Ming Tan

University of South Alabama, Mobile, Alabama, United States

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Publications (25)102.99 Total impact

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    ABSTRACT: Lactotransferrin (LTF), also known as lactoferrin, is a key component of innate immune defense. We previously reported that LTF was downregulated in nasopharyngeal carcinoma (NPC) and could suppress NPC cell proliferation. However, the relevance of the relationship between LTF expression and NPC clinical outcome has not been reported. This study aims to assess the possible correlations between LTF expression and clinical parameters and its potential prognostic predictive ability in the outcomes of patients with NPC. Complementary DNA (cDNA) microarray, quantitative real-time PCR (qRT-PCR), and immunohistochemistry (IHC) results suggested that LTF expression was significantly downregulated in NPC tissues compared to non-NPC tissues. LTF was negatively correlated with lymph node metastasis (P = 0.042), T stage (P < 0.001), clinical tumor-node-metastasis (TNM) stage (P = 0.022), and EBV-encoded RNA 1 (EBER-1) expression (r = -.167, P = 0.016). A survival analysis of 108 patients with NPC revealed that positive expression of LTF could predict a good prognosis [disease-free survival (DFS): P = 0.043, overall survival (OS): P = 0.040]. Multivariable analysis revealed that LTF could independently predict prognosis (DFS: HR = 0.414, P = 0.003; OS: HR = 0.309, P = 0.005). These observations indicated that LTF is a potential prognostic factor of NPC.
    Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine. 10/2014;
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    ABSTRACT: Human SPLUNC1 can suppress NPC tumor formation, however, the correlation between SPLUNC1expression and NPC patient prognosis has not been reported. In this study, we used a large-scale sample of 1,015 tissue cores to detect SPLUNC1 expression and its association with patient prognosis. SPLUNC1 expression was reduced in NPC samples compared to non-tumor nasopharyngeal epithelial (NPE) tissues. Positive expression of SPLUNC1 in NPC predicted a better prognosis (Disease Free Survival (DFS): P=0.034, Overall Survival (OS): P=0.048). Cox's Proportional Hazards Model revealed that SPLUNC1 could be a significant prognostic factor affecting DFS (P=0.027). A cDNA microarray analyzed by SAM and IPA revealed that an indirect interaction existed between SPLUNC1 and retinoic acid (RA) in the cancer regulatory network. To further investigate the molecular mechanisms involved, we utilized several bioinformatics tools and identified 12 retinoid X receptors (RXRs) heterodimer binding sites in the promoter region of the SPLUNC1 gene. The transcriptional activity of the SPLUNC1 promoter was up-regulated significantly by all-trans-retinoic acid (ATRA). SPLUNC1 and RA receptor expression were induced significantly by ATRA, and removal of ATRA led to a progressive loss of SPLUNC1 and RA receptor expression. ATRA inhibited proliferation and induced the differentiation of NPC cells. Interestingly, over-expression of SPLUNC1 sensitized NPC cells to ATRA, whereas knockdown of SPLUNC1 in HNE1 cells increased cell viability. Under SPLUNC1 knockdown conditions, differentiation was reversed with ATRA treatment. We concluded that SPLUNC1 could potentially predict prognosis for NPC patients and play an important role in ATRA-induced growth inhibition and differentiation in NPC cells.This article is protected by copyright. All rights reserved.
    FEBS Journal 08/2014; · 4.25 Impact Factor
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    ABSTRACT: Nasopharyngeal carcinoma (NPC) is a major head and neck cancer with high occurrence in Southeast Asia and southern China. To identify novel biomarkers for the early detection of NPC patients, 2D-DIGE combined with MALDI-TOF-MS analysis was performed to identify differentially expressed proteins in the carcinogenesis and progression of NPC using LCM-purified normal nasopharyngeal epithelial tissues and various stages of NPC biopsies. As a result, 26 differentially expressed proteins were identified, of which two proteins with sharp expressional changes in the carcinogenic process, ENO1 and CYPA, were validated by western blot analysis and identified as critical seed proteins in the functional network. Immunohistochemistry assay was further performed to detect the expression of the two proteins with a tissue microarray that included various stages of NPC tissues. The ability of these proteins to detect NPC early was evaluated via a receiver operating characteristic analysis. The results indicated that the combination of the two proteins could perfectly discriminate NNET and AH from stage I of NPC with high sensitivity and specificity, which is more effective than using either of the two proteins individually. In summary, the combination of ENO1 and CYPA can serve as potential molecular markers for the early detection of NPC.
