Oncology Research 23(4) Abstracts

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Oncology Research, Vol. 23, pp. 147-154, 2016
0965-0407/16 $90.00
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DOI: http://dx.doi.org/10.3727/096504016X14519157902645
E-ISSN 1555-3906
Copyright ©
2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

BMP-7 Attenuates TGF-β1-Induced Fibronectin Secretion and Apoptosis of NRK-52E Cells by the Suppression of miRNA-21

Zhong Yu, Xu Zai-Chun, Han Wun-Lun, and Zhu Yun-Yun

Department of Nephrology, Tongde Hospital of Zhejiang Province, Hangzhou, China

Bone morphogenetic protein-7 (BMP-7) inhibited the pathogenesis of renal injury in response to a variety of stimuli. However, little is known about the molecular regulation and mechanism of endogenous BMP-7 and its renoprotective functions. This study examined the regulation of BMP-7 and its role in the fibronectin secretion and apoptosis of NRK-52E cells resulting from transforming growth factor-b1 (TGF- β1) in vitro. Results showed that TGF- β1 promoted factor-associated suicide (FAS), FAS ligand (FASL), fibronectin (FN), and miRNA-21 expression, while it downregulated phospho-Smad1 (pSmad1), pSmad5, and pSmad8 expressions in NRK-52E cells. In contrast, BMP-7 alleviated TGF- β1-induced cell apoptosis, inhibited TGF- β1-induced higher expression of miRNA-21 and FN, and enhanced TGF- β1-attenuated phosphorylation of Smad1, Smad5, and Smad8. Furthermore, a chemical inhibitor of miRNA-21 also negatively affected TGF- β1-induced apoptosis and FN secretion. On the other hand, overexpression of miRNA-21 counteracted the inhibitory effect of BMP-7 on TGF- β1-induced FN secretion and apoptosis. However, BMP-7 showed no effects on TGF- β1-induced FN secretion and apoptosis following knockdown of miRNA-21. Taken together, these findings demonstrated that BMP-7 might inhibit TGF- β1-induced FN secretion and apoptosis by the suppression of miRNA-21 in NRK-52E cells.

Key words: Bone morphogenetic protein-7 (BMP-7); Transforming growth factor- β1 (TGF- β1); Fibronectin (FN) secretion; Apoptosis; miRNA-21, Smad

Address correspondence to Zhong Yu, Tongde Hospital of Zhejiang Province, No. 234 of Gucui Road, Hangzhou, China. Tel/Fax: +8657189972412; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 155-163, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14519157902681
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

miRNA-497 Negatively Regulates the Growth and Motility of Chondrosarcoma Cells by Targeting Cdc25A

Yandong Lu,*1 Fangguo Li,*1 Tao Xu,† and Jie Sun*1

*Department of Orthopaedic Traumatology, Tianjin Hospital, Tianjin, China
†Department of OrthopaedicsJixian People’s Hospital, Tianjin, China

Chondrosarcoma (CHS) is the second most common malignant bone sarcoma with increased risk of invasion and metastasis. However, the regulatory mechanisms of CHS tumorigenesis remain unknown. Here we investigated the novel role of miR-497 in regulating chondrosarcoma cell growth and cell cycle arrest. RT-PCR analysis showed that the expression of miR-497 is aberrantly downregulated in human chondrosarcoma samples and cells. After transfection with miR-497 mimic or antagomir, the proliferation and apoptosis of JJ012 and OUMS-27 chondrosarcoma cells were determined by CCK-8 assay and flow cytometric analysis, respectively. Results showed that the proliferation capacity of JJ012 and OUMS-27 cells was significantly decreased by miR-497 overexpression but increased by miR-497 repression. Apoptosis in both cell types was remarkably enhanced by miR-497 mimic but inhibited by miR-497 antagomir. By bioinformatics and luciferase reporter analysis, Cdc25A was proven to be a direct target of miR-497 in chondrosarcoma cells. Further studies indicated that miR-497 modulates the growth of chondrosarcoma cells by targeting Cdc25A, in which the cell cycle inhibitor p21 is involved through a p53-independent pathway. In conclusion, we demonstrated that miR-497 represents a potential tumor suppressor in human chondrosarcoma that regulates the growth of chondrosarcoma cells by targeting Cdc25A. This may provide a novel therapeutic target for chondrosarcoma.

