A review of in vivo and in vitro models of gastric cancer research

Introduction: Shanghai Jikai Gene Chemical Technology Co., Ltd. was established in 2002, has the largest lentivirus library in China, and is also the largest supplier of disease key genetic research services in China. It has accumulated more than 14 years of experimentation in the field of disease research! Here, we have compiled the experience of more than 10 research fields for everyone, and share the most practical essence with everyone! In the last issue, I helped you summarize the application of lentiviral tools in lung cancer research. In the previous issue, let's look at the current situation in this issue.

Gastric cancer is highly heterogeneous, and gastric cancer can be differentiated by conventional pathology. However, the widely used histopathological classification has gradually become difficult to adapt to the needs of clinical individualized diagnosis and treatment. The research on gastric cancer has entered the molecular level. As the saying goes, "A good start is half the battle." Today, let's talk about the choice of in vitro and in vivo models and the application of viral tools in gastric cancer research.

1. Which cell model do I need? Is it easy to operate?

A large number of omics studies have confirmed that gastric cancer is a very complicated disease. If you want to study a particular group of gastric cancer, there are two questions to be aware of: 1. Whether the cells and animal models used are consistent with the characteristics of the disease. 2. How to effectively operate the target gene in the model according to the needs of the experiment. For example, if you want to study the effect of a gene in gastric cancer on the p53 pathway, what kind of cells do you need to choose?

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Second, the cell experiment works well, how does the animal experiment do?

Animal experiments in gastric cancer research are mainly divided into three types: I spontaneous gastric cancer model; II induced gastric cancer model; III transplanted gastric cancer model. The first species is mainly achieved by constructing a transgenic animal, and the second species is induced by a chemical inducer or Helicobacter pylori (HP) infection, and the third species is directly inoculated into a nude mouse by a human tumor tissue or cell. Because of the low incubation conditions and hairlessness of nude mice, it is easy to observe the growth state of tumors dynamically, and the selection of inoculation methods and sites can achieve a satisfactory transfer effect. Therefore, nude mice are currently selected for human gastric cancer cell allograft migration.

For genetic manipulation in transplanted tumor models, it is more common to inoculate cells after lentivirus infection. If the virus is directly injected into the animal/tumor, the virus used must be specially purified to ensure high titer, low toxicity, and not easy to cause an inflammatory reaction.

Third, the in vitro and in vivo models have been selected, then what kind of lentiviral vector does my experiment need to use to manipulate the gene?

Promoters, fluorescent markers, and resistance tags are the three major factors we need to consider when choosing a carrier. Different components also require corresponding changes in the experiment. It is as simple as offering a map of God and customizing your exclusive carrier!

Shanghai Jikai Gene Chemical Technology Co., Ltd. was established in 2002 and has a BSL-2 level lentivirus packaging laboratory. The virus production line has passed the ISO9001 quality management system verification, and the monthly average custom genetic virus product packaging has exceeded 1000 times. Lentiviral production uses six QC assays, viral purity fractionation and absolute quantitative detection of viral titers to ensure virus quality.

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references

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[2] Li, Wenjuan, et al. "CIP2A is overexpressed in gastric cancer and its depletion leads to impaired clonogenicity, senescence, or differentiation of tumor cells." Clinical Cancer Research 14.12 (2008): 3722-3728.

[3] Wang, Jia-bin, et al. “CDK5RAP6 acts as a tumor suppressor in gastric cancer through inhibition of β-catenin signaling.” Cancer Letters (2016).

[4] Sun, Ruochuan, et al. "Down regulation of Thrombospondin2 predicts poor prognosis in patients with gastric cancer." Molecular cancer 13.1 (2014): 1.

[5] Zhang, Qi, et al. "Knockdown of S100P by lentiviral-mediated RNAi promotes apoptosis and suppresses the colony-formation ability of gastric cancer cells." Oncology reports 31.5 (2014): 2344-2350.

[6] Zhang, Qing, et al. "By recruiting HDAC1, MORC2 suppresses p21Waf1/Cip1 in gastric cancer." Oncotarget 6.18 (2015): 16461.

[7] Zhou, Jinfeng, et al. “Chaperone-mediated autophagy regulates proliferation by targeting RND3 in gastric cancer.” Autophagy 12.3 (2016): 515-528.

[8] Li, T., et al. "MicroRNA-296-5p increases proliferation in gastric cancer through repression of Caudal-related homeobox 1." Oncogene 33.6 (2014): 783-793.

[9] Asciutti, Stefania, et al. "Diverse mechanisms of Wnt activation and effects of pathway inhibition on proliferation of human gastric cancer cells." Oncogene 30.8 (2011): 956-966.

[10] Zhou, W., et al. “The AKT1/NF-kappaB/Notch1/PTEN axis has an important role in chemoresistance of gastric cancer cells.” Cell death & disease 4.10 (2013): e847.

[11] She, Jun-Jun, et al. "Side population cells isolated from KATO III human gastric cancer cell line have cancer stem cell-like characteristics." World J Gastroenterol 18.33 (2012): 4610-4617.

[12] Zhang, Y., et al. “SIRT1 Is Reduced in Gastric Adenocarcinoma and Acts as a Potential Tumor Suppressor in Gastric Cancer.” Gastrointestinal Tumors 2.3 (2015): 109-123.

[13]Su, Guo‐Qiang, et al. “Research of shRNAmir inhibitory effects towards focal adhesion kinase expression in the treatment of gastric cancer.” Oncology letters 9.2 (2015): 595-603.

[14] Hu, Hao, et al. "Real-time bioluminescence and tomographic imaging of gastric cancer in a novel orthotopic mouse model." Oncology reports 27.6 (2012): 1937.

[15] Chen, L., et al. "miR-1207-5p and miR-1266 suppress gastric cancer growth and invasion by targeting telomerase reverse transcriptase." Cell death & disease 5.1 (2014): e1034.


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