Oncology Research 22(3) Abstracts

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Oncology Research, Vol. 22, pp. 129–137, 2015
0965-0407/15 $90.00
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DOI: http://dx.doi.org/10.3727/096504015X
14267282610894
E-ISSN 1555-3906
Copyright ©
2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Review

Role of Vitamin D Metabolism and Activity on Carcinogenesis

Xiayu Wu, Tao Zhou, Neng Cao, Juan Ni, and Xu Wang

School of Life Sciences, The Engineering Research Center of Sustainable Development and Utilization of Biomass Energy, Ministry of Education, Yunnan Normal University, Kunming, Yunnan, China

The vitamin D endocrine system regulates a broad variety of independent biological processes, and its deficiency is associated with rickets, bone diseases, diabetes, cardiovascular diseases, and tuberculosis. Cellular and molecular studies have also shown that it is implicated in the suppression of cancer cell invasion, angiogenesis, and metastasis. Sunlight exposure and consequent increased circulating levels of vitamin D are associated with reduced occurrence and a reduced mortality in different histological types of cancer, including those resident in the skin, prostate, breast, colon, ovary, kidney, and bladder. The vitamin D receptor (VDR) as a steroid hormone superfamily of nuclear receptors is highly expressed in epithelial cells at risk for carcinogenesis, providing a direct molecular link by which vitamin D status impacts on carcinogenesis. Because VDR expression is retained in many human tumors, vitamin D status may be an important modulator of cancer progression in persons living with cancer. The aim of this review is to highlight the relationship between vitamin D, VDR, and cancer, summarizing several mechanisms proposed to explain the potential protective effect of vitamin D against the development and progression of cancer.

Key words: Vitamin D; Vitamin D receptor (VDR); Carcinogenesis; Cancer

Address correspondence to Xu Wang, Ph.D., School of Life Sciences, The Engineering Research Center of Sustainable Development and Utilization of Biomass Energy, Ministry of Education, Yunnan Normal University, Kunming, Yunnan, 650500, China. Tel/Fax: +86-871-65941366; E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 139–145, 2015
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DOI: http://dx.doi.org/10.3727/096504014X
13983417587366
E-ISSN 1555-3906
Copyright ©
2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

HIF-1 Dimerization Inhibitor Acriflavine Enhances Antitumor Activity of Sunitinib in Breast Cancer Model

Tao Yin,* Sisi He,* Guobo Shen,* and Yongsheng Wang*†

*State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy, West China School of Medicine, West China Hospital, Sichuan University, Chengdu, PR China
†Department of Thoracic Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, PR China

Antiangiogenic therapy is a promising strategy for cancer therapy. However, antiangiogenic therapy can induce intratumor hypoxia and hypoxia-inducible factor-1 (HIF-1) expression, which slows cancer progression. In our present study, we found that antiangiogenic therapy with sunitinib plus HIF-1 dimerization inhibitor acriflavine retarded tumor growth in a murine model of breast cancer. The combination of sunitinib with acriflavine significantly decreased vascular endothelial growth factor and TGF-
βexpression and reduced tumor vasculature followed by increased intratumor necrosis and apoptosis. Moreover, decreased accumulation of myeloid-derived suppressor cells in the spleen was observed after the combinational therapy. In conclusion, the combination of HIF-1 inhibition and antiangiogenic therapy may represent a novel strategy for cancer patients.

Key words: Hypoxia-inducible factor-1 (HIF-1); Acriflavine; Breast cancer; Antiangiogenic therapy

Address correspondence to Yongsheng Wang, Department of Thoracic Oncology, State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy, Cancer Center, West China Hospital, West China Medical School, Sichuan University, People’s South Road 3 section 17 number, Chengdu 610041, PR China. Tel: +86-28-85164063; Fax: +86-28-85164060; E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 147–157, 2015
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DOI: http://dx.doi.org/10.3727/096504015X
14298122915583
E-ISSN 1555-3906
Copyright ©
2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Induction of G2/M Arrest by Berberine via Activation of PI3K/Akt and p38 in Human Chondrosarcoma Cell Line

Seong-Hui EoJu-Hee Kim, and Song-Ja Kim

Department of Biological Sciences, College of Natural Sciences, Kongju National University, GongjuChungnamRepublic of Korea

Berberine
is a clinically important natural isoquinoline alkaloid found in many medicinal herbs. Berberine has been shown to have many pharmacological effects including antimicrobial, antitumor, and anti-inflammatory activities. However, the effects and mechanism of action of berberine have not been studied in chondrosarcoma. Therefore, the effects of berberine on proliferation in a human chondrosarcoma cell line (HTB-94) were investigated. Berberine inhibited cell proliferation in a concentration-dependent manner. We also determined that inhibition of cell proliferation by berberine occurred via G2/M phase arrest in HTB-94 cells. Berberine induced cell cycle arrest at the G2/M phase by upregulation of p53 and p21 expression and suppressed cyclin B1, cyclin-dependent kinase 1 (cdc2), cdc25c, and phosphorylated retinoblastoma tumor-suppressor protein (pRb) expression. In addition, berberine stimulated phosphorylation of protein kinase B (Akt) and p38 kinase. Inhibition of phosphatidylinositol 3-kinase (PI3K)/Akt with LY294002 (LY) and p38 kinase with SB203580 (SB), respectively, decreased berberine-induced p53 and p21 expression and restored cell proliferation and expression of cyclin B1, cdc2, cdc25c, and pRb cell cycle progression proteins. These results suggest that berberine-induced inhibition of cell proliferation by cell cycle arrest at the G2/M phases was regulated through PI3K/Akt and p38 kinase pathways in HTB-94 chondrosarcoma cells.