Key words: miR-497; Chondrosarcoma (CHS); Metastasis; Cdc25A; p21

1These authors provided equal contribution to this work.
Address correspondence to Jie Sun, Department of Orthopaedic Traumatology, Tianjin Hospital, Jiefang South Road No. 406, Hexi District, Tianjin 300211, China. Tel: +86-22-60910343; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 165-170, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14519157902726
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

miR-544a Promotes Breast Cancer Cell Migration and Invasion Reducing Cadherin 1 Expression

Pengwei Lu, Yuanting Gu, Lin Li, Fang Wang, and Xinguang Qiu

Department of General Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China

Accumulating evidence has reported the significant role of miRNAs in the underlying biology of tumors, including breast cancer. The purpose for this study was to investigate the potential effects of miR-544a in breast cancer migration and invasion. The human normal breast Hs578Bst cells and the human breast cancer MCF-7 and MDA-MB-231 cells were used to analyze the expression of miR-544a by RT-PCR. The effects of miR-544a on the two kinds of breast cancer cell migration and invasion were analyzed using the Matrigel and Transwell assay, respectively. miR-544a expression on the cell metastasis-related protein expression was also analyzed using Western blotting. Compared to the normal Hs578Bst cells, miR-544a was significantly downregulated in MCF-7 cells but was upregulated in MDA-MB-231 cells (p < 0.01). The overexpressed miR-544a significantly promotes the migrated and invaded MCF-7 cells (p < 0.05), which was opposite to that in MCAMB-231 cells (p < 0.05). Moreover, the cadherin 1 (CDH1) expression was negatively correlated to miR-544a expression in the two kinds of cells. Our study suggested that the overexpressed miR-544a may be a promoter for breast cancer migration and invasion by targeting CDH1.

Key words: Breast cancer; Cell migration; Cell invasion; miR-544a; Cadherin 1 (CDH1)

Address correspondence to Xinguang Qiu, Department of General Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe Road, Zhengzhou, Henan 450052, China. Tel: +86-0371-67967246; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 171-181, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14519995067562
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Inhibition of Liver Carcinoma Cell Invasion and Metastasis by Knockdown of Cullin7 In Vitro and In Vivo

Donghui Zhang,*1 Genling Yang,†1 Xidong Li,‡ Cheng Xu,* and Honglei Ge§

*Second Ward of Infectious Disease Department, Linyi People’s Hospital, Linyi, Shandong, China
†Third Ward of Jining Infectious Disease Hospital, Jining, Shandong, China
‡Six Ward of Infectious Disease Department, Linyi People’s Hospital, Linyi, Shandong, China
§Cardiothoracic Surgery Department, Liaohe Oil Field General Hospital, Panjin, Liaoning, China

Cullin7 is an E3 ubiquitin ligase. The Cullin7 protein family functions as a molecular scaffold to coordinate substrate ubiquitination in SkpCullin, and F-box-containing complex (SCF complex). Cullin7s control normal development and primary cellular processes and are characterized by a unique genomic network organization. Less is known about the involvement of Cullin7 with hepatocellular carcinoma (HCC). In this study, we found that Cullin7 showed a high expression in HCC tumor tissues, especially in metastatic HCC tumor tissues. Also, there was a negative correlation between Cullin7 expression and long survival. Silencing of Cullin7 in liver cancer cells can significantly reduce the migration, invasion, and metastatic abilities. Also, detection of epithelial–mesenchymal transition (EMT) marker expression showed that Cullin7 promotes epithelial–mesenchymal transformation of cancer cells. The results of this study helped to elucidate the oncogene functions of Cullin7 in liver cancers.

Key words: Cullin7; Hepatocellular carcinoma (HCC); Invasion; Metastasis

1These authors provided equal contribution to this work.
Address correspondence to Mr. Cheng Xu, Second Ward of Infectious Disease Department, Linyi People’s Hospital, Linyi, 276003 Shandong, China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 183-195, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14537290676865
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Clinical Outcome in Definitive Concurrent Chemoradiation With Weekly Paclitaxel and Carboplatin for Locally Advanced Esophageal and Junctional Cancer

