Cancer Research and Treatment

Special Article

How Can We Treat Cancer Disease Not Cancer Cells?: Kyu-Won Kim, Su-Jae Lee, Woo-Young Kim, Ji Hae Seo, Ho-Young Lee; Cancer Res Treat. 2017;49(1):1-9. Published online December 26, 2016; DOI: https://doi.org/10.4143/crt.2016.606

Since molecular biology studies began, researches in biological science have centered on proteins and genes at molecular level of a single cell. Cancer research has also focused on various functions of proteins and genes that distinguish cancer cells from normal cells. Accordingly, most contemporary anticancer drugs have been developed to target abnormal characteristics of cancer cells. Despite the great advances in the development of anticancer drugs, vast majority of patients with advanced cancer have shown grim prognosis and high rate of relapse. To resolve this problem, we must reevaluate our focuses in current cancer research. Cancer should be considered as a systemic disease because cancer cells undergo a complex interaction with various surrounding cells in cancer tissue and spread to whole body through metastasis under the control of the systemic modulation. Human body relies on the cooperative interaction between various tissues and organs, and each organ performs its specialized function through tissue-specific cell networks. Therefore, investigation of the tumor-specific cell networks can provide novel strategy to overcome the limitation of current cancer research. This review presents the limitations of the current cancer research, emphasizing the necessity of studying tissue-specific cell network which could be a new perspective on treating cancer disease, not cancer cells.

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Maria Goldberg, Michel G Mondragon-Soto, Ghaith Altawalbeh, Bernhard Meyer, Amir Kaywan Aftahy
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Oncogene.2020; 39(4): 739. CrossRef

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Original Articles

The Differential Gene Expression Profiles between Sensitive and Resistant Breast Cancer Cells to Adriamycin by cDNA Microarray: Myung-Ju Ahn, Ki-Hwan Lee, Joon-Ik Ahn, Dong-Hyun Yu, Hye-Sook Lee, Jung-Hye Choi, Joung Soon Jang, Jong Min Bae, Yong-Sung Lee; Cancer Res Treat. 2004;36(1):43-49. Published online February 29, 2004; DOI: https://doi.org/10.4143/crt.2004.36.1.43

Abstract PDF PubReader ePub

Purpose

Adriamycin® is one of the most commonly used drugs in the treatment of breast cancer. This study was performed to understand the molecular mechanisms of drug resistance in breast cancer cells.

Materials and Methods

We have analyzed the MCF-7 breast cell line and its adriamycin-resistant variants, MCF-7/ADR using human 10 K element cDNA microarrays.

Results

We defined 68 genes that were up-regulated (14 genes) or down-regulated (54 genes) in adriamycin resistant breast cancer cells. Several genes, such as G protein-coupled receptor kinase 5, phospholipase A2, guanylate cyclase 1, vimentin, matrix metalloproteinase 1 are up-regulated in drug resistant cells. Several genes, such as interferon, alpha-inducible protein 27, forkhead box M1, mitogen-activated protein kinase 6, regulator of mitotic spindle assembly 1 and tumor necrosis factor superfamily are down-regulated in adriamycin resistant cells. The altered expression of genes observed in microarray was verified by RT-PCR.

Conclusion

These findings show that cDNA microarray analysis can be used to obtain gene expression profiles reflecting the effect of anticancer drugs on breast cancer cells. Such data may lead to the assigning of signature expression profiles of drug-resistant tumors which may help predict responses to drugs and assist in the design of tailored therapeutic regimens to overcome drug resistance.

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cDNA Microarray Analysis of Differential Gene Expression in Gastric Cancer Cells Sensitive and Resistant to 5-Fluorouracil and Cisplatin
Myung-Ju Ahn, Young-Do Yoo, Ki-Hwan Lee, Joon-Ik Ahn, Dong-Hyun Yu, Hye-Sook Lee, Ho-Suck Oh, Jung-Hye Choi, Yong-Sung Lee
Cancer Research and Treatment.2005; 37(1): 54. CrossRef

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Study on the Apoptosis in Human Prostate and Breast Cancer Cells: Eun Jeong Kwon, Myung Sun Lee; J Korean Cancer Assoc. 1999;31(4):728-738.

