Cancer Research and Treatment

Original Articles

Gastrointestinal Cancer

The Establishment of a Fast and Safe Orthotopic Colon Cancer Model Using a Tissue Adhesive Technique: Hong-Tao Hu, Zhe Wang, Myung Ji Kim, Lu-Shang Jiang, Shi-Jun Xu, Jaeyun Jung, Eunji Lee, Jung-Hoon Park, Nader Bakheet, Sung Hwan Yoon, Kun Yung Kim, Ho-Young Song, Suhwan Chang; Cancer Res Treat. 2021;53(3):733-743. Published online December 15, 2020; DOI: https://doi.org/10.4143/crt.2020.494

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Purpose
We aimed to develop a novel method for orthotopic colon cancer model, using tissue adhesive in place of conventional surgical method.
Materials and Methods
RFP HCT 116 cell line were used to establish the colon cancer model. Fresh tumor tissue harvested from a subcutaneous injection was grafted into twenty nude mice, divided into group A (suture method) and group B (tissue adhesive method). For the group A, we fixed the tissue on the serosa layer of proximal colon by 8-0 surgical suture. For the group B, tissue adhesive (10 μL) was used to fix the tumor. The mortality, tumor implantation success, tumor metastasis, primary tumor size, and operation time were compared between the two groups. Dissected tumor tissue was analyzed for the histology and immunohistochemistry. Also, we performed tumor marker analysis.
Results
We observed 30% increase in graft success and 20% decrease in mortality, by using tissue adhesive method, respectively. The median colon tumor size was significantly increased by 4 mm and operation time was shortened by 6.5 minutes. The H&E showed similar tumor structure between the two groups. The immunohistochemistry staining for cancer antigen 19-9, carcinoembryonic antigen, cytokeratin 20, and Ki-67 showed comparable intensities in both groups. Real-time quantitative reverse transcription analysis showed eight out of nine tumor markers are unchanged in the tissue adhesive group. Western blot indicated the tissue adhesive group expressed less p-JNK (apototic marker) and more p-MEK/p-p38 (proliferation marker) levels.
Conclusion
We concluded the tissue adhesive method is a quick and safe way to generate orthotopic, colon cancer model.

Citations

Citations to this article as recorded by

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Nature Communications.2024;[Epub] CrossRef
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Jae Yun Jung, Hyun Jin Ryu, Seung-Hwan Lee, Dong-Young Kim, Myung Ji Kim, Eun Ji Lee, Yeon-Mi Ryu, Sang-Yeob Kim, Kyu-Pyo Kim, Eun Young Choi, Hyung Jun Ahn, Suhwan Chang
Cells.2021; 10(10): 2734. CrossRef

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Low Doses of Nonylphenol Promote Growth of Colon Cancer Cells through Activation of ERK1/2 via G Protein‒Coupled Receptor 30: Ming Xie, Jin-Long Liang, Han-Dong Huang, Mai-Jian Wang, Tao Zhang, Xue-Feng Yang; Cancer Res Treat. 2019;51(4):1620-1631. Published online May 15, 2019; DOI: https://doi.org/10.4143/crt.2018.340

Abstract PDF PubReader ePub

Purpose
Nonylphenol (NP) is an endocrine disruptor found in products such as cleaners, plastics, and detergents. It exerts actions similar to endogenous 17β-estradiol (E2) and is reported to influence various cancers. However, its role in colon cancer remains elusive.
Materials and Methods
Colon cancer cell lines COLO 205 and SW480 were employed in our study. The cells were treated with NP or E2 followed by measurement of apoptosis and proliferation using flow cytometry and MTT assays, respectively. G protein–coupled estrogen receptor 30 (GPR30) expression was visualized using immunofluorescence and Western blot. To investigate the underlying mechanism, the expression levels of GPR30, p-protein kinase A (PKA), c-myc, cyclin D1, and ERK1/2 were analyzed using Western blot. Meanwhile, the GPR30 antagonist G15 was utilized to validate the role of GPR30 in colon cancer progression. Finally, the effect of a GPR30 inhibitor on tumor growth was determined in vivo using tumor xenograft mouse models.
Results
NP facilitated the proliferation of colon cancer cells and induced apoptosis failure in vitro. Western blot revealed increased GPR30 expression levels in response to NP treatment. Cyclin D1, p-PKA, c-myc, and proliferating cell nuclear antigen, proteins that regulate the cell cycle, were all upregulated by NP, and NP-mediated ERK1/2 activation and subsequent cell proliferation were abrogated by the GPR30 inhibitor G15. Moreover, colon cancer mice that received G15 administration demonstrated impaired tumor growth in vivo.
Conclusion
Low dose NP promotes the growth of colon tumors through GPR30-mediated activation of ERK1/2 signaling.

Citations

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