    Journal of Proteomics 07/2014; · 4.09 Impact Factor
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    ABSTRACT: Compared to normal cells, cancer cells strongly upregulate glucose uptake and glycolysis to give rise to increased yield of intermediate glycolytic metabolites and the end product pyruvate. Moreover, glycolysis is uncoupled from the mitochondrial tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) in cancer cells. Consequently, the majority of glycolysis-derived pyruvate is diverted to lactate fermentation and kept away from mitochondrial oxidative metabolism. This metabolic phenotype is known as the Warburg effect. While it has become widely accepted that the glycolytic intermediates provide essential anabolic support for cell proliferation and tumor growth, it remains largely elusive whether and how the Warburg metabolic phenotype may play a role in tumor progression. We hereby review the cause and consequence of the restrained oxidative metabolism, in particular in tumor metastasis. Cells change or lose their extracellular matrix during the metastatic process. Inadequate/inappropriate matrix attachment generates reactive oxygen species (ROS) and causes a specific type of cell death, termed anoikis, in normal cells. Although anoikis is a barrier to metastasis, cancer cells have often acquired elevated threshold for anoikis and hence heightened metastatic potential. As ROS are inherent byproducts of oxidative metabolism, forced stimulation of glucose oxidation in cancer cells raises oxidative stress and restores cells' sensitivity to anoikis. Therefore, by limiting the pyruvate flux into mitochondrial oxidative metabolism, the Warburg effect enables cancer cells to avoid excess ROS generation from mitochondrial respiration and thus gain increased anoikis resistance and survival advantage for metastasis. Consistent with this notion, pro-metastatic transcription factors HIF and Snail attenuate oxidative metabolism, whereas tumor suppressor p53 and metastasis suppressor KISS1 promote mitochondrial oxidation. Collectively, these findings reveal mitochondrial oxidative metabolism as a critical suppressor of metastasis and justify metabolic therapies for potential prevention/intervention of tumor metastasis.
    Cancer letters 04/2014; · 5.02 Impact Factor
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    ABSTRACT: As a special class of short non-coding RNAs, microRNAs (a.k.a. miRNAs or miRs) have been reported to perform important roles in various biological processes by regulating respective target genes. However, significant barriers exist during biologists' conventional miR knowledge discovery. Emerging semantic technologies, which are based upon domain ontologies, can render critical assistance to this problem. Our previous research has investigated the construction of a miR ontology, named Ontology for MIcroRNA Target Prediction (OMIT), the very first of its kind that formally encodes miR domain knowledge. Although it is unavoidable to have a manual component contributed by domain experts when building ontologies, many challenges have been identified for a completely manual development process. The most significant issue is that a manual development process is very labor-intensive and thus extremely expensive. Therefore, we propose in this paper an innovative ontology development methodology. Our contributions can be summarized as: (i) We have continued the development and critical improvement of OMIT, solidly based on our previous research outcomes. (ii) We have explored effective and efficient algorithms with which the ontology development can be seamlessly combined with machine intelligence and be accomplished in a semi-automated manner, thus significantly reducing large amounts of human efforts. A set of experiments have been conducted to thoroughly evaluate our proposed methodology.