Abstract PDF: PURPOSE
Apoptosis is a form of cell death characterized by specific morphological changes in the dying cell including contraction of cytoplasm, chromatin condensation, and cellular fragmentation into membrane-bound bodies. A common biological marker of apoptosis is the degradation of nuclear DNA resulting in a ladder of nucleosome-sized DNA fragments when resolved by electrophoresis. The potential therapeutic implications of simultaneous activation of apoptosis in androgen-dependent and androgen-independent prostatic cells are clearly very important in the development of cancer treatment modalities for advanced prostate cancer. The efficacy of chemotherapeutic agents correlates with their ability to induce apoptosis, Therefore, quantification of experimentally induced apoptosis in cancer cell lines is likely to be a predictor of the outcome of treatment. The main objective of this study was to examine the induction of apoptosis as a new strategy for cancer therapy by cis-diamminedichloroplatinum (CDDP) or 12-0-tetradecanoyl phorbol 13-acetate (TPA) in human prostate (androgen-dependent LNCaP and androgen-independent DU-145), and breast cancer cells (MCF-7).
MATERIALS AND METHODS
DNA gel electrophoresis, flow cytometry and transmission electron microscopy for morphological analysis were used to further characterize drug response in human prostate and breast cancer cells.
RESULTS
Treatment of the LNCaP and DU-145 cells with CDDP or TPA resulted in dose-dependent growth inhibition and accumulation of cells in Ao (apoptotic region), and caused significant degradation of the genomic DNA into intemucleosomal-sized DNA fragments, indicating apoptosis. In contrast, MCF-7 cells showed little or no DNA fragmentation.
CONCLUSION
These studies suggest that a differential susceptibility to apoptosis and chemosensitivity may be related to the efficacy of chemotherapeutic .agents. CDDP and TPA may have clinical implication in the treatment of prostate cancer. In particular, cytotoxic effects of TPA may well lead to new possibilities for improved strategy.

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Genistein Induced Inginition of Cell Proliferation and Programmed Cell Death in the Human Cancer Cell Lines: Young Hyun Choi, Soo Jae Lee, Min Kim, Lijuan Zhang, Won Ho Lee, Kun Young Park; J Korean Cancer Assoc. 1998;30(4):800-808.

Abstract PDF: PURPOSE
Genistein, a natural isoflavonoid phyto-oestrogen present in plant foods including citrus fruits and soybean, is a specific inhibitor of tyrosine kinase and topoisomerase II. In this paper we examined the effect of genistein on cell cycle progression and programmed cell death in the human prostate carcinoma PC-3 and Ewing's sarcoma CHP-100 cells. MATERIAL AND METHODS: Effect of genistein on cell cycle was measured by DNA flow cytometric analysis. In order to understand anticancer effect of genistein on cell cycle, Western blot analysis, immune complex kinase assay, DAPI staining and DNA fragmentation analysis were conducted.
RESULTS
DNA flow cytometric analysis indicated that genistein induced cell cycle arrest at the G2/M transition phase. Western blot analyses showed that genistein selectively reduced expression of cyclin B1 and cdk2-dependent kinase activity in both cell lines. Genistein also induced apoptosis that was demonstrated by direct visualization of morphological nuclear changes and confirmed by the production of characteristic ladder patterns of genomic DNA fragmentation.
CONCLUSION
The chemopreventive activity of genistein is proven to be related with the induction of cell cycle arrest at the G2/M transition phase by reducing the expression of cyclin B1 and cdk2-dependent kinase activity, and also with the induction of apoptosis in the tested cancer cells.

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Role of Cell Surface Mucin on Invasion and Metastasis of HM7 Colon Cancer Cells: Wan Hee Yoon, Hae Duck Park, Kyu Lim, Byung Doo Hwang; J Korean Cancer Assoc. 1997;29(2):309-320.

Abstract PDF: PURPOSE
Mucinous colorectal cancers have a poorer prognosis than which colorectal cancer produce low amount of mucin, but the exact mechanism is not well understood. The present study was undertaken to elucidate the exact mechanism of invasion and metastasis of high mucin producing colon cancer cells using mucin glycosylation inhibitor, benzyl-alpha-N-acetylgalactosamine.
MATERIALS AND METHODS
To evaluate the effect of glycosylated mucin on invasion and metastasis, in vitro invasion, metalloproteinases (MMPs) activity, cell-matrix protein binding, cell-cell aggregation, as well as endothelial leukocyte adhesion molecule (ELAM-1) binding and cell surface expression of various mucin related antigens were analyzed.
RESULTS
MMPs activity in conditioned medium and invasion of ECM-coated porous filters by benzyl-alpha-GalNAc treated HM7 cells were decreased. There was no difference between control and treated HM7 cells in terms of matrix protein binding assay, but treated HM7 cells showed higher homotypic cell adhesion. The binding activity of treated HM7 cells to ELAM-1 was significantly decreased and fixed cell binding of MoAb SNH-3, 19-9 (specific for sialyl-Lewis X and sialyl-Lewis A) were also significantly decreased.
CONCLUSION
These results suggest that glycosylated mucin modulates ELAM-1 binding, MMPs activity and homotypic cell adhesion, therefore enhance invasive and metastatic properties of human colon cancer cells.

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