Oncology Research 20(10) Abstracts

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Oncology Research, Vol. 20, pp. 437–445, 2013
0965-0407/13 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504013X13685487925059
E-ISSN 1555-3906
Copyright © 2013 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

RITA Inhibits Growth of Human Hepatocellular Carcinoma Through Induction of Apoptosis

Haihe Wang,* Guofu Chen,† Hongzhi Wang,† and Chunbo Liu*

*Department of Pathogenobiology, Daqing Branch of Harbin Medical University, Daqing, China
†Department of General Surgery of Fifth Clinical Hospital of Harbin Medical University, Daqing, China

RBP-J-interacting and tubulin-associated (RITA) is a novel RBP-J-interacting protein that downregulates Notch-mediated transcription. The current study focuses on the antitumor effect of RITA in human hepatocellular carcinoma (HCC) and aims to explore its molecular mechanism. Thirty paired HCC and adjacent nontumoral liver samples were analyzed by real-time quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). RITA overexpression was induced by transfection of a pcDNA3.1-Flag-RITA plasmid into HepG2 cells. RITA knockdown was achieved by siRNA transfection. mRNA and protein expression of target genes were quantified by qRT-PCR and Western blotting, respectively. Cell proliferation and apoptosis were measured using MTT assay and flow cytometry. Our results demonstrate that adjacent nontumoral liver samples exhibited increased RITA expression compared to HCC tissues (p < 0.05); RITA levels were associated with tumor differentiation status. Overexpression of RITA suppressed cell proliferation and promoted early apoptosis, while its silencing promoted cell growth dramatically (p < 0.05). RITA overexpression upregulated p53 and reduced cyclin E levels, whereas silencing of RITA had the opposite effect on p53 and cyclin E expression. Our in vitro results represent the first evidence that RITA might suppress tumor growth and induce apoptosis in HCCs, and may be a potent antitumoral agent for HCC treatment that deserves further exploration.

Key words: RBP-J-interacting and tubulin-associated (RITA); Hepatocellular carcinoma (HCC); Notch; Apoptosis

Address correspondence to Haihe Wang, Department of Pathogenobiology, Daqing Branch of Harbin Medical University, Daqing163319, China. Tel: +86-459-8153049; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 20, pp. 447–455, 2013
0965-0407/13 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504013X13685487925176
E-ISSN 1555-3906
Copyright © 2013 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Enhancement of Antitumor Activity by Combination of Tumor Lysate-Pulsed Dendritic Cells and Celecoxib in a Rat Glioma Model

Hongtao Zhang,*1 Miao Tian,†1 Chunming Xiu,* Yunbo Wang,* and Guotai Tang*

*Department of Neurosurgery, Yantai Yuhuangding Hospital Affiliated to Qingdao University School of Medicine, Yantai, Shandong, China
†Department of Cardiology, Yantai Yuhuangding Hospital Affiliated to Qingdao University School of Medicine, Yantai, Shandong, China

Using dendritic cell (DC)-based vaccines for treatment of gliomas has emerged as a meaningful and feasible treatment approach for inducing long-term survival, but this approach so far has failed to generate significant clinical responses. In the present study, we demonstrated that glioma lysate-pulsed DCs in combination with celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor, showed more significantly enhanced antitumor activity with increased apoptosis of tumor cells, reduced neovascularization, and developed a strong cytotoxic T lymphocyte (CTL) response in tumor-bearing rats. Celecoxib may reduce production of prostaglandin E2 and modulate the balance between T helper 1 (Th1) cytokines and T helper 2 (Th2) cytokines by increasing the pivotal Th1 cytokine interleukin-12 and reducing Th2 cytokine interleukin-10. Taken together, our results demonstrated that selective inhibition of COX-2 using celecoxib combined with DC-based immunotherapy could act as an important novel strategy for improving future treatment of malignant gliomas.

