Re-expression of cell adhesion molecule inhibits growth and induces apoptosis of human pancreatic cancer cell line PANC-1

Liu, Zhiqing; Zhu, Liang; Hua, Qi; Li, Demin; Xie, Zuoqi; Ke, Xiaoyu; Zhao, Qiu

doi:10.1007/s11596-011-0673-z

Cited by 5 publications

(5 citation statements)

References 20 publications

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“…Our data show for the first time a linkage between HPV16 positivity and CADM1 methylation in OPSCC. CADM1 plays a role in cell–cell adhesion and reduced expression of this gene is correlated with lymph node metastasis . Interestingly, CADM1 was also often methylated in cervical cancer (Fig.…”

Section: Discussionmentioning

confidence: 91%

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HPV‐positive oropharyngeal squamous cell carcinoma is associated with TIMP3 and CADM1 promoter hypermethylation

et al. 2014

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Oropharyngeal squamous cell carcinoma (OPSCC) is associated with human papillomavirus (HPV) in a proportion of tumors. HPV-positive OPSCC is considered a distinct molecular entity with a prognostic advantage compared to HPV-negative cases. Silencing of cancer-related genes by DNA promoter hypermethylation may play an important role in the development of OPSCC. Hence, we examined promoter methylation status in 24 common tumor suppressor genes in a group of 200 OPSCCs to determine differentially methylated genes in HPV-positive versus HPV-negative primary OPSCC. Methylation status was correlated with HPV status, clinical features, and patient survival using multivariate methods. Additionally, methylation status of 16 cervical squamous cell carcinomas (SCC) was compared with HPV-positive OPSCC. Using methylation-specific probe amplification, HPV-positive OPSCC showed a significantly higher cumulative methylation index (CMI) compared to HPV-negative OPSCC (P=0.008). For the genes CDH13, DAPK1, and RARB, both HPV-positive and HPV-negative OPSCC showed promoter hypermethylation in at least 20% of the tumors. HPV status was found to be an independent predictor of promoter hypermethylation of CADM1 (P < 0.001), CHFR (P = 0.027), and TIMP3 (P < 0.001). CADM1 and CHFR showed similar methylation patterns in OPSCC and cervical SCC, but TIMP3 showed no methylation in cervical SCC in contrast to OPSCC. Methylation status of neither individual gene nor CMI was associated with survival. These results suggest that HPV-positive tumors are to a greater extent driven by promotor hypermethylation in these tumor suppressor genes. Especially CADM1 and TIMP3 are significantly more frequently hypermethylated in HPV-positive OPSCC and CHFR in HPV-negative tumors.

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Section: Discussionmentioning

confidence: 91%

“…CADM1 plays a role in cell-cell adhesion and reduced expression of this gene is correlated with lymph node metastasis [46]. Interestingly, CADM1 was also often methylated in cervical cancer (Fig.…”

Section: Discussionmentioning

confidence: 91%

HPV‐positive oropharyngeal squamous cell carcinoma is associated with TIMP3 and CADM1 promoter hypermethylation

et al. 2014

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“…Our finding demonstrated that CADM1 was a target gene of miR-196b in PANC-1 cells. CADM1, which is also called as TSCL1, has been reported to be involved in cell adhesion, migration, and apoptosis 22 – 24 . Besides, previous study has found that CADM1 expression was down-regulated in different types of cancers, including gastric cancer, breast cancer, and lung carcinoma 25 – 27 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-196b inhibits late apoptosis of pancreatic cancer cells by targeting CADM1

Wang

Zhou

Liu

et al. 2017

Sci Rep

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Pancreatic cancer (PC), as the leading cause of cancer death worldwide, is one of the deadliest tumors with a very low 5-year survival rate. Therefore, it is urgent to seek new biomarkers of PC for more accurate and reliable treatments. To identify the differentially expressed miRNAs (DEM) in PC tissues, we performed the systematic microarray and qRT-PCR analyses. We found miR-196b was the top dysregulated DEM in PC tissues as compared with the corresponding adjacent tissues, and positively correlated with poor differentiation, tumor size, lymphatic invasion and TNM stage. Furthermore, the late apoptosis rate was significantly reduced, while the cell proliferation was increased in PANC-1 and ASPC-1 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 response to the alteration of miR-196b. Moreover, blockade of CADM1 could decrease the late apoptosis in PANC-1 cells as up-regulated by inhibition of miR-196b. Finally, luciferase report assay confirmed that CADM1 was the direct target gene of miR-196b. Overexpression of miR-196b in PC tissues can increase the late apoptosis of pancreatic cancer cells by targeting CADM1. These findings suggested miR-196b is a potential target for diagnosis and therapeutics of human pancreatic cancer.

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“…Loss of heterozygosity for the CADM1 gene and methylation of the CADM1 promoter is shown to promote PC progression, with CADM1 promoter hypermethylation detected in nonsmall cell lung cancer, pancreatic, hepatocellular, and prostate cancers. 64,67,[73][74][75]…”

Section: Cell Adhesion Moleculementioning

confidence: 99%

“…Cell adhesion molecule 1 was also reported to suppress PDAC metastasis by inducing cell cycle arrest at the G 1 phase and promoting cellular apoptosis. Loss of heterozygosity for the CADM1 gene and methylation of the CADM1 promoter is shown to promote PC progression, with CADM1 promoter hypermethylation detected in nonsmall cell lung cancer, pancreatic, hepatocellular, and prostate cancers 64,67,73–75 …”

Section: Cell Adhesion Moleculementioning

confidence: 99%

Metastasis Suppressor Genes in Pancreatic Cancer

et al. 2021

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Pancreatic cancer, especially pancreatic ductal adenocarcinoma (PDAC), has for long remained a deadly form of cancer characterized by high mortality rates resulting from metastasis to multiple organs. Several factors, including the late manifestation of the disease, partly amplified by lack of efficient screening methods, have hampered the drive to design an effective therapeutic strategy to treat this deadly cancer. Understanding the biology of PDAC progression and identifying critical genes regulating these processes are essential to overcome the barriers toward effective treatment. Metastasis suppressor genes have been shown to inhibit multiple steps in the metastatic cascade without affecting primary tumor formation and are considered to hold promise for treating metastatic cancers. In this review, we catalog the bona fide metastasis suppressor genes reported in PDAC and discuss their known mechanism of action.

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Re-expression of cell adhesion molecule inhibits growth and induces apoptosis of human pancreatic cancer cell line PANC-1

Cited by 5 publications

References 20 publications

HPV‐positive oropharyngeal squamous cell carcinoma is associated with TIMP3 and CADM1 promoter hypermethylation

HPV‐positive oropharyngeal squamous cell carcinoma is associated with TIMP3 and CADM1 promoter hypermethylation

MicroRNA-196b inhibits late apoptosis of pancreatic cancer cells by targeting CADM1

Metastasis Suppressor Genes in Pancreatic Cancer

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