Jun-Nian Zheng

Nevada cancer institute, Las Vegas, Nevada, United States

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Publications (77)206.32 Total impact

  • No preview · Article · Apr 2016
  • Wen-Qi Du · Jun-Nian Zheng · Dong-Sheng Pei
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    ABSTRACT: Introduction: The salt-inducible kinases originally cloned in adrenal glands of high salt diet-fed rats, generally named as SIKs, are highly evolutionarily conserved serine/threonine protein kinases belonging to a family of AMP-activated protein kinase (AMPK). Overexpression of SIK2 and SIK3 is discovered in many tumors. Whereas, SIK1 expression was significantly lower in tumors than in normal tissues. Areas covered: The main aim of our review is to introduce the signaling pathways as well as its mechanisms underlying their activity regulation, and especially the roles they play in cancer, which may shed light on the prospects of the cancer prevention and therapeutic targeting of SIKs in the future. Expert opinion: It is conceivable that SIKs, mainly stimulated by ACTH, LKB1, TGF-β, and autophosphorylation, play crucial roles in regulating multiple signal pathways in cancer cells and controlling a series of cellular processes including cell proliferation and cell apoptosis. More recent studies about SIKs are emerging, and their overexpression is found in a few specific types of cancers. However, correlations between SIKs and carcinogenesis remain to be fully elucidated.
    No preview · Article · Nov 2015 · Expert Opinion on Therapeutic Targets
  • Jin Bai · Yan-Su Chen · Peng-Jin Mei · Qing-Hua Liu · Ying Du · Jun-Nian Zheng
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    ABSTRACT: PinX1, a conserved nuclear protein, could maintain telomere integrity and plays an important role in regulating telomerase activity. It has been reported that the expression of PinX1 is down-regulated in some cancer and associated with cancer prognosis. However, the value of PinX1 in gliomas has not been studied. In this study, two independent retrospective gliomas cohorts with the corresponding gliomas tissue microarrays (TMAs) were established to detect the expression level of PinX1 and the correlation of PinX1 expression with the clinicopathological features and the patients' survival. Compared with non-cancerous brain tissues, PinX1 protein levels were remarkably up-regulated in gliomas (P = 0.001), and further increased from benign gliomas tissues to malignant gliomas tissues (P = 0.090). Moreover, high PinX1 expression was significantly positively associated with gliomas WHO grade in the training set (P = 0.019) and the validation set (P = 0.037). High PinX1 expression significantly correlated with a worse 5-year overall (P = 0.016) and disease-specific survival (P = 0.026). Simultaneously, the multivariate COX regression analysis showed that PinX1 was an independent unfavorable prognostic factor for 5-year overall survival (hazard ratio (HR) = 2.078, P = 0.015) and disease-specific survival (HR = 2.429, P = 0.012) after adjusting with age, sex and WHO grade in gliomas. In conclusion, PinX1 expression may serve as a prognostic and predictive biomarker for gliomas.
    No preview · Article · Aug 2015 · International journal of clinical and experimental pathology
  • Dong-Sheng Pei · Jie-Hui Di · Wen-Qi Du · Jun-Nian Zheng
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    ABSTRACT: The transcription factor p53 plays a critical role in maintaining homeostasis as it relates to cellular growth, proliferation, and metabolism. In an effort to identify novel p53 target genes, a microarray approach was utilized to identify Rap2B as a robust candidate gene. Rap2B belongs to the Rap family and its increased expression can be found in a variety of human tumors. Here, we demonstrate that Rap2B can regulate the motility of tumor cells as well as mouse normal cells. Noteworthy, p53 modulated cell motility in the low glucose levels. The effect of p53 on cell migration was mediated through its target gene, Rap2B. As a target gene of p53, the investigations of Rap2B potential function will provide novel insight into an unexpected role for p53 in cell migration with implications in embryogenesis or inflammatory response. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    No preview · Article · Jul 2015 · Molecular Carcinogenesis
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    ABSTRACT: As one of the members of the PLC family, the phosphoinositide-specific phospholipase Cε (PLCε) has been shown to play pivotal roles in multiple signal pathways and control a variety of cellular functions. A number of studies have shown that aberrant regulation of PLCε was involved in various types of animal and human cancer. However, the role of PLCε in cancer remains elusive. In this review, we provide an overview of the PLCε, especially its roles in multiple signal pathways, and summarize the recent findings that highlight the roles of PLCε in carcinogenesis and cancer progression, making an avenue to provide a novel therapeutic strategy for the treatment of cancer. A literature search mainly paying attention to the network of PLCε involved in tumorigenesis and development was performed in electronic databases. PLCε plays a key role in medicating the development and progression of human cancers with highest potency to be a target of cancer prevention and treatment.
