Cyclin-dependent kinase inhibitor 3 is overexpressed in hepatocellular carcinoma and promotes tumor cell proliferation

2012 ◽  
Vol 420 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Chunyang Xing ◽  
Haiyang Xie ◽  
Lin Zhou ◽  
Wuhua Zhou ◽  
Wu Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Kinase Inhibitor ◽  
Cyclin Dependent Kinase ◽  
Tumor Cell Proliferation ◽  
Cyclin Dependent Kinase Inhibitor

Expression of β-Catenin in Hepatocellular Carcinoma

2001 ◽  
Vol 71 (3) ◽  
pp. 116-125
Author(s):  
Norina Basa ◽  
Daniela Lazar ◽  
Remus Cornea ◽  
Sorina Taban ◽  
Melania Ardelean ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Mitotic Index ◽  
Histological Grade ◽  
Proliferation Index ◽  
Tumor Cell Proliferation ◽  
Ki 67 ◽  
B Virus ◽  
Development And Evolution

Alteration of β-catenin expression is involved in the development and evolution of hepatocellular carcinoma (HCC); β-catenin is able to influence tumor cell proliferation. We analyzed the immunohistochemical (IHC) expression of β-catenin on a group of 32 patients diagnosed with HCC using the anti-β-catenin monoclonal antibody (clone E247). We correlated the expression of β-catenin with the proliferation index of Ki-67 (PI Ki-67), the mitotic index (MI) and other clinical and pathological features. We observed an altered β-catenin expression in 58.38% of all HCC cases. This expression was insignificantly correlated with tumor size (]5 cm) (p = 0.683), histological grade G1-G2 (p = 0.307), vascular invasion (p = 0.299) and advanced pT stage (p = 0.453); we obtained a significantly higher MI in HCC with altered β-catenin expression (p = 0.018), as compared to HCC without overexpression (1.66 � 1.37) (p = 0.038) and a PI Ki-67 of 22.49 � 20.1 and 28.24 � 18.2, respectively in tumors with altered β-catenin expression with insignificant differences compared to HCC without overexpression (25.95 � 15.2) (p = 0.682 and p = 0.731, respectively). According to the results we obtained, aberrant β-catenin expression in HCC was correlated with a high mitotic index, therefore playing an important role in tumor progression by stimulating tumor cell proliferation; non-nuclear β-catenin overexpression can have a pathological significance in HCC, especially in cases of HCC associated with hepatitis B virus (HBV) infection.

scholarly journals Δ40p53α suppresses tumor cell proliferation and induces cellular senescence in hepatocellular carcinoma cells

2016 ◽  
Vol 130 (3) ◽  
pp. 614-625 ◽  
Author(s):  
Akinobu Ota ◽  
Haruhisa Nakao ◽  
Yumi Sawada ◽  
Sivasundaram Karnan ◽  
Md Wahiduzzaman ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Cellular Senescence ◽  
Carcinoma Cells ◽  
Tumor Cell Proliferation ◽  
Hepatocellular Carcinoma Cells

scholarly journals SNRPB-mediated RNA splicing drives tumor cell proliferation and stemness in hepatocellular carcinoma

Aging ◽  
2020 ◽  
Author(s):  
Yu-Ting Zhan ◽  
Lei Li ◽  
Ting-Ting Zeng ◽  
Ning-Ning Zhou ◽  
Xin-Yuan Guan ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Rna Splicing ◽  
Tumor Cell Proliferation

scholarly journals BAP31 Promotes Tumor Cell Proliferation by Stabilizing SERPINE2 in Hepatocellular Carcinoma

2020 ◽  
Vol 8 ◽  
Author(s):  
Xiyang Zhang ◽  
Dongbo Jiang ◽  
Shuya Yang ◽  
Yuanjie Sun ◽  
Yang Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Colony Formation ◽  
Clinical Stage ◽  
Tumor Cell Proliferation ◽  
Ki 67 ◽  
Hcc Cells

Hepatocellular carcinoma (HCC) patients are mostly diagnosed at an advanced stage, resulting in systemic therapy and poor prognosis. Therefore, the identification of a novel treatment target for HCC is important. B-cell receptor-associated protein 31 (BAP31) has been identified as a cancer/testis antigen; however, BAP31 function and mechanism of action in HCC remain unclear. In this study, BAP31 was demonstrated to be upregulated in HCC and correlated with the clinical stage. BAP31 overexpression promoted HCC cell proliferation and colony formation in vitro and tumor growth in vivo. RNA-sequence (RNA-seq) analysis demonstrated that serpin family E member 2 (SERPINE2) was downregulated in BAP31-knockdown HCC cells. Coimmunoprecipitation and immunofluorescence assays demonstrated that BAP31 directly binds to SERPINE2. The inhibition of SERPINE2 significantly decreased the BAP31-induced cell proliferation and colony formation of HCC cells and phosphorylation of Erk1/2 and p38. Moreover, multiplex immunohistochemistry staining of the HCC tissue microarray showed positive associations between the expression levels of BAP31, SERPINE2, its downstream gene LRP1, and a tumor proliferation marker, Ki-67. The administration of anti-BAP31 antibody significantly inhibited HCC cell xenograft tumor growth in vivo. Thus, these findings suggest that BAP31 promotes tumor cell proliferation by stabilizing SERPINE2 and can serve as a promising candidate therapeutic target for HCC.

Myc Targets Cks1 To Provoke Proliferation and Lymphomagenesis.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2618-2618
Author(s):  
Ulrich Keller ◽  
Jennifer B. Old ◽  
Jonas Nilsson ◽  
Lisa Nilsson ◽  
Kirsteen Maclean ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
B Cells ◽  
Burkitt Lymphoma ◽  
Poor Prognosis ◽  
Transcriptional Activity ◽  
Kinase Inhibitor ◽  
Ex Vivo ◽  
Cyclin Dependent Kinase ◽  
Cyclin Dependent Kinase Inhibitor ◽  
Induced Apoptosis

Abstract Reduced levels of the cyclin dependent kinase inhibitor p27Kip1 connote poor prognosis in cancer. In human Burkitt lymphoma, and in pre-cancerous B cells and lymphomas arising in Eμ-Myc transgenic mice, p27Kip1 expression is markedly reduced. Furthermore, the Cks1 component of the SCFSkp2 complex that is necessary for p27Kip1 ubiquitylation and degradation, and to a lesser extent Skp2, are induced by Myc ex vivo and in Eμ-Myc B-cells and lymphomas, and up-regulation of CKS1 and SKP2 are hallmarks of Burkitt lymphoma. While loss of Skp2 has rather modest effects, the deletion of Cks1 in Eμ-Myc B-cells elevates p27Kip1 levels, reduces proliferation and delays lymphoma development. In contrast, Myc-induced apoptosis and transcriptional activity are not affected by Cks1 (or Skp2) loss. Therefore, Myc accelerates cell proliferation and promotes tumorigenesis through its ability to selectively induce Cks1.

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