PKM2 regulates neural invasion of and predicts poor prognosis for human hilar cholangiocarcinoma
The therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a variety of cancers, while their roles in treatment of and prognosis for hilar cholangiocarcinoma (HC) remain unclear. In this study, we determined the exp...
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Published in | Molecular cancer Vol. 14; no. 9155; p. 193 |
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14.11.2015
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Abstract | The therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a variety of cancers, while their roles in treatment of and prognosis for hilar cholangiocarcinoma (HC) remain unclear. In this study, we determined the expression of PKM2 in and its impact on biology and clinical outcome of human HC.
The regulation and function of PKM2 in HC pathogenesis was evaluated using human tissues, molecular and cell biology, and animal models, and its prognostic significance was determined according to its impact on patient survival.
We found that expression of hexokinase 1 and the M2 splice isoform of PK (PKM2) was upregulated in HC tissues and that this expression correlated with tumor recurrence and outcome. PKM2 expression was increased in HC cases with chronic cholangitis as demonstrated by isobaric tags for relative and absolute quantification. High PKM2 expression was highly correlated with high syndecan 2 (SDC2) expression and neural invasion. PKM2 downregulation led to a decrease in SDC2 expression. Treatment with metformin markedly suppressed PKM2 and SDC2 expression at both the transcriptional and posttranscriptional levels and inhibited HC cell proliferation and tumor growth.
PKM2 regulates neural invasion of HC cells at least in part via regulation of SDC2. Inhibition of PKM2 and SDC2 expression contributes to the therapeutic effect of metformin on HC. Therefore, PKM2 is an independent prognostic factor and potential therapeutic target for human HC. |
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AbstractList | The therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a variety of cancers, while their roles in treatment of and prognosis for hilar cholangiocarcinoma (HC) remain unclear. In this study, we determined the expression of PKM2 in and its impact on biology and clinical outcome of human HC. The regulation and function of PKM2 in HC pathogenesis was evaluated using human tissues, molecular and cell biology, and animal models, and its prognostic significance was determined according to its impact on patient survival. We found that expression of hexokinase 1 and the M2 splice isoform of PK (PKM2) was upregulated in HC tissues and that this expression correlated with tumor recurrence and outcome. PKM2 expression was increased in HC cases with chronic cholangitis as demonstrated by isobaric tags for relative and absolute quantification. High PKM2 expression was highly correlated with high syndecan 2 (SDC2) expression and neural invasion. PKM2 downregulation led to a decrease in SDC2 expression. Treatment with metformin markedly suppressed PKM2 and SDC2 expression at both the transcriptional and posttranscriptional levels and inhibited HC cell proliferation and tumor growth. PKM2 regulates neural invasion of HC cells at least in part via regulation of SDC2. Inhibition of PKM2 and SDC2 expression contributes to the therapeutic effect of metformin on HC. Therefore, PKM2 is an independent prognostic factor and potential therapeutic target for human HC. The therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a variety of cancers, while their roles in treatment of and prognosis for hilar cholangiocarcinoma (HC) remain unclear. In this study, we determined the expression of PKM2 in and its impact on biology and clinical outcome of human HC. The regulation and function of PKM2 in HC pathogenesis was evaluated using human tissues, molecular and cell biology, and animal models, and its prognostic significance was determined according to its impact on patient survival. We found that expression of hexokinase 1 and the M2 splice isoform of PK (PKM2) was upregulated in HC tissues and that this expression correlated with tumor recurrence and outcome. PKM2 expression was increased in HC cases with chronic cholangitis as demonstrated by isobaric tags for relative and absolute quantification. High PKM2 expression was highly correlated with high syndecan 2 (SDC2) expression and neural invasion. PKM2 downregulation led to a