    PLoS ONE 01/2014; 9(7):e100855. · 3.53 Impact Factor
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    ABSTRACT: Recent studies have revealed that long non-coding RNAs participate in all steps of cancer initiation and progression by regulating protein-coding genes at the epigenetic, transcriptional, and post-transcriptional levels. Long non-coding RNAs are in turn regulated by other genes, forming a complex regulatory network. The regulation networks between the p53 tumor suppressor and these RNAs in nasopharyngeal carcinoma remains unclear. The aims of this study were to investigate the regulatory roles of the TP53 gene in regulating long non-coding RNA expression profiles and to study the function of a TP53-regulated long non-coding RNA (LOC401317) in the nasopharyngeal carcinoma cell line HNE2. Long non-coding RNA expression profiling indicated that 133 long non-coding RNAs were upregulated in the human NPC cell line HNE2 cells following TP53 overexpression, while 1057 were downregulated. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. Further studies indicated that LOC401317 is directly regulated by p53 and that ectopic expression of LOC401317 inhibits HNE2 cell proliferation in vitro and in vivo by inducing cell cycle arrest and apoptosis. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage. Collectively, these results suggest that LOC401317 is directly regulated by p53 and exerts antitumor effects in HNE2 nasopharyngeal carcinoma cells.
    PLoS ONE 01/2014; 9(11):e110674. · 3.53 Impact Factor
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    ABSTRACT: Triple-negative breast cancer (TNBC) is a highly diverse group that is associated with an aggressive phenotype. Its treatment has been challenging due to its heterogeneity and absence of well-defined molecular targets. Thus, there is an urgent need to identify novel agents with therapeutic application. NF-κB is over-expressed in many breast cancers; thus, inactivation of the NF-κB pathway could serve as a therapeutic target. Here we report for the first time the anti-tumor activity of panepoxydone (PP), a NF-κB inhibitor isolated from an edible mushroom, in several breast cancer cell lines.
    PLoS ONE 01/2014; 9(6):e98370. · 3.53 Impact Factor
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    Acta Biochimica et Biophysica Sinica 12/2013; · 1.81 Impact Factor
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    ABSTRACT: The M2 isoform of pyruvate kinase (PKM2) plays an important role in aerobic glycolysis and is a mediator of the Warburg effect in tumors. It was previously thought that tumor cells switch expression of PKM from normal tissue-expressed PKM1 to tumor-specific PKM2 via an alternative splicing mechanism. This view was challenged by a recent report demonstrating that PKM2 is already the major PKM isoform expressed in many differentiated normal tissues. Here, through analyses on sixteen tumor types using the cancer genome atlas RNA-Seq and exon array datasets, we confirmed that isoform switch from PKM1 to PKM2 occurred in glioblastomas but not in other tumor types examined. Despite lacking of isoform switches, PKM2 expression was found to be increased in all cancer types examined, and correlated strongly to poor prognosis in head and neck cancers. We further demonstrated that elevated PKM2 expression correlated well with the hypomethylation status of intron 1 of the PKM gene in multiple cancer types, suggesting epigenetic regulation by DNA methylation as a major mechanism in controlling PKM transcription in tumors. Our study suggests that isoform switch of PKM1 to PKM2 in cancers is tissue-specific and targeting PKM2 activity in tumors remains a promising approach for clinical intervention of multiple cancer types.
    Oncotarget 08/2013; · 6.64 Impact Factor
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    ABSTRACT: Cancer cells are markedly different from normal cells with regards to how their metabolic pathways are used to fuel cellular growth and survival. Two basic metabolites that exemplify these differences through increased uptake and altered metabolic usage are glucose and glutamine. These molecules can be catabolized to manufacture many of the building blocks required for active cell growth and proliferation. The alterations in the metabolic pathways necessary to sustain this growth have been linked to therapeutic resistance, a trait that is correlated with poor patient outcomes. By targeting the metabolic pathways that import, catabolize, and synthesize essential cellular components, drug-resistant cancer cells can often be resensitized to anticancer treatments. The specificity and efficacy of agents directed at the unique aspects of cancer metabolism are expected to be high; and may, when in used in combination with more traditional therapeutics, present a pathway to surmount resistance within tumors that no longer respond to current forms of treatment. Cancer Res; 73(9); 1-9. ©2013 AACR.