    No preview · Article · Jun 2015 · Journal of Cancer Research and Clinical Oncology
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    ABSTRACT: Recent studies suggest that SATB1 is a promising therapeutic target for prostate cancer. To develop novel SATB1-based therapeutic agents for prostate cancer, in this study, we aimed to construct ZD55-SATB1, an oncolytic adenovirus ZD55 carrying shRNA targeting SATB1, and investigate its effects on the inhibition of prostate cancer growth and metastasis. ZD55-SATB1 was constructed and used to infect human prostate cancer cell lines DU145 and LNCaP. The inhibitory effect of ZD55-SATB1 on SATB1 expression was evaluated by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis. The cytotoxicity of ZD55-SATB1 was detected by MTT assay. Cell invasion was detected by Matrigel invasion assay. The in vivo antitumor activities of ZD55-SATB1 were evaluated in xenograft mouse model. We found that ZD55-SATB1 selectively replicated and significantly reduced SATB1 expression in DU145 and LNCaP cells. ZD55-SATB1 effectively inhibited the viability and invasion of DU145 and LNCaP cells in vitro and inhibited prostate cancer growth and metastasis in xenograft nude mice. In conclusion, replicative oncolytic adenovirus armed with SATB1 shRNA exhibits effective antitumor effect in human prostate cancer. Our study provides the basis for the development of ZD55-SATB1 for the treatment of prostate cancer.
    No preview · Article · Jun 2015 · Tumor Biology
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    ABSTRACT: As one of the COP9 signalosome complex, CSN5 (also known as Jab1) has been confirmed overexpression in many human cancers and affected multiple pathways associating with cell proliferation and apoptosis. Correlation of CSN5 overexpression with poor prognosis for cancer provides evidence that it is involved in the tumorigenesis. However, little is known about the functional role and the underlying mechanism of CSN5 in gastric cancer progression. In the current study, the effect of CSN5 siRNA (small-interfering RNA) on the proliferation and apoptosis of human gastric cancer cells (AGS and MKN45) were examined. Our results showed that knockdown of CSN5 could inhibit proliferation and promote apoptosis of gastric cancer cells. Additionally, suppression of CSN5 expression contributed to the increased expression levels of p53 and Bax. In conclusion, CSN5 overexpression is significantly correlated with gastric cancer progression, and CSN5 could be a novel target in gastric cancer therapy. Copyright © 2015 Elsevier Ltd. All rights reserved.
    No preview · Article · May 2015 · Bioorganic & medicinal chemistry letters
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    ABSTRACT: CHIP (c-terminal Hsp70-interacting protein) is an E3 ligase which may play different roles in different cancers. The elucidation of the VHL-HIF-1α(hypoxia inducible factor-1α)-VEGF (vascular endothelial growth factor) pathway has led to the development of targeted therapy in renal cell carcinoma (RCC). However, little is known about the role of CHIP and the relationship between CHIP and VEGF-VEGFR2 (VEGF receptor 2) pathway in RCC. In this study, we found that the expression of CHIP was downregulated and significantly correlated with pT status (P = 0.022) and TNM stage (P = 0.022) in 304 RCC and 35 normal renal tissues using tissue microarray. Moreover, low expression of CHIP is a strong and independent negative prognostic value for RCC. In vitro, CHIP negatively regulated RCC cell migration, invasion and angiogenesis. In addition, ELISA tests showed that restoration of CHIP inhibited, while knockdown promoted, the secreted level of VEGF. Furthermore, western blot indicated that the VEGFR2 protein level was reduced after CHIP overexpression. Our findings demonstrate for the first time that CHIP may be involved in RCC angiogenesis through regulating VEGF secretion and expression of VEGFR2. CHIP may serve as promising prognostic biomarker of angiogenesis and may constitute a potential therapeutic target in RCC.