Vanita Noronha,* Kumar Prabhash,* Amit Joshi,* Vijay Maruti Patil,* Sanjay Talole,† Dipti Nakti,* Arvind Sahu,* Srushti Shah,‡ Sarbani Ghosh-Laskar,§ Prachi S. Patil,¶ Shaesta A. Mehta,¶ Nirmala Jambhekar,# Abhishek Mahajan,** and Nilendu Purandare††

*Department of Medical Oncology, Tata Memorial Hospital, Mumbai, India
†Department of Epidemiology and Biostatistics, Tata Memorial Hospital, Mumbai, India
‡Clinical Research Secretariat, Tata Memorial Hospital, Mumbai, India
§Department of Radiation Oncology, Tata Memorial Hospital, Mumbai, India
¶Department of Digestive Diseases and Clinical Nutrition, Tata Memorial Hospital, Mumbai, India
#Department of Pathology, Tata Memorial Hospital, Mumbai, India
**Department of Radiodiagnosis, Tata Memorial Hospital, Mumbai, India
††Department of Nuclear Medicine, Tata Memorial Hospital, Mumbai, India

There are little data on the efficacy and safety of taxane/platinum with definitive radiotherapy (RT) for esophageal/ GEJ cancer. This article is a retrospective analysis of patients who received weekly paclitaxel 50 mg/ m2 and carboplatin AUC 2 with radical definitive RT for locally advanced esophageal/GEJ cancer. Between February 2011 and July 2014, 179 patients were included. The median age was 54 years. Ninety-two percent of patients had squamous histology. Mean RT dose was 58.7 Gy in 32 fractions over 53 days, with mean of six chemotherapy cycles. Fifty-six percent of patients developed ≥grade 3 acute toxicities, commonly febrile neutropenia (12%) and infection (11%); ≥grade 3 laboratory abnormalities included hyponatremia (38%), leukopenia (49%), neutropenia (27%), and anemia (16%). Twelve percent of patients developed ≥grade 3 chronic toxicity. Fatal toxicities included six during CRT, eight within 30 days of completing CRT, and three chronic. Radiologic response was 49% (CR 5.6%, PR 43%). Follow-up endoscopy showed remission in 53% and residual disease in 14%. At a median follow-up of 28 months, median PFS was 11 months (95% CI: 8–13.9), median OS was 19 months (95% CI: 15.4–22.6), and estimated 1-year, 2-year, and 3-year survivals were 70%, 47%, and 39%, respectively. Weekly paclitaxel–carboplatin concurrently with definitive RT is efficacious with manageable toxicity. [The trial was registered with the Clinical Trials Registry-India (CTRI), registration number: CTRI/2014/07/004776.]

Key words: Chemoradiation; Definitive chemoradiotherapy; Esophageal; Esophagogastric cancer; Paclitaxel; Radical

Address correspondence to Dr. Kumar Prabhash, Department of Medical Oncology, Tata Memorial Hospital, Dr. E Borges Marg, Parel, Mumbai 400012, India. Tel: +91 9224182898; Fax: +02224171734; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 197-203, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14537290676919
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

FGF19 Contributes to Tumor Progression in Gastric Cancer by Promoting Migration and Invasion

Shuang Wang,* Daqi Zhao,† Ruihua Tian,* Hailong Shi,* Xiangming Chen,* Wenzhi Liu,* and Lin Wei*

*Department of Clinical Oncology, The Central Hospital of TaianTaian, Shandong, People’s Republic of China
†Department of Radiation Oncology, The Central Hospital of TaianTaian, Shandong, People’s Republic of China

Gastric cancer is the fourth most common type of cancer and second leading cause of cancer-related death in the world. Since patients are often diagnosed at a late stage, very few effective therapies are left in the arsenal. FGF19, as a hormone, has been reported to promote tumor growth in various types of cancer; however, its function in gastric cancer remains unknown. In the current study, we showed that FGF19 is overexpressed in gastric cancer and is associated with depth of invasion, lymph node metastasis, and TNM stage. In addition, in vitro experiments demonstrated that FGF19 is able to enhance migration and invasion abilities of gastric cancer cells. Given its great potency in gastric cancer progression, FGF19 may be an effective target of treatment for advanced gastric cancer patients.

Key words: Gastric cancer; FGF19; Migration; Invasion

Address correspondence to Lin Wei, M.D., Department of Clinical Oncology, The Central Hospital of TaianLongtan Road 29, Taian, 271000, Shandong Province, People’s Republic of China. Tel: +0086-538 8261 699; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it