Key words: Glioma; Dendritic cells (DCs); Celecoxib; Cyclooxygenase 2 (COX-2); Immunotherapy

1These authors provided equal contribution to this work.
Address correspondence to Miao Tian, M.D., Department of Cardiology, Yantai Yuhuangding Hospital Affiliated to Qingdao University School, No. 20 Yuhuangding East Road, Yantai City, Shandong, 264000, China. Tel: +86-15953511957; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 20, pp. 457–465, 2013
0965-0407/13 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504013X13685487925211
E-ISSN 1555-3906
Copyright © 2013 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

BTG2 Overexpression Increases the Radiosensitivity of Breast Cancer Cells In Vitro and In Vivo

Xudong Hu,*†‡ Ligang Xing,*‡ Yang Jiao,§ Jiaying Xu,§ Xingwu Wang,‡ Anqin Han,*‡ and Jinming Yu*‡

*Department of Radiation Oncology, Shandong Tumor Hospital and Institute, Jinan, China
†Postdoctoral Working Station of Tianjin Medical University, Tianjin, China
‡Key Laboratory of Radiation Oncology of Shandong Province, Shandong Tumor Hospital and Institute, Jinan, China
§School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, Jiangsu, China

Antiproliferative gene B-cell translocation gene, member 2 (BTG2) is a member of the BTG/TOB antiproliferative gene family. In this study, we investigated the effect of BTG2 gene overexpression on the radiosensitivity of breast cancer cells in vitro and in vivo. Results show that in human breast cancer cell line MCF-7 stably overexpressing BTG2 gene, cell sensitivity to ionizing radiation increased. The MCF-7-BTG2 cells were more susceptible to radiation-caused apoptosis with decreased cyclin B1, cyclin D1, Ku70, FEN-1, and XRCC1 protein expression as well as increased BAX protein expression. The findings indicate for the first time that BTG2 can improve the radiosensitivity of breast cancer cells by affecting cell cycle distribution, enhancing radiation-induced apoptosis, and inhibiting DNA repair-related protein expression.

Key words: B-cell translocation gene, member 2 (BTG2); Breast cancer; Radiosensitivity; Xenograft

Address correspondence to Jinming Yu, Department of Radiation Oncology, Shandong Tumor Hospital and Institute, No. 440, Jiyan Road, Jinan, 250117, China. Tel: +86-531-87984729; Fax: +86-531-87984079; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 20, pp. 467–472, 2013
0965-0407/13 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504013X13685487925257
E-ISSN 1555-3906
Copyright © 2013 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

The Role of HOXA9 in Human Laryngeal Squamous Cell Carcinoma

Xin Sun,* Bin Liu,* Wenyue Ji,* Xiaolin Ma,* Xinqi Wang,* and Hui Gu†

*Department of Otorhinolaryngology, Shengjing Hospital, China Medical University, Shenyang City, Liaoning Province, P. R. China
†Central Laboratory, Shengjing Hospital, China Medical University, Shenyang City, Liaoning Province, P. R. China

The present study was performed to investigate the expression of HOXA9 in human laryngeal squamous cell carcinoma and its possible roles in the progression. The levels of HOXA9 mRNA and protein were evaluated in human laryngeal squamous cell carcinoma. Hep-2 cells were transfected with h-HOXA9-siRNA. CCK-8 was used to analyze cell proliferation. Flow cytometry (FCM) was used to analyze cell cycle. The mobility of cells was tested by transwell migration assay. The expression of HOXA9 in laryngeal squamous cell carcinoma was significantly higher than normal mucosa tissues. In in vitro experiments, downregulation of HOXA9 strongly inhibited cell growth in Hep-2 by arresting cells in G1 phase (p < 0.05). Transwell migration assay showed that more HOXA9-negative cells migrated to the lower side of the membrane than positive ones (p < 0.01). HOXA9 acts as an oncogene in laryngeal squamous cell carcinoma. It could promote the proliferation and migration of Hep-2 cells.