    Cancer Research 04/2013; · 9.28 Impact Factor
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    ABSTRACT: HSF1, a master regulator of heat shock responses, plays an important role in tumorigenesis. In this study we demonstrated that HSF1 is required for chemotherapeutic agents -induced cytoprotective autophagy through transcriptional upregulation of autophagy related gene ATG7. Interestingly, this is independent of HSF1s heat shock response function. Treatment of cancer cells with FDA approved chemotherapeutic agent Carboplatin induced autophagy and growth inhibition, which was significantly increased upon knockdown of HSF1. Mechanistic studies revealed that HSF1 regulates autophagy by directly binding to ATG7 promoter and transcriptionally upregulating its expression. Significantly, breast cancer patient sample study revealed that higher ATG7 expression level is associated with poor patient survival. This novel finding was further confirmed by analysis of two independent patient databases, demonstrating a prognostic value of ATG7. Furthermore, a strong positive correlation was observed between levels of HSF1 and ATG7 in triple negative breast cancer patient samples, thus validating our in-vitro findings. This is the first study identifying a critical role for HSF1 in controlling cytoprotective autophagy through regulation of ATG7, which is distinct from HSF1s function in heat shock response. This is also the first study demonstrating a prognostic value of ATG7 in breast cancer patients. These findings strongly argue that combining chemotherapeutic agents with autophagy inhibition by repressing HSF1/ATG7 axis represents a promising strategy for future cancer treatment.
    Journal of Biological Chemistry 02/2013; · 4.65 Impact Factor
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    ABSTRACT: Chemoresistance is a major obstacle in cancer treatment. Our previous studies have shown that miR-125b plays an important role in chemoresistance. Here we report a novel mechanism that upregulation of miR-125b through Wnt signaling by Snail enriches cancer stem cells. Overexpression of Snail dramatically increases the expression of miR-125b, through Snail activated Wnt/beta-catenin/TCF4 axis. Snail confers chemoresistance by repressing Bak1 through upregulation of miR-125b. Restoring the expression of Bak1 or depleting miR-125b re-sensitizes Snail-expressing cancer cells to Taxol, indicating that miR-125b is critical in Snail-induced chemoresistance. Moreover, overexpression of miR-125b significantly increases the cancer stem cell population (CD24-CD44+), while depletion of miR-125b or rescue of the expression of Bak1 increases the non-stem cell population (CD24+CD44+) in Snail-overexpressing cells. These findings strongly support that miR-125b functions as a key mediator in Snail-induced cancer stem cells and chemoresistance. This novel mechanism for Snail-induced stem cell propagation and chemoresistance may have important implications in the development of strategies for overcoming cancer cell resistance to chemotherapy.
    Journal of Biological Chemistry 12/2012; · 4.65 Impact Factor
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    ABSTRACT: It is well known that ErbB2, a receptor tyrosine kinase, localizes to the plasma membrane. Here we describe a novel observation that ErbB2 also localizes in mitochondria of cancer cells and patient samples. We found that ErbB2 translocates into mitochondria through association with mtHSP70. Additionally, mitochondrial ErbB2 (mtErbB2) negatively regulates mitochondrial respiratory functions. Oxygen consumption and activities of complexes of the mitochondrial electron transport chain were decreased in mtErbB2-overexpressing cells. Mitochondrial membrane potential and cellular ATP levels were also decreased. In contrast, mtErbB2 enhanced cellular glycolysis. The translocation of ErbB2 and its impact on mitochondrial function are kinase dependent. Interestingly, cancer cells with higher levels of mtErbB2 were more resistant to the ErbB2-targeting antibody trastuzumab. Our study provides a novel perspective on the metabolic regulatory function of ErbB2 and reveals that mtErbB2 has an important role in the regulation of cellular metabolism and cancer cell resistance to therapeutics.
