|CSC-DC009522||Panoply™ Human MIIP Knockdown Stable Cell Line||Inquiry|
|CSC-SC009522||Panoply™ Human MIIP Over-expressing Stable Cell Line||Inquiry|
|CDCB158570||Human MIIP ORF clone (BC008068)||Inquiry|
|CDCB186458||Rabbit MIIP ORF clone (XM_008275379.1)||Inquiry|
|CDCH389248||Human MIIP ORF clone(NM_021933.3)||Inquiry|
|CDCH389249||Mouse MIIP ORF clone(NM_001025365.2)||Inquiry|
|CDCR370493||Rat Miip ORF Clone(NM_001017450.1)||Inquiry|
|CDCS417955||Human MIIP ORF Clone (BC008068)||Inquiry|
|CDFR003453||Rat Miip cDNA Clone(NM_001017450.1)||Inquiry|
|MiUTR1R-03111||MIIP miRNA 3'UTR clone||Inquiry|
|MiUTR3H-10218||MIIP miRNA 3'UTR clone||Inquiry|
Migration invasion inhibitor protein (MIIP), also known as invasion inhibitor protein 45, inhibits the migration, invasion and proliferation of tumor such as glioma, colorectal cancer, endometrial cancer, lung cancer, and breast cancer.
The MIIP gene is located on chromosome 1p36, which is frequently deleted in a variety of tumors including breast cancer, meningioma, prostate cancer, neuroblastoma and colorectal cancer. MIIP has 10 exons spanning 12.6 kb of genomic DNA.
MIIP Gene and Glioma
Compared to normal brain tissue, the expression of MIIP is decreased in glioblastoma. MIIP is a tumor suppressor gene of glioma, and the introduction of MIIP can reduce the incidence of glioma. Studies have shown that MIIP does not play a major role in gliomas through genetic mutation. In aggressive gliomas, MIIP can be inactivated by tumor-specific splicing, resulting in abnormal and unstable MIIP isomers.
MIIP Gene and Colorectal Cancer
MIIP single copy deletion is significantly associated with low expression of MIIP, lymph node metastasis and distant metastasis. In addition, the incidence of MIIP single copy deletion in colorectal cancer is significantly higher than that in colorectal adenoma and normal mucosa. MIIP single copy deletion is not associated with known genetic abnormalities associated with colorectal cancer (TP53, APC, PIK3CA, KRAS, NRAS, TGFBR2, SMAD4, MSH6 and MSH3). These results suggest that MIIP inactivation in colorectal cancer is mainly due to single copy deletion of MIIP gene, and MIIP single copy deletion may be a relatively new and important molecular abnormality in the development of colorectal cancer.
MIIP Gene and Endometrial Carcinoma
Someone has found that MIIP is highest expressed in normal endometrium, slightly lower in atypical hyperplasia endometrium, and lowest in endometrial carcinoma. Furthermore, the low expression of MIIP in endometrial carcinoma is positively correlated with deep myometrial infiltration, lymph node metastasis and evevated FIGO stage, suggesting that MIIP may also play an oncogene role in endometrial carcinoma. However, the role and mechanism of MIIP in endometrial carcinoma need further study.
MIIP Gene and Non-small Cell Lung Cancer
The expression of MIIP is an independent prognostic factor affecting overall survival, and patients with low MIIP expression have poor overall survival. The mRNA and protein expression levels of MIIP in NSCLC are significantly lower than those in matched normal tissues. In addition, the expression of MIIP mRNA and protein in lung adenocarcinoma is significantly higher than that in squamous cell carcinoma, and negatively correlated with tumor grade. Survival analysis shows that the 5-year survival rate of patients with MIIP-positive expression is significantly higher than that of negative expression.
MIIP Gene and Breast Cancer
The expression of MIIP mRNA and protein is decreased in breast cancer tissues, and the expression of MIIP is significantly decreased in patients with advanced breast cancer and those with a maximum diameter > 2 cm. Survival analysis shows that patients with LOH in SNP rs2295283 have shorter survival time. These results suggest that the low expression of MIIP and LOH may lead to poor prognosis in breast cancer patients.
MIIP Gene and Esophageal Squamous Cell Carcinoma
MIIP has an inhibitory effect in glioma, colorectal cancer, endometrial cancer, non-small cell lung cancer and breast cancer. However, the opposite result has been found in esophageal squamous cell carcinoma, where the expression of MIIP is significantly increased. Moreover, the high expression of MIIP in poorly differentiated esophageal cancer is significantly higher than that in well differentiated and moderately differentiated cases. Survival analysis shows that patients with lower MIIP expression have better overall survival and disease-free survival. Multivariate analysis shows that MIIP expression is an independent prognostic factor for overall survival and disease-free survival of esophageal cancer. Since MIIP is rarely studied in squamous cell carcinoma, the role and mechanism of MIIP in squamous cell carcinoma need further study.
As a new candidate tumor suppressor gene, MIIP can inhibit tumor cell migration, invasion, proliferation and genomic instability through multiple downstream target proteins. Although mitosis and cell migration seem to be two distinct processes, they are closely related by the sharing of microtubule mechanisms. It is not clear how MIIP and other regulatory molecules in the cells organizes these delicate procedures in an orderly manner.
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