Key words: Laryngeal squamous cell carcinoma (LSCC); HOXA9; Oncogene; Proliferation; Migration

Address correspondence to Dr. Wenyue Ji, Department of Otorhinolaryngology, Shengjing Hospital, China Medical University, Shenyang 110004, P. R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 20, pp. 473–482, 2013
0965-0407/13 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504013X13715991125684
E-ISSN 1555-3906
Copyright © 2013 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Inhibition of Tumor Growth and Alteration of Associated Macrophage Cell Type by an HO-1 Inhibitor in Breast Carcinoma-Bearing Mice

Rui Deng,* Shi-Min Wang,* Tao Yin,* Ting-Hong Ye,* Guo-Bo Shen,* Ling Li,* Jing-Yi Zhao,† Ya-Xiong Sang,* Xiao-Gang Duan,* and Yu-Quan Wei*

*State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Cheng Du, Sichuan, P. R. China
†Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, Chengdu, Sichuan, P. R. China

Heme oxygenase-1 [HO-1, also called heat shot protein 32 (HSP32)] can specifically metabolize heme to carbon monoxide, biliverdin, and ferrous iron and plays an important role in the processes of anti-inflammation, tissue protection, and antioxidative stress reaction. It has been reported that HO-1 can promote tumorigenesis and metastasis of many tumors. However, the detailed mechanisms of how HO-1 affects tumor progress are not clear. Here, we used ZnPPIX (a specific inhibitor of HO-1) to evaluate its potential effects on mouse breast cancer and tumor-associated macrophages (TAMs). We found out that mouse 4T1 breast cancer growth can be effectively suppressed through inhibition of HO-1 in vitro and in vivo. Moreover, in the 4T1 mouse model, when HO-1 was suppressed in TAMs, alternatively activated macrophages (M2 type) switched to classically activated macrophages (M1 type). In conclusion, 4T1 breast cancer growth was modulated by HO-1 expression. Furthermore, inhibition of HO-1 may induce tumor-associated immune response by activating TAMs’ alternative proliferation. These data suggest that HO-1 may be an important target of breast cancer treatment.

Key words: Heme oxygenase (HO-1); 4T1; ZnPPIX; Tumor-associated macrophages (TAMs)

Address correspondence to Prof. Dr. Yu-quan Wei, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Ren ming Road South 17, 3rd section, Cheng Du, Sichuan 610041, P. R. China. Tel: +86-028-85503817; Fax: +86-028-85503817; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 20, pp. 483–490, 2013
0965-0407/13 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504013X13685487925130
E-ISSN 1555-3906
Copyright © 2013 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Prolonged Disease Stability With Trabectedin in a Heavily Pretreated Elderly Patient With Metastatic Leiomyosarcoma of the Thigh and Renal Failure: A Case Report and Review of the Literature

Danilo Galizia, Erica Palesandro, Anna Maria Nuzzo, Ymera Pignochino, Sandra Aliberti, Massimo Aglietta, and Giovanni Grignani

Medical Oncology Unit, Institute for Cancer Research and Treatment, Fondazione del Piemonte per l’ Oncologia Candiolo, Turin, Italy

Leiomyosarcoma represents about 24% of all soft tissue sarcomas and can originate from retroperitoneum, uterus, or extremities. Adequate local control may be achieved with surgery and radiotherapy. In the presence of unresectable metastases either doxorubicin- or gemcitabine-based chemotherapy is the standard of treatment. Nevertheless, prognosis remains poor regardless of the selected chemotherapy regimen, and new effective therapeutic agents for patients with advanced leiomyosarcoma are needed. Trabectedin, a promising new DNA-damaging agent with a mechanism of action that is different from that of traditional alkylating agents, is approved in Europe for the treatment of patients with advanced soft tissue sarcoma, after failure of anthracyclines and ifosfamide, or who are unsuited to receive these agents and in combination with pegylated liposomal doxorubicin (PLD) for the treatment of patients with relapsed platinum-sensitive ovarian cancer. We present a case of a 76-year-old patient with progressive metastatic lung lesions from a previously resected primary leiomyosarcoma of the thigh and moderate renal failure, who achieved 17 months of disease stability during third-line treatment with trabectedin. Trabectedin was not associated with any cumulative toxicity and was consistently well tolerated for a total of 22 treatment cycles. Current evidence on trabectedin is also presented.

Key words: Leiomyosarcoma; Lung metastases; Soft tissue sarcoma; Thigh; Trabectedin

Address correspondence to Danilo Galizia, M.D., Medical Oncology Unit, Institute for Cancer Research and Treatment, Fondazione del Piemonte per l’ Oncologia, Strada Provinciale 142 km 3,95 10060 Candiolo, Torino, Italy. Tel: +390119933623; Fax: +390119933290; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it