Juntang Guo

Publications (4)11.13 Total impact

• Article: Drosophila Eyes Absent Homologue 2 is up-regulated in lung adenocarcinoma

  Juntang Guo, Chaoyang Liang, Lihua Ding, Naikang Zhou, Qinong Ye
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  ABSTRACT: ObjectiveLung cancer has emerged as a leading cause of cancer death in the world. Eyes Absent (EYA) is an important and conserved transcriptional regulator of development. The aim of the present study was to identify the expression of Drosophila Eyes Absent Homologue 2 (EYA2) in non-small cell lung cancer (NSCLC) and to investigate their correlation with clinical parameters. MethodsFresh, paired lung samples (n = 59) of NSCLC were obtained by surgical resection at the Department of Thoracic Surgery of the People’s Liberation Army General Hospital. Expression of EYA2 were examined by Western blot and immunohistochemical analysis in specimens of NSCLC and paired normal lung tissue. Clinical data, pathologic result and Ki67 expression were collected and subsequent correlation with EYA2 expression was analyzed. ResultsEYA2 expression was found located in cytoplasm and nucleus, but mostly in cytoplasm. The expression of EYA2 increased in NSCLC by Western blot and immunohistochemistry, which was correlated with histology type, but not correlated with gender, age, pTNM stage, histological differentiation and lymph node metastasis. Compared with normal lung tissue, the expression of EYA2 significantly was up-regulated in lung adenocarcinoma, while no significant difference in lung squamous cell carcinoma. Expression of EYA2 was uncorrelated with expression of Ki67 in NSCLC. ConclusionExpression of EYA2 was augmented in lung adenocarcinoma. EYA2 is likely participating in tumorigenesis and development of lung adenocarcinoma as transcriptional activator.
  The Chinese-German Journal of Clinical Oncology 04/2012; 8(12):681-684.
• Article: Downregulation and growth inhibitory role of FHL1 in lung cancer.

  Chang Niu, Chaoyang Liang, Juntang Guo, Long Cheng, Hao Zhang, Xi Qin, Qunwei Zhang, Lihua Ding, Bin Yuan, Xiaojie Xu, Jiezhi Li, Jing Lin, Qinong Ye
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  ABSTRACT: Four and a half Lin-11, Isl-1, Mac-3 (LIM) protein 1 (FHL1) has been linked to carcinogenesis. However, the role of FHL1 in lung cancer remains unclear and the detailed mechanism underlying its tumor suppressive role is poorly understood. The purpose of this study was to examine FHL1 expression in lung cancer patients and to investigate how it was associated with lung cancer cell growth. Immunoblotting and immunohistochemistry showed that FHL1 protein was downregulated in over 90% of 80 lung cancer patients. FHL1 expression was strongly correlated with tumor histological types (p < 10(-4) ) and the differentiation of the tumor (p = 0.002). FHL1 inhibited anchorage-dependent and -independent growth of human lung cancer cell lines. The inhibitory effects of FHL1 on lung cancer cell growth were associated with both the G1 and the G2/M cell cycle arrest concomitant with a marked inhibition of cyclin A, cyclin B1 and cyclin D as well as the induction of the cyclin dependent kinase inhibitors p21 (WAF1/CIP1) and p27 (Kip1). Direct intratumoral injection of an adenovirus expressing FHL1 dramatically suppressed the growth of A549 lung cancer cells in nude mice. Our data suggest that reduced expression of FHL1 may play an important role in the development and progression of lung cancer and that FHL1 may be a useful target for lung cancer gene therapy.
  International Journal of Cancer 06/2011; 130(11):2549-56. · 5.44 Impact Factor
• Source

  Available from: PubMed Central

  Article: Giant solitary fibrous tumor of the pleura: an analysis of five patients.

  Juntang Guo, Xiangyang Chu, Yu-E Sun, Lianbin Zhang, Naikang Zhou
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  ABSTRACT: Solitary fibrous tumor of the pleura (SFTP) represents a clinical entity rarely encountered, especially in giant forms. Complete surgical resection for giant tumor of pleura is a challenge. The aim of this article is to present five new cases of giant SFTP, and to discuss their clinical characteristics and the treatment strategy of such neoplasms. We performed a retrospective review of the clinical records of five patients who underwent surgery for a huge SFTP (>18 cm in diameter) between 2007 and 2009. Four patients were symptomatic. All five patients underwent angiography and embolization of the tumor-supplying vessels within 24 h of surgery. All giant tumors were removed completely by extended postlateral thoracotomy with moderate intraoperative bleeding. Two wedge resections and one lobectomy were performed in three cases where the parenchyma had been encroached. Tumors in three patients were pathologically benign; those in the other two were malignant. The symptoms disappeared in all cases after surgery. Complete resection remains the mainstay of cure for giant SFTP. We recommend preoperative angiography and embolization for giant SFTP which can reduce the risk of hemorrhage and can contribute to piecemeal removal for radical excision.
  World Journal of Surgery 11/2010; 34(11):2553-7. · 2.36 Impact Factor
• Article: Knockdown of c-FLIP(L) enhanced AD5-10 anti-death receptor 5 monoclonal antibody-induced apoptosis in human lung cancer cells.

  Feng Chen, Juntang Guo, Yaxi Zhang, Yu Zhao, Naikang Zhou, Shilian Liu, Yanxin Liu, Dexian Zheng
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  ABSTRACT: It is reported that the agonistic antibodies against death receptors 4 and 5 (DR4, DR5) are cytotoxic to various cancer cells. In the present study, the sensitivity of five human lung cancer cell lines to previously reported AD5-10 agonistic antibody against DR5 were investigated. Of these cell lines, A549 and small cell lung cancer showed a moderate sensitivity to AD5-10 and three other cell lines were resistant. Cell line H460 is resistant to AD5-10 despite a high level of cell-surface DR5 expression. We demonstrated that the resistance of H460 cells to AD5-10 was not related to the expression level of DR5, but the expression and cleavage of c-FLIP(L) in the cells. Inhibition of endogenous c-FLIP(L) expression by siRNA significantly enhanced AD5-10-induced cell death in these lung cancer cells. We further showed that this sensitizing effect was associated with decreased expression of Bcl-2 family proteins Bid and Bcl-X(L), change of mitochondrial membrane potential, release of cytochrome c from mitochondria, and caspase activation. Therefore, these data provide evidence that c-FLIP(L) is involved in the resistance of lung cancer cells to AD5-10-induced apoptosis. Moreover, immunohistochemistry on paraffin-embedded tissue revealed that c-FLIP(L) was expressed in 87.9% (29 of 33) of lung carcinoma tissues from the patients, but little in tissues from normal controls. This suggests that inhibition of c-FLIP(L) expression might be a potential strategy for lung cancer therapy, especially for those lung cancers resistant to the agonistic antibody against death receptors.
  Cancer Science 03/2009; 100(5):940-7. · 3.33 Impact Factor