decrease in SDC2 expression. Treatment with metformin markedly suppressed PKM2 and SDC2 expression at both the transcriptional and posttranscriptional levels and inhibited HC cell proliferation and tumor growth. PKM2 regulates neural invasion of HC cells at least in part via regulation of SDC2. Inhibition of PKM2 and SDC2 expression contributes to the therapeutic effect of metformin on HC. Therefore, PKM2 is an independent prognostic factor and potential therapeutic target for human HC. BACKGROUNDThe therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a variety of cancers, while their roles in treatment of and prognosis for hilar cholangiocarcinoma (HC) remain unclear. In this study, we determined the expression of PKM2 in and its impact on biology and clinical outcome of human HC.METHODSThe regulation and function of PKM2 in HC pathogenesis was evaluated using human tissues, molecular and cell biology, and animal models, and its prognostic significance was determined according to its impact on patient survival.RESULTSWe found that expression of hexokinase 1 and the M2 splice isoform of PK (PKM2) was upregulated in HC tissues and that this expression correlated with tumor recurrence and outcome. PKM2 expression was increased in HC cases with chronic cholangitis as demonstrated by isobaric tags for relative and absolute quantification. High PKM2 expression was highly correlated with high syndecan 2 (SDC2) expression and neural invasion. PKM2 downregulation led to a decrease in SDC2 expression. Treatment with metformin markedly suppressed PKM2 and SDC2 expression at both the transcriptional and posttranscriptional levels and inhibited HC cell proliferation and tumor growth.CONCLUSIONSPKM2 regulates neural invasion of HC cells at least in part via regulation of SDC2. Inhibition of PKM2 and SDC2 expression contributes to the therapeutic effect of metformin on HC. Therefore, PKM2 is an independent prognostic factor and potential therapeutic target for human HC. Background The therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a variety of cancers, while their roles in treatment of and prognosis for hilar cholangiocarcinoma (HC) remain unclear. In this study, we determined the expression of PKM2 in and its impact on biology and clinical outcome of human HC. Methods The regulation and function of PKM2 in HC pathogenesis was evaluated using human tissues, molecular and cell biology, and animal models, and its prognostic significance was determined according to its impact on patient survival. Results We found that expression of hexokinase 1 and the M2 splice isoform of PK (PKM2) was upregulated in HC tissues and that this expression correlated with tumor recurrence and outcome. PKM2 expression was increased in HC cases with chronic cholangitis as demonstrated by isobaric tags for relative and absolute quantification. High PKM2 expression was highly correlated with high syndecan 2 (SDC2) expression and neural invasion. PKM2 downregulation led to a decrease in SDC2 expression. Treatment with metformin markedly suppressed PKM2 and SDC2 expression at both the transcriptional and posttranscriptional levels and inhibited HC cell proliferation and tumor growth. Conclusions PKM2 regulates neural invasion of HC cells at least in part via regulation of SDC2. Inhibition of PKM2 and SDC2 expression contributes to the therapeutic effect of metformin on HC. Therefore, PKM2 is an independent prognostic factor and potential therapeutic target for human HC. Background The therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a variety of cancers, while their roles in treatment of and prognosis for hilar cholangiocarcinoma (HC) remain unclear. In this study, we determined the expression of PKM2 in and its impact on biology and clinical outcome of human HC. Methods The regulation and function of PKM2 in HC pathogenesis was evaluated using human tissues, molecular and cell biology, and animal models, and its prognostic significance was determined according to its impact on patient survival. Results We found that expression of hexokinase 1 and the M2 splice isoform of PK (PKM2) was upregulated in HC tissues and that this expression correlated with tumor recurrence and outcome. PKM2 expression was increased in HC cases with chronic cholangitis as demonstrated by isobaric tags for relative and absolute quantification. High PKM2 expression was highly correlated with high syndecan 2 (SDC2) expression and neural invasion. PKM2 downregulation led to a decrease in SDC2 expression. Treatment with metformin markedly suppressed PKM2 and SDC2 expression at both the transcriptional and posttranscriptional levels and inhibited HC cell proliferation and tumor growth. Conclusions PKM2 regulates neural invasion of HC cells at least in part via regulation of SDC2. Inhibition of PKM2 and SDC2 expression contributes to the therapeutic effect of metformin on HC. Therefore, PKM2 is an independent prognostic factor and potential therapeutic target for human HC. Keywords: Prognosis, Metabolism, Biomarkers, PKM2, hilar cholangiocarcinoma |
