|CSC-DC002282||Panoply™ Human CADM1 Knockdown Stable Cell Line||Inquiry|
|CSC-SC002282||Panoply™ Human CADM1 Over-expressing Stable Cell Line||Inquiry|
|CDCB184989||Rabbit CADM1 ORF clone (XM_008261037.1)||Inquiry|
|CDCL183012||Human CADM1 ORF clone(NM_014333.3)||Inquiry|
|CDCL183013||Mouse CADM1 ORF clone(NM_018770.3)||Inquiry|
|CDCR040702||Human CADM1 ORF clone (NM_001098517.1)||Inquiry|
|CDCR040706||Mouse Cadm1 ORF clone (NM_001025600.1)||Inquiry|
|CDCR040710||Mouse Cadm1 ORF clone (NM_207675.2)||Inquiry|
|CDCR040712||Mouse Cadm1 ORF clone (NM_207676.2)||Inquiry|
|CDCR369543||Rat Cadm1 ORF Clone(NM_001012201.1)||Inquiry|
|CDCS407429||Human CADM1 ORF Clone (BC047021)||Inquiry|
|CDCS407430||Human CADM1 ORF Clone (BC125103)||Inquiry|
|CDFG017562||Mouse Cadm1 cDNA Clone(NM_001025600.1)||Inquiry|
|CDFH002596||Human CADM1 cDNA Clone(NM_001098517.1)||Inquiry|
|CDFL002108||Mouse Cadm1 cDNA Clone(NM_207675.2)||Inquiry|
|CDFL002109||Mouse Cadm1 cDNA Clone(NM_207676.2)||Inquiry|
|CDFR002626||Rat Cadm1 cDNA Clone(NM_001012201.1)||Inquiry|
|MiUTR1M-02456||CADM1 miRNA 3'UTR clone||Inquiry|
|MiUTR1M-02457||CADM1 miRNA 3'UTR clone||Inquiry|
|MiUTR1M-02458||CADM1 miRNA 3'UTR clone||Inquiry|
|MiUTR1M-02459||CADM1 miRNA 3'UTR clone||Inquiry|
|MiUTR1R-02608||CADM1 miRNA 3'UTR clone||Inquiry|
|MiUTR4H-TG01568||CADM1 miRNA 3'UTR clone||Inquiry|
|SHG132913||shRNA set against Mouse Cadm1(NM_001025600.1)||Inquiry|
|SHG132949||shRNA set against Human CADM1(NM_014333.3)||Inquiry|
|SHG132967||shRNA set against Mouse Cadm1(NM_207675.2)||Inquiry|
|SHG132985||shRNA set against Mouse Cadm1(NM_018770.3)||Inquiry|
|SHG133003||shRNA set against Mouse Cadm1(NM_207676.2)||Inquiry|
|SHH253589||shRNA set against Mouse CADM1 (NM_018770.3)||Inquiry|
|SHH253593||shRNA set against Rat CADM1 (NM_001012201.1)||Inquiry|
Recent Research Progress
Cell adhesion molecule 1 (CADM1), also known as synaptic cell adhesion molecule (SynCAMs), tumor suppressor in lung cancer 1 (TSLC1) or immunoglobulin superfamily, member 4 (IGSF4), is a cell adhesion molecules that context-dependent roles as a tumor suppressor or an oncogene in different cancers. CADM1 expression is associated with a variety of human cancers, including gastric cancer (GC), squamous cell carcinoma (SqCC), Merkel cell carcinoma (MCC), pancreatic cancer (PC), and hepatocellular carcinoma (HCC).
CADM1 and GC
Abnormal expression of microRNAs has been shown to play a key role in the development and progression of GC. Recent studies have shown that inhibition of miR-126 effectively reduced migration and invasion of gastric cancer cell lines. Bioinformatics and luciferase reporter assays showed that miR-126 specifically targeted the 3'-Untranslated Regions (3'-UTR) of CADM1 and regulated its expression. Down-regulation of CADM1 enhanced migration and invasion of GC cell lines. In addition, the expression of miR-126 was negatively correlated with CADM1 in tumor tissues obtained from gastric cancer patients, and the high expression of miR-126 combined with the low expression of CADM1 may be a risk factor for patients with stage 1 gastric cancer. In conclusion, studies have shown that miR-126 enhances the migration and invasion of GC cells by down-regulating CADM1.