    Preview · Article · May 2015 · Scientific Reports
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    ABSTRACT: PIN2/TRF1-interacting telomerase inhibitor 1 (PinX1) is a novel cloned gene which has been identified as a major haploinsufficient tumor suppressor essential for maintaining telomerase activity, the length of telomerase and chromosome stability. This study explored the clinical significance and biological function of PinX1 in human clear cell renal cell carcinoma (ccRCC). The clinical relevance of PinX1 in ccRCC was evaluated using tissue microarray and immunohistochemical staining in two independent human ccRCC cohorts. Our data demonstrated that PinX1 expression was dramatically decreased in ccRCC tissues compared with normal renal tissues and paired adjacent non-tumor tissues. Low PinX1 expression was significantly correlated with depth of invasion, lymph node metastasis and advanced TNM stage in patients, as well as with worse overall and disease-specific survival. Cox regression analysis revealed that PinX1 expression was an independent prognostic factor for ccRCC patients. Moreover, PinX1 inhibited the migration and invasion of ccRCC by suppressing MMP-2 expression and activity via NF-κB-dependent transcription in vitro. In vivo studies confirmed that PinX1 negatively regulated ccRCC metastasis and the expression of MMP-2 and NF-κB-p65. These findings indicate that PinX1 suppresses ccRCC metastasis and may serve as a ccRCC candidate clinical prognostic marker and a potential therapeutic target.
    Preview · Article · May 2015 · Oncotarget
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    ABSTRACT: The neutrophil-to-lymphocyte ratio (NLR) is a strong predictor of mortality in patients with colorectal, lung, gastric cancer, pancreatic and metastatic renal cell carcinoma. We here evaluated whether preoperative NLR is an independent prognostic factor for non-metastatic renal cell carcinoma (RCC). Data from 327 patients who underwent curative or palliative nephrectomy were evaluated retrospectively. In preoperative blood routine examination, neutrophils and lymphocytes were obtained. The predictive value of NLR for non-metastatic RCC was analyzed. The NLR of 327 patients was 2.72±2.25. NLR <1.7 and NLR ≥1.7 were classified as low and high NLR groups, respectively. Chi-square test showed that the preoperative NLR was significantly correlated with the tumor size (P=0.025), but not with the histological subtype (P=0.095)and the pT stage (P=0.283). Overall survival (OS) and disease-free survival (DFS) were assessed using the Kaplan-Meier method. Effects of NLR on OS (P=0.007) and DFS (P=0.011) were significant. To evaluate the independent prognostic significance of NLR, multivariate COX regression models were applied and identified increased NLR as an independent prognostic factor for OS (P=0.015), and DFS (P=0.019). Regarding patient survival, an increased NLR represented an independent risk factor, which might reflect a higher risk for severe cardiovascular and other comorbidities. An elevated blood NLR may be a biomarker of poor OS and DFS in patients with non-metastatic RCC.
    No preview · Article · May 2015 · Asian Pacific journal of cancer prevention: APJCP
  • Qing-Hua Liu · Mei-Lin Shi · Jin Bai · Jun-Nian Zheng
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    ABSTRACT: The aim of this study was to investigate the clinical significance of annexin a1 (ANXA1) and provide molecular evidence to support that decreased ANXA1 expression could enhance cancer migration and invasion in pancreatic ductal adenocarcinoma (PDAC). Immunohistochemistry of a tissue microarray with 162 surgically resected PDAC specimens was performed to examine the expression of ANXA1. We also investigated the relationship between ANXA1 expression and clinicopathological factors and prognosis of PDAC patients. We further studied the role of ANXA1 in PDAC cell proliferation, migration and invasion by cell proliferation assay, migration assay and matrigel invasion assay with reduced ANXA1 expression by RNAi. Western blotting was used to detect matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) expression. We also detected MMP-9 enzyme activity by gelatin zymography. Decreased expression of ANXA1 was significantly associated with poor differentiation, lymph node metastasis and advanced TNM stage of PDAC patients (p<0.05). Moreover, decreased expression of ANXA1 was correlated with poor survival (p<0.05). Furthermore, we found that ANXA1 knockdown inhibited cell proliferation, induced G1 phase cell cycle arrest, increased PDAC cell migration and invasion capacity compared with controls. In addition, Western blotting showed that ANXA1 knockdown increased the MMP-9 protein level and decreased TIMP-1 expression. Gelatin zymography showed that MMP-9 enzyme activity was also elevated. Negative ANXA1 expression is a most unfavorable prognostic factor for PDAC patients. ANXA1 knockdown inhibits cell proliferation by inducing G1 phase cell cycle arrest and increases migration and invasion of PDAC cells through up-regulating MMP-9 expression and activity, implying that ANXA1 may serve as a promising prognostic biomarker and therapeutic target for PDAC.