ArticleNumber | 193 |
Audience | Academic |
Author | Fang, Wenzheng Jin, Guangzhi Xie, Keping Yu, Allan Chen, Ying Yu, Wenlong Li, Zhaosheng Zhang, Xiaoli Xu, Dongyun Xia, Tian Yu, Guanzhen |
Author_xml | – sequence: 1 givenname: Guanzhen surname: Yu fullname: Yu, Guanzhen email: qiaoshanqian@aliyun.com, qiaoshanqian@aliyun.com organization: Department of Gastroenterology, Hepatology and Nutrition, Unit 1466, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, 77030, USA. qiaoshanqian@aliyun.com – sequence: 2 givenname: Wenlong surname: Yu fullname: Yu, Wenlong organization: Department of Surgery, Eastern Hepatobiliary Hospital, Shanghai, People's Republic of China – sequence: 3 givenname: Guangzhi surname: Jin fullname: Jin, Guangzhi organization: Department of Pathology, Eastern Hepatobiliary Hospital, Shanghai, People's Republic of China – sequence: 4 givenname: Dongyun surname: Xu fullname: Xu, Dongyun organization: Department of Oncology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, People's Republic of China – sequence: 5 givenname: Ying surname: Chen fullname: Chen, Ying organization: Department of Pathology, Changhai Hospital, Shanghai, People's Republic of China – sequence: 6 givenname: Tian surname: Xia fullname: Xia, Tian organization: Department of Gastroenterology, Hepatology and Nutrition, Unit 1466, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, 77030, USA – sequence: 7 givenname: Allan surname: Yu fullname: Yu, Allan organization: Department of Gastroenterology, Hepatology and Nutrition, Unit 1466, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, 77030, USA – sequence: 8 givenname: Wenzheng surname: Fang fullname: Fang, Wenzheng organization: Department of Oncology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, People's Republic of China – sequence: 9 givenname: Xiaoli surname: Zhang fullname: Zhang, Xiaoli organization: Department of Pathology, Chinese People's Liberation Army, No 411 Hospital, Shanghai, People's Republic of China – sequence: 10 givenname: Zhaosheng surname: Li fullname: Li, Zhaosheng email: zhaoshenli.smmu.edu@hotmail.com organization: Department of Gastroenterology, Changhai Hospital, Shanghai, 200433, People's Republic of China. zhaoshenli.smmu.edu@hotmail.com – sequence: 11 givenname: Keping surname: Xie fullname: Xie, Keping email: kepxie@mdanderson.org organization: Department of Gastroenterology, Hepatology and Nutrition, Unit 1466, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, 77030, USA. kepxie@mdanderson.org |
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Snippet | The therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a variety of... Background The therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a... BACKGROUNDThe therapeutic and prognostic value of the glycolytic enzymes hexokinase, phosphofructokinase, and pyruvate kinase (PK) has been implicated in a... |
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SubjectTerms | Adult Aged Animals Biological markers Carrier Proteins - genetics Carrier Proteins - metabolism Cell Line, Tumor Cell Proliferation - genetics Cell Proliferation - physiology Cells Gene Expression Regulation, Neoplastic - genetics Gene Expression Regulation, Neoplastic - physiology Hexokinase - genetics Hexokinase - metabolism Humans Klatskin Tumor - genetics Klatskin Tumor - metabolism Klatskin Tumor - pathology Male Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Inbred BALB C Middle Aged Neoplasm Recurrence, Local - genetics Neoplasm Recurrence, Local - metabolism Neoplasm Recurrence, Local - pathology Prognosis Protein Isoforms - genetics Protein Isoforms - metabolism Syndecan-2 - genetics Syndecan-2 - metabolism Thyroid Hormone-Binding Proteins Thyroid Hormones - genetics Thyroid Hormones - metabolism |
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Title | PKM2 regulates neural invasion of and predicts poor prognosis for human hilar cholangiocarcinoma |
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