CKLF-like MARVEL transmembrane domain-containing 5

Studies have reported that: 1) the levels of CMTM5-v1 in the malignant tissues of patients with prostate cancer are lower than the levels in their nearby normal prostate gland tissues^[9] as well as in the tissues of patients with benign prostate hyperplasia;^[10] 2) patients with lower prostate cancer tissue levels of CMTM5-v1 have higher prostate cancer Gleason scores and therefore poorer prognoses than patients with higher prostate cancer tissue levels of CMTM5-v1;^[9] and 3) the forced overexpression of CMTM5-v1 in cultured DU145 cells (a human prostate cancer cell line) reduces, while the forced higher expression of the CMTM5-v1 levels increases, their proliferation and migration.^[4][9][10] Similar findings for an unspecified CMTM5 isoform are reported in ovarian cancer,^[4][11] hepatocellular carcinoma,^[4][12] pancreatic cancer,^[4][13] non-small-cell lung carcinoma,^[4][14] renal cell carcinoma,^[4][15] and breast cancer.^[16] The forced over expression of CMTM5-v1 in Huh7 human hepatic cells also inhibited the ability of these cells to grow in a mouse model of cancer.^[12] Finally, various cancer human cell lines including those of the liver, breast, prostate, colon, stomach, nasopharynx, laryngopharynx, esophagus, lung, and cervix express low levels of, or no, CMTM5-v1 and concurrently have highly methylated CpG sites near to the CMTM5 gene.^[17] These findings suggest that the CMTM5 gene may act as a tumor suppressor gene, i.e. a normal gene whose product(s) inhibit the development and/or progression of various cancers. The findings also support further studies to confirm and expand these relationships and determine if the expression of CMTM5 isoforms can be used as tumor markers for these cancers severities/prognoses and/or targets as for treating them.^[4]

A case–control study of hospitalized patients found that the blood plasma levels of CMTM5 protein and CMTM5 messenger RNA (i.e. mRNA) in 350 patients with coronary artery disease were significantly higher than a matched group of 350 patients without this disease.^[18] The same research group similarly studied 124 hospitalized patients who had in place a coronary artery stent. They found that high blood plasma levels of CMTM5 mRNA were associated with a higher rate of subsequently developing stenosis (i.e. narrowing) in their stents than patients with lower levels of this mRNA.^[19] Furthermore, the forced overexpression of the CMTM5 gene inhibited the proliferation and migration of cultured human endothelial cells,^[19][20] while the forced suppression of the CMTM5 gene promote the proliferation of these cells.^[20] These studies suggest that the CMTM5 gene, one of its mRNAs, and/or one of its CMTM5 proteins may promote atherosclerosis-based coronary artery disease and the stenosis of coronary artery stents and do so by inhibiting vascular endothelial cells from functioning to inhibit atherosclerosis and stent occlusion. More studies are necessary to confirm and further define these relationships; to determine if expression of the CMTM5 gene's or its products can be used as makers for patient susceptibilities to coronary artery/stent occlusions; and to determine if this gene or its products can be used clinically as targets for preventing or decreasing the frequency of these occlusions.^[19][20]