    No preview · Article · Apr 2015 · Asian Pacific journal of cancer prevention: APJCP
  • Peng-Jin Mei · Yan-Su Chen · Ying Du · Jin Bai · Jun-Nian Zheng
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    ABSTRACT: PinX1 induces apoptosis and suppresses cell proliferation in some cancer cells, and the expression of PinX1 is frequently decreased in some cancer and negatively associated with metastasis and prognosis. However, the precise roles of PinX1 in gliomas have not been studied. In this study, we found that PinX1 obviously reduced the gliomas cell proliferation through regulating the expressions of cell cycle-relative molecules to arrest cell at G1 phase and down-regulating the expression of component telomerase reverse transcriptase (hTERT in human), which is the hardcore of telomerase. Moreover, PinX1 could suppress the abilities of gliomas cell wound healing, migration and invasion via suppressing MMP-2 expression and increasing TIMP-2 expression. In conclusion, our results suggested that PinX1 may be a potential suppressive gene in the progression of gliomas.
    No preview · Article · Mar 2015 · Medical Oncology
  • Jin-Xia Wu · Ding-Guo Zhang · Jun-Nian Zheng · Dong-Sheng Pei
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    ABSTRACT: The p53 transcription factor is a critical regulator of the cell cycle, DNA repair, and apoptosis. Recent evidences suggest that p53 may contribute to the regulation of cell invasion and migration. Rap2a, a member of the small GTPase superfamily, mediate diverse cellular events such as cell adhesion, migration and proliferation through various signaling pathways. In this study, we identify that Rap2a is a novel target of p53 and is induced upon DNA damage in a p53-dependent manner. Upon DNA damage, p53 directly binds to the promoter of Rap2a and activates its transcription. We show that Rap2a is significantly upregulated in many types of tumors. In addition, the ectopic expression of Rap2a enhances the migration and invasive ability of cancer cells and increases activities of matrix metalloproteinase MMP2 and MMP9. In contrast, the inactivation of Rap2a inhibits cell invasion and activities of MMP2 and MMP9. We also show that Rap2a regulates the phosphorylation level of Akt. Collectively, our results show that ectopic expression of Rap2a has a key role in enhancing migration, invasion and metastasis by up-regulating p-Akt. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Feb 2015 · Cellular Signalling
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    ABSTRACT: p21-Activated kinase 5 (PAK5) is the last identified member of the PAK family. The PAKs are highly conserved serine/threonine and effector proteins for Cdc42 and Rac and are essential in regulating cell motility and survival. Previous studies have demonstrated that PAK5 played a pivotal role in apoptosis, proliferation, cancer migration, and invasion. However, the biological function of PAK5 in hepatocellular carcinoma, as well as its underlying mechanism, still remains to be fully elucidated. In the present study, we demonstrated that PAK5 markedly inhibited cisplatin-induced apoptosis and promoted cell proliferation in hepatocellular carcinoma cells. Moreover, our results showed that overexpression of PAK5 contributed to cell cycle regulation. In order to elucidate the underlying mechanism of PAK5 on cisplatin-induced apoptosis and cell cycle regulation, we also examined the protein expressions of chk2 and p-chk2. In summary, our study investigated the role of PAK5 in cisplatin-induced cellular processes and provided evidence of its underlying mechanism.
