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Functional Similarity of Anticancer Drugs by MTT Bioassay | OMICS International | Abstract
ISSN: 1948-5956

Journal of Cancer Science & Therapy
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Functional Similarity of Anticancer Drugs by MTT Bioassay

Takaki Hiwasa1*,Takanobu Utsumi1, Mari Yasuraoka1, Nana Hanamura1, Hideaki Shimada2, Hiroshi Nakajima3, Motoo Kitagawa4, Yasuo Iwadate4,5, Ken-ichiro Goto6, Atsushi Takeda7, Kenzo Ohtsuka8, Hiroyoshi Ariga9 and Masaki Takiguchi1

1Department of Biochemistry, and Genetics, Chiba University, Graduate School of Medicine, Chuo-ku, Chiba 260-8670, Japan

2Department of Surgery, School of Medicine, Toho University, Ota-ku, Tokyo 143-8541, Japan

3Department of Molecular Genetics, Chiba University, Graduate School of Medicine, Chuo-ku, Chiba 260-8670, Japan

4Department of Molecular and Tumor Pathology, Chiba University, Graduate School of Medicine, Chuo-ku, Chiba 260-8670, Japan

5Department of Neurological Surgery, Chiba University, Graduate School of Medicine, Chuo-ku, Chiba 260-8670, Japan

6Department of Orthopaedic Surgery, National Hospital Organization, Shimoshizu Hospital, Yotsukaido, Chiba 284-0003, Japan

7Laboratory of Biochemistry, Graduate School of Nutritional Sciences, Sagami Women’s University, Sagamihara, Kanagawa 252-0383, Japan

8Laboratory of Cell & Stress Biology, Department of Environmental Biology, Chubu University, Matsumoto-cho, Kasugai, Aichi 487-8501, Japan

9Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita-ku, Sapporo 060-0812, Japan

*Corresponding Author:
Dr. Takaki Hiwasa
Associate Professor, Department of Biochemistry and Genetics
Chiba University, Graduate School of Medicine
1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Tel: 81-43-226-2541
E-mail: hiwasa_ [email protected]

Received Date: July 11, 2011; Accepted Date: December 15, 2011; Published Date: December 17, 2011

Citation: Hiwasa T, Utsumi T, Yasuraoka M, Hanamura N, Shimada H, et al. (2011) Functional Similarity of Anticancer Drugs by MTT Bioassay. J Cancer Sci Ther 3: 250-255. doi: 10.4172/1948-5956.1000099

Copyright: © 2011 Hiwasa T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

We prepared normal or Ha-ras-transformed NIH3T3 cells transfected stably or transiently with various tumorrelated genes. The chemosensitivity of the transfected clones to 16 anticancer drugs was compared to the parental control cells using the MTT assay. The chemosensitivity changes induced by transfected genes were calculated and expressed numerically as the Drug Chemosensitivity Index (DCI). High DCI values (indicating resistance) were frequently observed in cells expressing C/EBP?, C/EBP?, p53, p21, PTEN, dominant-negative MDM2, caspases, HSP90, COUP-TF1 and decorin. In contrast, transfectants expressing ras, src, erbB2 and calpastatin had low DCI values, indicating increased sensitivity. Thus, it may be possible to predict the sensitivity of cancer cells toward anticancer drugs based on the expression levels of these genes. We then performed a regression analysis of DCI values between anticancer drugs. The correlation coefficients (r) were relatively high between cisplatin, camptothecin, mitomycin C and etoposide, suggesting that the mechanisms of action of these drugs are similar. The r values of aclarubicin, vincristine, taxol and cytarabine were low, suggesting that each of these drugs has a different and unique effect. This analysis may provide a rationale for design of combination chemotherapy regimens.

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