    Nature Communications 12/2012; 3:1271. · 10.74 Impact Factor
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    ABSTRACT: Cancer cells exhibit altered glucose metabolism characterized by a preference for aerobic glycolysis or the Warburg effect, and the cells resist matrix detachment-induced apoptosis, which is called anoikis, a barrier to metastasis. It remains largely unclear whether tumor metabolism influences anoikis and metastasis. Here we show that when detached from the matrix, untransformed mammary epithelial cells undergo metabolic reprogramming by markedly upregulating pyruvate dehydrogenase (PDH) kinase 4 (PDK4) through estrogen-related receptor gamma (ERRγ), thereby inhibiting PDH and attenuating the flux of glycolytic carbon into mitochondrial oxidation. To decipher the significance of this metabolic response, we found that depletion of PDK4 or activation of PDH increased mitochondrial respiration and oxidative stress in suspended cells, resulting in heightened anoikis. Conversely, overexpression of PDKs prolonged survival of cells in suspension. Therefore, decreased glucose oxidation following cell detachment confers anoikis resistance. Unlike untransformed cells, most cancer cells demonstrate reduced glucose oxidation even under attached conditions, and thus they inherently possess a survival advantage when suspended. Normalization of glucose metabolism by stimulating PDH in cancer cells restores their susceptibility to anoikis and impairs their metastatic potential. These results suggest that the Warburg effect, more specifically, diminished glucose oxidation, promotes anoikis resistance and metastasis and that PDKs are potential targets for antimetastasis therapy.
    Molecular and Cellular Biology 03/2012; 32(10):1893-907. · 5.04 Impact Factor
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    ABSTRACT: Computational techniques have been adopted in medical and biological systems for a long time. There is no doubt that the development and application of computational methods will render great help in better understanding biomedical and biological functions. Large amounts of datasets have been produced by biomedical and biological experiments and simulations. In order for researchers to gain knowledge from original data, nontrivial transformation is necessary, which is regarded as a critical link in the chain of knowledge acquisition, sharing, and reuse. Challenges that have been encountered include: how to efficiently and effectively represent human knowledge in formal computing models, how to take advantage of semantic text mining techniques rather than traditional syntactic text mining, and how to handle security issues during the knowledge sharing and reuse. This paper summarizes the state-of-the-art in these research directions. We aim to provide readers with an introduction of major computing themes to be applied to the medical and biological research.
    World journal of biological chemistry. 02/2012; 3(2):27-33.
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    ABSTRACT: MicroRNA is a set of small RNA molecules mediating gene expression at post-transcriptional/translational levels. Most of well-established high throughput discovery platforms, such as microarray, real time quantitative PCR, and sequencing, have been adapted to study microRNA in various human diseases. The total number of microRNAs in humans is approximately 1,800, which challenges some analytical methodologies requiring a large number of entries. Unlike messenger RNA, the majority of microRNA (>60%) maintains relatively low abundance in the cells. When analyzed using microarray, the signals of these low-expressed microRNAs are influenced by other non-specific signals including the background noise. It is crucial to distinguish the true microRNA signals from measurement errors in microRNA array data analysis. In this study, we propose a novel measurement error model-based normalization method and differentially-expressed microRNA detection method for microRNA profiling data acquired from locked nucleic acids (LNA) microRNA array. Compared with some existing methods, the proposed method significantly improves the detection among low-expressed microRNAs when assessed by quantitative real-time PCR assay.
    PLoS ONE 01/2012; 7(5):e37537. · 3.53 Impact Factor
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    ABSTRACT: MicroRNAs (miRNAs) play important roles in various biological processes by regulating their target genes. Therefore, miRNAs are closely associated with development, diagnosis, and prognosis for many diseases. The prediction of miRNA targets remains a challenging task for biologists because it involves an extremely large amount of data sources to be explored: to manually integrate information of identified targets and related information from various sources is time-consuming and error-prone; most of all, it is subject to biologists' limited prior knowledge. In this paper we investigated an ontology-based knowledge sharing framework to assist biologists in unraveling important roles of miRNAs in human disease in an automated and more efficient manner, (i) We developed the very first domain-specific ontologies in the miRNA field, Ontology for MicroRNA Target (OMIT), (ii) According to the global metadata model defined in ontologies, heterogeneous data sources were annotated and seamlessly integrated and stored into a central Resource Description Framework (RDF) data repository, (iii) We then enabled ontology-based queries, instead of traditional SQL queries, by inferring new statements from RDF data triples. Consequently we were able to acquire hidden knowledge originally implicit and unclear, yet critical, to biologists.