    No preview · Article · Jan 2015 · Tumor Biology
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    ABSTRACT: p42.3 is a tumor-specific gene and found to be over-expressed in many tumor cell lines and primary tumor tissues. It plays a significant role in neoplastic transformation and tumor progression. To date, the association between p42.3 and Renal-Cell Carcinoma (RCC) has not been reported. This study investigated the biological effects and mechanisms of p42.3 in RCC progression. In this study, we found that p42.3 is overexpressed in various kinds of RCC cells, and knockdown of p42.3 dramatically reduced cell proliferation and invasion in vitro. Our studies revealed that overexpression of p42.3 accelerates the epithelial-mesenchymal transition (EMT) progression and induces RCC cells proliferation and invasion. Further studies show that p42.3 may involve in activation of β-catenin and participate in RCC cell invasion. Combined, these data indicate that p42.3 contributes to promoting RCC cells proliferation and invasion through accelerates the EMT progression and β-catenin activation.
    No preview · Article · Dec 2014 · International Journal of Clinical and Experimental Medicine
  • Hu Song · Wei Xu · Jun Song · Yong Liang · Wei Fu · Xiao-Cheng Zhu · Chao Li · Jun-Sheng Peng · Jun-Nian Zheng
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    ABSTRACT: Lin28 plays important roles in the development, maintenance of pluripotency and progression of various types of cancers. Lin28 represses the biogenesis of let-7 microRNAs and is implicated in both development and tumorigenesis. Oncogenic regulation of let-7 microRNAs has been demonstrated in several human malignancies, yet their correlation with Lin28 has not yet been studied in gastric cancer. Therefore, in the present study, we explored the possible mechanisms involved in the effects by Lin28 on the proliferation, migration, cell cycle arrest and apoptosis in gastric cancer cells via alteration of let-7 miRNA. The expression levels of Lin28 and let-7 were detected by real-time PCR in gastric cancer cell lines in vitro. Lin28 was overexpressed in the BGC-823 cells via lentiviral transfection, and let-7 expression was assessed. Cell proliferation and migration capabilities were investigated by MTT and Transwell assays, while cell cycle distribution and the apoptosis rate were detected using flow cytometry. The expression of Lin28 was moderately expressed in the GES cells while underexpressed in the BGC-823, SGC-7901 and HGC-27 cells. Let-7a miRNA was highly expressed in the GES, BGC-823, SGC-7901 and HGC-27 cells. Overexpression of Lin28 was inversely correlated with the downregulated expression of let-7a, and markedly suppressed the proliferation, migration, cell cycle progression and induced apoptosis in the BGC-823 cells. These findings demonstrated that overexpression of Lin28 can suppress the biological behavior of gastric cancer in vitro, and let-7 miRNA may play an important role in the process. We suggest that Lin28 may be a candidate predictor or an anticancer therapeutic target for gastric cancer patients.
    No preview · Article · Dec 2014 · Oncology Reports
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    Guan Jiang · Rong-Hua Li · Chao Sun · Yan-Qun Liu · Jun-Nian Zheng
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    ABSTRACT: Malignant melanoma is the most aggressive and deadly form of skin cancer. Dacarbazine (DTIC) has been the approved first-line treatment for metastatic melanoma in routine clinical practice. However, response rates with single-agent DTIC are low. The objective of this study was to compare the efficacy and safety of DTIC with or without placebo and DTIC-based combination therapies in patients with advanced metastatic melanoma. We searched from electronic databases such as The Cochrane Library, MEDLINE, EBSCO, EMBASE, Ovid, CNKI, and CBMDisc from 2003 to 2013. The primary outcome measures were overall response and 1-year survival, and the secondary outcome measurements were adverse events. Nine randomized controlled trials (RCTs) involving 2,481 patients were included in the meta-analysis. DTIC-based combination therapies was superior to DTIC alone in overall response (combined risk ratio [RR] = 1.60, 95% confidence interval [CI]: 1.27-2.01) and 1-year survival (combined RR = 1.26, 95% CI: 1.14-1.39). Patients with DTIC-based combination therapies had higher incidence of adverse events including nausea (combined RR = 1.23, 95% CI: 1.10-1.36), vomiting (combined RR = 1.73, 95% CI: 1.41-2.12) and neutropenia (combined RR = 1.75, 95% CI: 1.42-2.16) compared to the group for DTIC alone. These data suggested that DTIC-based combination therapies could moderately improve the overall response and the 1-year survival but increased the incidence of adverse events. Further large-scale, high-quality, placebo-controlled, double-blind trials are needed to confirm this conclusion.