CADM1 and SqCC
Although squamous cell carcinoma (SqCC) in the lungs, head and neck, esophagus, and cervix accounts for up to 30% of cancer deaths, the mechanisms regulating disease progression are still not fully understood. Down-regulation of epigenetic silencing or loss of heterozygosity by CADM1 is accompanied by an increase in tumor cell invasion and metastatic potential, making it an attractive candidate for regulating SqCC progression. Recently, Valathh et al. have identified the key functional role of CADM1 in the progression of SqCC (Figure 1). The extracellular domain of CADM1 limits tumor growth and metastasis by interacting with human epidermalgrowth factor receptor-2 (HER2) and integrinα6β4 (Itgα6β4) on the cell surface. The CADM1-HER2-Itgα6β4 signaling complex reduces downstream signal transducers and activators of transduction-3 (STAT3) activity, which is an important regulator of SqCC proliferation and invasion.
Figure 1. Model of CADM1 activity in SqCC. (Vallath, et al. Scientific Reports, 2016)
CADM1 and MCC
MCC is a clinically aggressive neuroendocrine skin cancer; 80% of cases are associated with the Merkel cell polyomavirus (MCPyV). Recent studies have demonstrated that MCPyV-associated MCCs show significantly lower CADM1 expression and higher mal T-cell differentiation protein (MAL) expression than MCPyV-negative MCCs. The high expression of CADM1 and the down-regulation of MAL expression in MCC were significantly associated with adverse outcomes. These findings suggest that CADM1 and MAL may act as oncoproteins and tumor suppressors in tumorigenesis of MCC, respectively.
CADM1 and PC
PC, as the leading cause of cancer death worldwide, is one of the deadly tumors with a very low 5-year survival rate. Therefore, there is an urgent need to seek new biomarkers for PCs for more accurate and reliable treatment. Wang et al. found that miR-196b was the least regulated differentially expressed miRNAs (DEM) in PC tissue compared to the corresponding adjacent tissue and is positively correlated with poor differentiation, tumor size, lymphatic invasion, and tumor node metastasis (TNM) staging. Moreover, the late apoptosis rate was significantly reduced, while the cell proliferation was increased in PANC-1 (human pancreatic cancer cell line) and ASPC-1 (Human pancreatic adenocarcinoma cell-lines) cell-lines after treatment with miR-196b mimics. The qRT-PCR and Western blot analysis demonstrated that the level of CADM1 in PANC-1 cells responded to changes in miR-196b. Furthermore, blocking CADM1 reduced late apoptosis in PANC-1 cells as up-regulated by inhibiting miR-196b. Finally, luciferase reporter assays confirmed that CADM1 was a direct target gene for miR-196b. Overexpression of miR-196b in PC tissue can increase late apoptosis of pancreatic cancer cells by targeting CADM1.
CADM1 and HCC
HCC is the most common primary liver cancer and has been recognized as one of the leading causes of death in patients with cirrhosis, and its incidence is expected to increase in the future. Recent studies have found that down-regulation of CADM1 expression was frequently detected in HCC cells and clinical samples. Restoration of CADM1 expression in HCC cell lines significantly inhibited cell growth and negatively regulated G1/S conversion. Overexpression of CADM1 can inhibit the tumorigenicity of HCC cells in vitro and in vivo. Western blot analysis showed that ectopic expression of CADM1 in HCC cells was associated with increased expression of retinoblastoma (Rb) protein.
In summary, there is increasing evidence that CADM1 is closely associated with tumorigenesis in various cancers. CADM1 plays a dual role and, depending on the cell type, can inhibit or promote human tumorigenesis. Therefore, there is an urgent need to explore the mechanism of action of CADM1 in various cancers to obtain more accurate and reliable treatments.
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