    Bioinformatics and Biomedicine Workshops (BIBMW), 2012 IEEE International Conference on; 01/2012
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    ABSTRACT: Identification and characterization of the important roles microRNAs (miRNAs) perform in human cancer is an increasingly active research area. Unfortunately, prediction of miRNA target genes remains a challenging task to cancer researchers. Current processes are time-consuming, error-prone, and subject to biologists' limited prior knowledge. Therefore, we propose a domain-specific knowledge base built upon Ontology for MicroRNA Targets (OMIT) to facilitate knowledge acquisition in miRNA target gene prediction. We describe the ontology design, semantic annotation and data integration, and user-friendly interface and conclude that the OMIT system can assist biologists in unraveling the important roles of miRNAs in human cancer. Thus, it will help clinicians make sound decisions when treating cancer patients.
    Pharmaceutical Research 08/2011; 28(12):3101-4. · 4.74 Impact Factor
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    ABSTRACT: In many types of cancer, the expression of the immunoregulatory protein B7-H3 has been associated with poor prognosis. Previously, we observed a link between B7-H3 and tumor cell migration and invasion, and in present study, we have investigated the role of B7-H3 in chemoresistance in breast cancer. We observed that silencing of B7-H3, via stable short hairpin RNA or transient short interfering RNA transfection, increased the sensitivity of multiple human breast cancer cell lines to paclitaxel as a result of enhanced drug-induced apoptosis. Overexpression of B7-H3 made the cancer cells more resistant to the drug. Next, we investigated the mechanisms behind B7-H3-mediated paclitaxel resistance and found that the level of Stat3 Tyr705 phosphorylation was decreased in B7-H3 knockdown cells along with the expression of its direct downstream targets Mcl-1 and survivin. The phosphorylation of Janus kinase 2 (Jak2), an upstream molecule of Stat3, was also significantly decreased. In contrast, reexpression of B7-H3 in B7-H3 knockdown and low B7-H3 expressing cells increased the phosphorylation of Jak2 and Stat3. In vivo animal experiments showed that B7-H3 knockdown tumors displayed a slower growth rate than the control xenografts. Importantly, paclitaxel treatment showed a strong antitumor activity in the mice with B7-H3 knockdown tumors, but only a marginal effect in the control group. Taken together, our data show that in breast cancer cells, B7-H3 induces paclitaxel resistance, at least partially by interfering with Jak2/Stat3 pathway. These results provide novel insight into the function of B7-H3 and encourage the design and testing of approaches targeting this protein and its partners.
    Molecular Cancer Therapeutics 06/2011; 10(6):960-71. · 5.60 Impact Factor
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    ABSTRACT: Trastuzumab shows remarkable efficacy in treatment of ErbB2-positive breast cancers when used alone or in combination with other chemotherapeutics. However, acquired resistance develops in most treated patients, necessitating alternate treatment strategies. Increased aerobic glycolysis is a hallmark of cancer and inhibition of glycolysis may offer a promising strategy to preferentially kill cancer cells. In this study, we investigated the antitumor effects of trastuzumab in combination with glycolysis inhibitors in ErbB2-positive breast cancer. We found that trastuzumab inhibits glycolysis via downregulation of heat shock factor 1 (HSF1) and lactate dehydrogenase A (LDH-A) in ErbB2-positive cancer cells, resulting in tumor growth inhibition. Moreover, increased glycolysis via HSF1 and LDH-A contributes to trastuzumab resistance. Importantly, we found that combining trastuzumab with glycolysis inhibition synergistically inhibited trastuzumab-sensitive and -resistant breast cancers in vitro and in vivo, due to more efficient inhibition of glycolysis. Taken together, our findings show how glycolysis inhibition can dramatically enhance the therapeutic efficacy of trastuzumab in ErbB2-positive breast cancers, potentially useful as a strategy to overcome trastuzumab resistance.
    Cancer Research 04/2011; 71(13):4585-97. · 9.28 Impact Factor

Publication Stats

292 Citations
102.99 Total Impact Points

Institutions

  • 2010–2014
    • University of South Alabama
      • Department of Cell Biology and Neuroscience
      Mobile, Alabama, United States
  • 2013
    • Central South University
      • Cancer Research Institute
      Ch’ang-sha-shih, Hunan, China
    • IDIBELL Bellvitge Biomedical Research Institute
      Barcino, Catalonia, Spain