MAL

Official Full Name

mal, T cell differentiation protein

Organism

Homo sapiens

GeneID

4118

Background

The protein encoded by this gene is a highly hydrophobic integral membrane protein belonging to the MAL family of proteolipids. The protein has been localized to the endoplasmic reticulum of T-cells and is a candidate linker protein in T-cell signal transduction. In addition, this proteolipid is localized in compact myelin of cells in the nervous system and has been implicated in myelin biogenesis and/or function. The protein plays a role in the formation, stabilization and maintenance of glycosphingolipid-enriched membrane microdomains. Down-regulation of this gene has been associated with a variety of human epithelial malignancies. Alternative splicing produces four transcript variants which vary from each other by the presence or absence of alternatively spliced exons 2 and 3. [provided by RefSeq, May 2012]

Synonyms

HLD28; MVP17; VIP17;

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Detailed Information

Brief Introduction

The MAL gene is located at 2q11.1 and contains 4 exons and 3 introns with a cDNA length of 1051 bp. MAL proteins are expressed in respiratory cells, gastrointestinal cells and other epithelial cells. The structure of MAL proteins is similar to that of chimeric proteins, which construct pores on cell membranes as molecular transporters to pass through lipid bilayers. The MAL protein not only expresses T cell receptor, but also expresses T11 antigen, indicating that MAL may participate in the signal transduction of T cell membrane through these two pathways.

Deletion of MAL gene expression is associated with the occurrence and development of various malignant tumors such as cervical cancer, ovarian cancer, oral cancer, laryngeal cancer, breast cancer, esophageal cancer, gastric cancer, intestinal cancer, and kidney cancer.

MAL Gene and Cancer

In esophageal cancer tissues, the expression of MAL gene is down-regulated or absent. Moreover, the MAL gene also plays a regulatory role in the differentiation and keratinization of esophageal epithelial cells. Studying its regulatory mechanisms can be helpful to elucidate the mechanism of esophageal cancer.

MAL gene is an important tumor suppressor gene in the progression of gastric cancer. The normal gastric mucosa also expresses MAL gene, but the MAL genes differ between cells. MAL is strongly expressed in parietal cells and main cells, but not in muscle tissue cells and sub-mucosal cells. There is a significant difference in the methylation rate of MAL gene between gastric cancer and normal gastric mucosa tissues. Methylation of MAL gene is an important cause of MAL gene inactivation, and methylation in different regions leads to different prognosis of gastric cancer.

The changes of MAL gene methylation are closely related to the occurrence of lung cancer, and the detection of plasma MAL gene methylation can be used as a potential early diagnostic indicator for lung cancer, which is helpful to differentiate lung cancer from pulmonary tuberculosis.

The methylation rate of MAL gene decreases successively in colorectal cancer, colorectal adenocarcinoma, and highly proliferative polyps. The methylation status of MAL gene has nothing to do with clinical features such as gender, age, tumor location, lymph node metastasis, and tumor stage. MAL methylation promoter occurs in most degenerative and malignant colorectal cancers, which may make MAL gene a real diagnostic target for early colorectal cancer.

In a word, the expression of MAL gene has changed in many tumors, and there are many related expression mechanisms. Gene methylation is the main mechanism of MAL gene inactivation.

References:

Huang Daye, et al. Significance of plasma MAL gene methylation in early diagnosis of lung cancer [J]. Modern oncology, 2016, (13): 2055-2058. DOI: 10.3969/j.issn.1672-4992.2016.13.013.
Liu Boxin, et al. Methylation status of MAL gene promoter region in EC9706 cells and human esophageal squamous cell carcinoma tissues [J]. Journal of Zhengzhou University (Medical Edition), 2013, (4): 440-443. DOI: 10.3969/j.issn.1671-6825.2013.04.002.
Liu Boxin, et al. MAL Gene and Tumor [J]. International Journal of Oncology, 2011, (12): 885-887. DOI: 10.3760/cma.j.issn.1673-422X.2011.12.002.

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