Key words: Berberine; Chondrosarcoma; Proliferation; Cell cycle arrest

Address correspondence to Song-Ja Kim, Ph.D., Department of Biological Sciences, College of National Sciences, Kongju National University, 182 Shinkwan-Dong, Gongju 314-701, Republic of Korea. Tel: +82-41-850-8507; Fax: +82-41-850-0927; E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 159–165, 2015
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DOI: http://dx.doi.org/10.3727/096504015X
14298122915628
E-ISSN 1555-3906
Copyright ©
2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

IL-24 Induces Apoptosis via Upregulation of RNA-Activated Protein Kinase and Enhances Temozolomide-Induced Apoptosis in Glioma Cells

Chang-Wei Hu,* Gang-Feng Yin,* Xi-Rui Wang,* Bao-Wen Ren,* Wen-Gao Zhang,* Qing-Ling Bai,* Yan-Ming Lv,† Wen-Ling Li,‡ and Wen-Qing Zhao§

*Third Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou, China
†First Department of Oncology Surgery, Cangzhou Central Hospital, Cangzhou, China|
‡Department of Functional Neurosurgery, Hebei People’s Hospital, Shijiazhuang, China
§Department of Neurosurgery, Hebei People’s Hospital, Shijiazhuang, China

Human interleukin-24 (IL-24) has been found recently to play a tumor-suppressor role in a variety of tumors, including gliomas. However, the exact mechanism of glioma tumor suppression by IL-24 remains unclear. We collected by surgery 30 gliomas at different grades and evaluated IL-24 and double-stranded RNA-activated protein kinase (PKR) expression using fluorescence quantitative real-time PCR and immunohistochemical techniques. Two human glioma cell lines, U87 and U251, were transfected with Ad5F35-IL24 via recombinant adenovirus-mediated gene transfer and apoptosis, as well as PKR and eIF-2
α expression analyzed. The results showed that IL-24 and PKR expression decreased with increasing tumor grade. Compared with cells of the control groups, Ad5F35-IL24-infected U87 and U251 cells exhibited a significantly increased apoptosis and elevated PKR, eIF-2α, p-PKR, and p-eIF-2α levels, while the expression of Bcl-2 was decreased. Finally, IL-24 also sensitized apoptosis of glioma cells to temozolomide (TMZ). This study indicates that IL-24 upregulates expression and activation of PKR, further increasing expression and activation of eIF-2α, and decreasing Bcl-2 to promote apoptosis. IL-24 also increases chemosensitivity of glioma cells to TMZ.

Key words: Interleukin-24 (IL-24); RNA-activated protein kinase (PKR); eIF-2
α; Glioma

Address correspondence to Chang-Wei Hu, Third Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou 061000, China. E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 167–176, 2015
0965-0407/15 $90.00
+ .00
DOI: http://dx.doi.org/10.3727/096504015X
14298122915664
E-ISSN 1555-3906
Copyright ©
2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

shRNA Depletion of cIAP1 Sensitizes Human Ovarian Cancer Cells to Anticancer Agent-Induced Apoptosis

Hong Jin,*1 You-Yuan Dong,†1 Hong Zhang,‡ Ying Cui,* Kai Xie,* and Ge Lou*

*Department of Gynecology, Harbin Medical University Cancer Hospital, Harbin, China
†Department of Epidemic Prevention, Fuqiang Street Community Health Service Center of Daqing Oil Field, Daqing, China
‡Department of Otorhinolaryngology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China

Emerging evidence suggests a potential role of cellular inhibitor of apoptosis protein 1 (cIAP1) in the development of human ovarian cancer. However, its function in the progression of ovarian cancer has not been clearly determined. Our study aimed to investigate the effect of cIAP1 gene depletion on the chemosensitivity of ovarian cancer cells. We developed a novel short hairpin RNA (shRNA) plasmid specifically targeting cIAP1. Cell proliferation, invasion, and apoptosis of the shRNA-transfected cells were evaluated using MTT, Transwell chamber, and flow cytometric assays, respectively. The concentration of MMP-9 in the supernatant was detected by ELISA. Targeted depletion of cIAP1 by shRNA significantly reduced expression levels of cIAP1 mRNA and protein, leading to inhibition of cell proliferation and invasion capability in SKOV3 cells. At the same time, cIAP1 downregulation decreased the secretion of MMP-9. shRNA depletion of cIAP1 enhanced chemosensitivity of ovarian cancer cells to Taxol and carboplatin
-induced apoptosis. cIAP1 is associated with tumor progression in human ovarian cancer. Therefore, cIAP1 might be a potential target for therapeutic anticancer drugs.

Key words: Cellular inhibitor of apoptosis protein 1 (cIAP1); Ovarian cancer; RNA interference (RNAi); Cell proliferation; Invasion; Chemosensitivity; Taxol; Carboplatin

1These authors provided equal contribution to this work.
Address correspondence to Dr. Ge Lou, Department of Gynecology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin 150081, Heilongjiang Province, China. E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it