    Preview · Article · Dec 2014 · PLoS ONE
  • Qing-Hua Liu · Mei-Lin Shi · Chao Sun · Jin Bai · Jun-Nian Zheng
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    ABSTRACT: Chemotherapy is one of the important methods for treatment in tumors. However, many tumor patients may experience tumor recurrence because of treatment failure due to chemoresistance. Although many signaling pathways could influence chemoresistance of tumor cells, the extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway has gained significant attention because of its implications in signaling and which has crosstalk with other signaling pathways. Extensive studies conclude that ERK1/2 pathway is responding to chemoresistance in many kinds of malignant tumors. The aim of this review is to discuss on the role of ERK1/2 pathway in chemoresistance and therapy of tumors. A comprehensive understanding of ERK1/2 pathway in chemoresistance of tumors could provide novel avenues for treatment strategies of tumors. Copyright © 2014 Elsevier Ltd. All rights reserved.
    No preview · Article · Dec 2014 · Bioorganic & Medicinal Chemistry Letters
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    Ren-Fu Chen · Yue-Yan Li · Lian-Tao Li · Qian Cheng · Guan Jiang · Jun-Nian Zheng
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    ABSTRACT: Renal cell carcinoma is the most frequent kidney malignancy and patients with metastatic disease have a poor prognosis. Suppressed apoptosis and marked invasiveness are distinctive features of renal cell carcinoma. In the present study, a dual‑regulated oncolytic adenovirus expressing the interluekin (IL)‑24 gene (Ki67‑ZD55‑IL‑24) was constructed utilizing the Ki67 promoter to replace the native viral promoter of the E1A gene. Whether the combination of Ki67‑ZD55‑IL‑24‑mediated gene virotherapy and radiotherapy produced increased cytotoxicity in renal cell carcinoma cells via mitochondrial apoptotic cell death was investigated. The data indicated that this novel strategy has the potential to be further developed into an effective approach to treat renal cell carcinoma. The results showed that the combination of Ki67‑ZD55‑IL‑24 and radiotherapy significantly enhanced anti‑tumour activity via increasing the induction of apoptosis in melanoma cells compared with the other agents.
    Preview · Article · Nov 2014 · Molecular Medicine Reports
  • Jie Yang · Qing Zhang · Ke Li · Hong Yin · Jun-Nian Zheng
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    ABSTRACT: The use of peptide‑based vaccines as therapeutics aims to elicit immune responses through antigenic epitopes derived from tumor antigens. Peptide‑based vaccines are easily synthesized and chemically stable entities, and of note, they are absent of oncogenic potential. However, their application is more complicated as the success of an effective peptide‑based vaccine is determined by numerous parameters. The success thus far has been limited by the choice of tumor antigenic peptides, poor immunogenicity and incorporation of strategies to reverse cancer‑mediated immune suppression. In the present review, an overview of the mechanisms of peptide‑based vaccines is provided and antigenic peptides are categorized with respect to their tissue distribution in order to determine their usefulness as targets. Furthermore, certain approaches are proposed that induce and maintain T cells for immunotherapy. The recent progress indicates that peptide‑based vaccines are preferential for targeted therapy in cancer patients.
    No preview · Article · Nov 2014 · International Journal of Molecular Medicine

Publication Stats

379 Citations
206.32 Total Impact Points


  • 2015
    • Nevada cancer institute
      Las Vegas, Nevada, United States
  • 2005-2015
    • Xuzhou Medical College
      • • Laboratory of Biological Cancer Therapy
      • • Research Center for Biochemistry and Molecular Biology
      Suchow, Jiangsu, China