown caused Hep3B proliferation inhibition.…”

Section: Discussionmentioning

confidence: 99%

“…Survivin, a member of the inhibitor of apoptosis protein family, has been implicated as a protector against cell apoptosis; the aberrant high expression of this factor in cancers is closely correlated with advanced disease and poor overall survival (20,21). According to previous studies, CENP-H siRNA decreases the protein expression of survivin, indicating apoptosis induction (12,18). Wang et al (22) found that siRNA knockdown of CENP-H mRNA promoted FaDu cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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

Hou

et al. 2017

Oncology Reports

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Abstract. The genomic alterations of hepatocellular carcinoma (HCC) are still unclear. Centromere protein-H (CENP-H) has been shown to be associated with many solid tumors. Our previous study found that CENP-H was upregulated in HCC and was related to patient prognosis. However, the biological functions of CENP-H in HCC and the possible underlying mechanisms have not been well elucidated. In the present study, we demonstrated that CENP-H knockdown inhibited the proliferation of Hep3B cells and decreased colony formation ability of single cells in vitro. Furthermore, CENP-H knockdown induced Hep3B cell apoptosis, and apoptotic bodies were observed using transmission electron microscopy. The protein expression of cleaved caspase-3 was upregulated in Hep3B cells after CENP-H knockdown. Additionally, a Bax/Bcl-2 ratio imbalance with a significant increase of Bax and a substantial decrease of Bcl-2 at both the mRNA and protein levels were determined in this study. In an animal experiment, CENP-H knockdown blocked the growth of Hep3B subcutaneous xenografts. Immunohistochemistry revealed that the protein expression of cleaved caspase-3 and Bax was increased, whereas the protein expression of Bcl-2 and Ki-67 was decreased in subcutaneous xenografts of the CENP-H-knockdown group. In summary, CENP-H may be involved in cell proliferation and apoptosis of HCC cells through the mitochondrial apoptotic pathway. Combined with previous studies, the data provide a new perspective on HCC development and progression.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

Hou

et al. 2017

Oncology Reports

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“…It was first reported to be upregulated in colorectal cancers, and the ectopic expression of CENPH induced chromosome instability (CIN) in diploid cell lines [11]. Shigeishi and our laboratory reported that CENPH was also upregulated in oral squamous cell carcinoma, nasopharyngeal carcinoma (NPC), breast cancer, esophageal carcinoma, non‐small‐cell lung cancer, and tongue cancer [12–17]. Moreover, higher CENPH expression is associated with poor prognosis for patients [12–17].…”

Section: Introductionmentioning

confidence: 99%

“…Shigeishi and our laboratory reported that CENPH was also upregulated in oral squamous cell carcinoma, nasopharyngeal carcinoma (NPC), breast cancer, esophageal carcinoma, non‐small‐cell lung cancer, and tongue cancer [12–17]. Moreover, higher CENPH expression is associated with poor prognosis for patients [12–17]. We have previously demonstrated that CENPH is more highly expressed in NPC tumors and cell lines and immortalized nasopharyngeal epithelial cells than in normal tissues and normal nasopharyngeal epithelial cells (NPECs).…”

Section: Introductionmentioning

confidence: 99%

Sp1 and Sp3 are involved in the full transcriptional activity of centromere protein H in human nasopharyngeal carcinoma cells

Zhao¹,

Wang²,

Xie³

et al. 2012

The FEBS Journal

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The overexpression of centromere protein H (CENPH), one of the fundamental components of the human active kinetochore, has been shown to be closely associated with human cancers. However, the mechanism of its transcriptional regulation has not been reported. The aim of the present study was to investigate the regulatory elements for the transcriptional regulation of CENPH in nasopharyngeal carcinoma cells. To characterize the CENPH promoter and identify regulatory elements, we cloned 1015 bp ()975 ⁄ +40 bp) of the 5¢-flanking region of the CENPH gene from immortalized normal nasopharyngeal epithelial cells (Bmi-1 ⁄ NPEC). Functional analysis established a minimal region ()140 ⁄ )87 bp) involved in the regulation of human CENPH promoter activity. Through site-directed mutagenesis, a transactivation assay, chromatin immunoprecipitation, and electrophoretic mobility shift assay, we found that the Sp1 ⁄ Sp3 transcription factors could bind to the CENPH promoter in vitro and in vivo, and that they regulated CENPH promoter activation in human nasopharyngeal carcinoma cells. Furthermore, Sp1 and Sp3 were highly expressed in nasopharyngeal carcinoma cells. Knockdown of Sp1 and Sp3 by small interfering RNA or inhibition of Sp1 and Sp3 activity by mithramycin A decreased CENPH mRNA expression, whereas the exogenous expression of Sp1 and Sp3 upregulated CENPH mRNA expression. Taken together, our results indicate that Sp1 and Sp3 bind to the CENPH minimal promoter and function as a regulator of the transcription of CENPH in human nasopharyngeal carcinomas.

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Upregulation of centromere protein H is associated with progression of renal cell carcinoma

Lin

Shi

et al. 2015

J Mol Hist

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Centromere protein H (CENPH), one of the essential component of active kinetochore, plays an important role in carcinogenesis of many cancer types. However, its expression signature and prognostic significance of renal cell carcinoma (RCC) are unclear. In the present study, we concluded that the expression of CENPH was prominently upregulated in RCC specimens and three RCC cell lines (ACHN, 786-O and A704). Immunohistochemical analysis revealed that RCCs exhibited higher levels of CENPH expression than normal renal tissues in paraffin-embedded archival specimens. Further statistical analysis suggested the upregulation of CENPH was positively correlated with the Fuhrman grade (P = 0.001), distant metastasis (P = 0.024) and clinical stage (P = 0.014). In addition, the CENPH served as an independent predictor of overall survival of RCC patients in multivariate analysis (P = 0.018). Furthermore, our in vitro assays of RCC cell lines indicated that knockdown of CENPH reduced cell proliferation, inhibited cell growth, and increased cell apoptosis. In conclusion, our data suggest that CENPH is a novel molecule involved in RCC progression, which provides a potential biomarker and therapeutic target.

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Upregulation of CENP-H in tongue cancer correlates with poor prognosis and progression

Abstract: Background: Centromere protein H (CENP-H) is one of the fundamental components of the human active kinetochore. Recently, CENP-H was identified to be associated with tumorigenesis. This study was aimed to investigate the clinicopathologic significance of CENP-H in tongue cancer.

Cited by 22 publications

References 32 publications

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

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

Sp1 and Sp3 are involved in the full transcriptional activity of centromere protein H in human nasopharyngeal carcinoma cells

Upregulation of centromere protein H is associated with progression of renal cell carcinoma

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