MIEN1

Official Full Name

migration and invasion enhancer 1

Organism

Homo sapiens

GeneID

84299

Background

Involved in negative regulation of apoptotic process; positive regulation of cell migration; and positive regulation of filopodium assembly. Located in cytoplasmic side of plasma membrane and cytosol. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

C35; ORB3; XTP4; RDX12; C17orf37;

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Detailed Information

Recent Research Progress

Migration and invasion enhancer 1 (MIEN1), also known as C17orf37, ORB3, C35 or MGC14832, a novel gene located in the 17q12-21 region of human chromosome, plays an important role in the biological process of tumor metastasis. MIEN1 has been reported to be dysregulated in various cancers, such as colorectal cancer (CRC) non-small cell lung cancer (NSCLC), prostate cancer, oral squamous cell carcinoma (OSCC) and breast cancer (BC).

MIEN1 and CRC

According to statistics released by the World Health Organization, CRC was the third most common form of cancer among men and the second highest among women worldwide. Recent studies have shown that MIEN1 is mainly expressed in CRC tissues in comparison to normal colorectal tissues and non-cancerous tissues adjacent to tumors. Furthermore, its expression is closely related to the invasion behavior of CRC. These results indicate the potential of using MIEN1 as a biomarker or therapeutic target for CRC management. MIEN1 expression should be analyzed in a larger sample and its biological role in CRC progression and drugs targeting the molecule should be studied in the future.

MIEN1 and NSCLC

MicroRNAs (miRNAs) are involved in the development and progression of tumors. MiR-26b is reported to be significantly down-regulated in NSCLC. However, the underlying mechanisms of miR-26b involvement in the development and progression of NSCLC remains poorly understood. Recently, some studies have shown that miR-26b inhibits cell metastasis in NSCLC by targeting MIEN1. MiR-26b was significantly down-regulated, and MIEN1 was significantly up-regulated in both NSCLC tissues and cell lines. The expression level of miR-26b was negatively correlated with the expression level of MIEN1 mRNA in clinical NSCLC tissues. Furthermore, MIEN1 was confirmed to be a direct target of miR-26b by dual luciferase reporter gene assay, and MIEN1 expression was down-regulated by miR-26b in NSCLC cells. In terms of function, transwell and wound healing assays demonstrated that miR-26b significantly inhibited invasion and migration of NSCLC cells, which was simulated by siRNA knockdown of MIEN1 and reversed by pcDNA/MIEN1 overexpression of MIEN1. Finally, miR-26b can regulate the nuclear factor kappa B (NF-kB)/ MMP-9 / VEGF pathway in NSCLC cells. Taken together, these findings reveal that miR-26b suppresses NSCLC metastasis by targeting MIEN1 via NF-kB/MMP-9/ VEGF pathways, implicating a potential prognostic biomarker and therapeutic target for NSCLC treatment.

MIEN1 and prostate cancer

Recently MIEN1 has been shown to enhance the migration and invasion of prostate cancer cells, which are two key processes in cancer progression. Compared with cancer cells, the new miRNA, hsa-miR-940 (miR-940), was identified and verified to be highly expressed in immortalized normal cells and is a regulator of MIEN1. Analysis of human prostate tumors and their matched normal tissues confirmed that miR-940 is highly expressed in normal tissues compared to its low to negligible expression in the tumors. Although MIEN1 is a direct target of miR-940, miR-940 alters MIEN1 RNA in a quantitative and cell-dependent context, while altering its downstream effectors. MiR-940 inhibits cell migration and invasion potential, attenuates its anchorage-independent growth capacity, and increases E-cadherin expression, suggesting its role in mesenchymal-epithelial transition (MET).

MIEN1 and OSCC

OSCC is a highly malignant tumor with the potential to invade local and distant sites and promote lymph node metastasis. Major players underlying the molecular mechanisms behind tumor progression are yet to be fully explored. Smrithi Rajendiran et al. investigated the expression and role of MIEN1 in oral cancer progression using an in vitro model, patient derived oral tissues and existing TCGA data. Expression analysis using immortalized normal cells and cancer cells indicates an increase in the expression of MIEN1 in cancer. Measurements performed after MIEN1 knockdown in OSC-2 (metastatic oral cell lines) cells showed a decrease in migration, invasion, and filopodia formation; whereas MIEN1 overexpression in DOK (a dysplastic cell) cells increased these characteristics and also up-regulated some Akt/NF-kB effectors. This indicates the important role of MIEN1 in the progression of oral cancer. In summary, MIEN1 expression is not only positively correlated with oral cancer progression, but also appears to be a key molecular determinant in migration and invasion of oral cancer cells, thus playing a possible role in their metastatic dissemination.

MIEN1 and BC

BC is a common malignant tumor in women, and migration and invasion are the main causes of early tumor spread. Recent studies have found that MIEN1 was overexpressed in BC and MDA-MB-231 cells were suppressed by inhibiting MIEN1 expression using short hairpin RNA (shRNA). MIEN1 may play a significant role in the progression of BC and is a potential molecular target for cancer chemotherapy.

In conclusion, although MIEN1 is not a direct oncogene, it aids cancer progression by playing a key role in distinct processes of migration and invasion of cancer cells. Therefore, MIEN1 may be a more appropriate and reliable biomarker for tumor diagnosis and prognosis, and may also be a new therapeutic target for cancer therapy.

References:

Xuan Dong, et al. C35 is overexpressed in colorectal cancer and is associated tumor invasion and metastasis. BioScience Trends, 2015, 9(2):117-121.
Dongmei Li, et al. MicroRNA-26b suppresses the metastasis of non-small cell lung cancer by targeting MIEN1 via NF-kB/MMP-9/VEGF pathways. Biochemical and Biophysical Research Communications, 2016, 472: 465e470
Rajendiran, et al. MicroRNA-940 suppresses prostate cancer migration and invasion by regulating MIEN1. Molecular Cancer, 2014, 13:250
Smrithi Rajendiran, et al. MIEN1 promotes oral cancer progression and implicates poor overall survival. Cancer Biology & Therapy, 2015, 16(6): 876--885;
Kpetemey, et al. MIEN1, a novel interactor of Annexin A2, promotes tumor cell migration by enhancing AnxA2 cell surface expression. Molecular Cancer, 2015, 14:156
Smrithi Rajendiran, et al. MIEN1 is tightly regulated by SINE Alu methylation in its promoter. Oncotarget, 2016
Zhao et al. Migration and invasion enhancer 1 (MIEN1) is overexpressed in breast cancer and is a potential new therapeutic molecular target. Genetics and Molecular Research, 2016, 16 (1): gmr16019380
Kun Yin, et al. Overexpression of C35 in breast carcinomas is associated with tumor progression and lymphnode metastasis. BioScience Trends, 2015, 9(6):386-392

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