Anti‐tumor Efficacy of Paclitaxel against Human Lung Cancer Xenografts

Yamori, Takao; Sato, Shigeo; Chikazawa, Hirotaka; Kadota, Toshihito

doi:10.1111/j.1349-7006.1997.tb00350.x

Cited by 58 publications

(46 citation statements)

References 13 publications

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“…Four GC cell lines (St-4, MKN1, MKN45, and MKN74) are components of the JFCR39 panel of human cancer cell lines described previously (23,24). Of these, St-4 was established in our foundation in 1990 (25).…”

Section: Cell Lines and Cell Culturementioning

confidence: 99%

M-COPA, a Golgi Disruptor, Inhibits Cell Surface Expression of MET Protein and Exhibits Antitumor Activity against MET-Addicted Gastric Cancers

et al. 2016

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The Golgi apparatus is responsible for transporting, processing, and sorting numerous proteins in the cell, including cell surfaceexpressed receptor tyrosine kinases (RTK). The small-molecule compound M-COPA [2-methylcoprophilinamide (AMF-26)] disrupts the Golgi apparatus by inhibiting the activation of Arf1, resulting in suppression of tumor growth. Here, we report an evaluation of M-COPA activity against RTK-addicted cancers, focusing specifically on human gastric cancer (GC) cells with or without MET amplification. As expected, the MET-addicted cell line MKN45 exhibited a better response to M-COPA than cell lines without MET amplification. Upon M-COPA treatment, cell surface expression of MET was downregulated with a concurrent accumulation of its precursor form. M-COPA also reduced levels of the phosphorylated form of MET along with the downstream signaling molecules Akt and S6. Similar results were obtained in additional GC cell lines with amplification of MET or the FGF receptor FGFR2. MKN45 murine xenograft experiments demonstrated the antitumor activity of M-COPA in vivo. Taken together, our results offer an initial preclinical proof of concept for the use of M-COPA as a candidate treatment option for MET-addicted GC, with broader implications for targeting the Golgi apparatus as a novel cancer therapeutic approach. Cancer Res; 76(13); 3895-903. Ó2016 AACR.

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Section: Cell Lines and Cell Culturementioning

confidence: 99%

M-COPA, a Golgi Disruptor, Inhibits Cell Surface Expression of MET Protein and Exhibits Antitumor Activity against MET-Addicted Gastric Cancers

et al. 2016

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“…Four clinically available drugs (fluorouracil, doxifluridine, 36) paclitaxel [37][38][39] and irinotecan [40][41][42] ) were chosen as models of test compounds and examined their anti-metastatic ability. Either drug is known to inhibit cancer cell growth by its own mechanism.…”

Section: Discussionmentioning

confidence: 99%

Development and Characterization of a Model of Liver Metastasis Using Human Colon Cancer HCT-116 Cells

Ishizu

Sunose²,

Yamazaki

et al. 2007

Biological & Pharmaceutical Bulletin

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The control of cancer metastasis is one of the most important strategies for cancer therapy from the current viewpoint of considerable limitations of surgical cancer resection. During the process of metastasis, metastasizing tumor cells interact with various host cells (platelets, lymphocytes and endothelial cells), extracellular matrix and basement membranes, leading to the development of metastases. [1][2][3][4][5][6][7][8][9] Experimental models are essential for the analysis of the mechanisms of cancer metastasis and a number of animal models have been developed. Although these have been extremely useful for the elucidation of the mechanism of cancer metastasis, the number of metastatic models based on human cancer cell lines is limited. 6,7,[10][11][12] From a clinical point of view, the liver is the most common target organ for metastasis of cancers of the digestive system, especially hematogenous metastasis of colon cancer, and the prognosis for cases with liver metastasis is extremely poor. Millikan et al. 13) reported that, considering the metastasis of colon cancer, up to 25% of patients have synchronous hepatic metastasis and 50% develop metachronous metastasis. Welch and Donaldson 14) reported that the liver is the most frequent target organ of hematogenous metastasis from colon cancer and 40-70% of the deaths from colon cancer involved liver metastasis. Russell et al. 15) reported that the first relapse site of 80% of colon cancer was the liver and 32% of the recurrence was only in the liver. Furthermore, liver metastasis often was observed after radical surgery.16) Therefore, analyzing the mechanism of liver metastasis and the improving its treatment are the most important considerations for improving the survival rate in colon cancer.To this end, suitable experimental models are needed for liver metastasis of human gastro-intestinal cancer. There are some models, for example, one of which was developed by Morikawa et al. 17) However, their number and variety are quite limited. In this study, to develop a liver-metastasis model of gastro-intestinal cancer, we screened human gastric cancer and colon cancer cell lines for their liver-metastatic potential, and found that one of the colon adenocarcinoma cell line, HCT-116, was suitable for developing such a model. The suitability of the HCT-116 liver metastasis model for the evaluation of anti metastatic reagents was confirmed using paclitaxel and irinotecan as model drugs. MATERIALS AND METHODSMice Animal care and treatment was performed in accordance with the guidelines of the animal use and care committee of Japanese Foundation for Cancer Research, and conformed to the NIH 'Guide for the Care and Use of Laboratory Animals'. All procedures were approved by the above committee. Seven-to-nine week old female nude mice (BALB/C nu/nu) were purchased from Charles River Japan, Inc. The mice were maintained in the laboratory for animal experimentation in a Specific Pathogen Free environment.Cell Lines The human colon and stomach cancer cell lines us...

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“…The antitumor efficacy was assessed by estimating tumor volume (in mm 3 ), calculated as (L · W 2 ) ⁄ 2, where L is tumor length (in mm) and W is tumor width (in mm). (17,18) Peritoneal xenograft model. KLM1 cells (1 · 10 7 ) were injected into the intraperitoneal cavity of mice.…”

Section: Methodsmentioning

confidence: 99%

Antitumor effects of α‐bisabolol against pancreatic cancer

et al. 2011

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In the present study, we investigated whether a-bisabolol, a sesquiterpene alcohol present in essential oils derived from a variety of plants, has antitumor effects against pancreatic cancer. a-Bisabolol induced a decrease in cell proliferation and viability in pancreatic cancer cell lines (KLM1, KP4, Panc1, MIA Paca2), but not in pancreatic epithelial cells (ACBRI515). a-Bisabolol treatment induced apoptosis and suppressed Akt activation in pancreatic cancer cell lines. Furthermore, a-bisabolol treatment induced the overexpression of early growth response-1 (EGR1), whereas EGR1 siRNA decreased the a-bisabolol-induced cell death of KLM1 cells. Tumor growth in both subcutaneous and peritoneal xenograft nude mouse models was significantly inhibited by intragastric administration of 1000 mg ⁄ kg of a-bisabolol, once a week for three weeks. The results indicate that a-bisabolol could be a novel therapeutic option for the treatment of pancreatic cancer. (Cancer Sci 2011; 102: 2199-2205

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Anti‐tumor Efficacy of Paclitaxel against Human Lung Cancer Xenografts

Cited by 58 publications

References 13 publications

M-COPA, a Golgi Disruptor, Inhibits Cell Surface Expression of MET Protein and Exhibits Antitumor Activity against MET-Addicted Gastric Cancers

M-COPA, a Golgi Disruptor, Inhibits Cell Surface Expression of MET Protein and Exhibits Antitumor Activity against MET-Addicted Gastric Cancers

Development and Characterization of a Model of Liver Metastasis Using Human Colon Cancer HCT-116 Cells

Antitumor effects of α‐bisabolol against pancreatic cancer

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