CEACAM6 induces epithelial-mesenchymal transition and mediates invasion and metastasis in pancreatic cancer

Chen, Jianmin; Li, Qiang; An, Yong; Lv, Nan; Xue, Xiaofeng; Wei, Jishu; Jiang, Kuirong; Wu, Junli; Gao, Wentao; Qian, Zhiguo; Dai, Chaoliu; Xu, Zekuan

doi:10.1016/j.pan.2013.04.084

Cited by 16 publications

(23 citation statements)

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“…This could result from the inhibition of CDK6 that we observed in these cells, loss of CDK6 being a marker of several PDAC cell line invasiveness [44]. This may also be due to other properties of miR-29a that depend on the cellular context: increased invasion through MMP2, E-cadherin and KLF4 in colorectal cancer cells [45], decreased invasion in gastric [46], lung and pancreatic cancer cells [47], or decreased invasion and metastasis probably through the inhibition of CEACAM6 in pancreatic cancer [48]. Additionally, we found that overexpression of miR-29a or miR-330-5p sensitizes PDAC cells to gemcitabine and induces a decrease of Akt pathway activation.…”

Section: Discussionmentioning

confidence: 77%

Micro-RNAs miR-29a and miR-330-5p function as tumor suppressors by targeting the MUC1 mucin in pancreatic cancer cells

Tréhoux

Lahdaoui

Delpu

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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MUC1 is an oncogenic mucin overexpressed in several epithelial cancers, including pancreatic ductal adenocarcinoma, and is considered as a potent target for cancer therapy. To control cancer progression, miRNAs became very recently, major targets and tools to inhibit oncogene expression. Inhibiting MUC1 using miRNAs appears thus as an attractive strategy to reduce cancer progression. However, potent miRNAs and associated mechanisms regulating MUC1 expression remain to be identified. To this aim, we undertook to study MUC1 regulation by miRNAs in pancreatic cancer cells and identify those with tumor suppressive activity. MiRNAs potentially targeting the 3'-UTR, the coding region, or the 5'-UTR of MUC1 were selected using an in silico approach. Our in vitro and in vivo experiments indicate that miR-29a and miR-330-5p are strong inhibitors of MUC1 expression in pancreatic cancer cells through direct binding to MUC1 3'-UTR. MUC1 regulation by the other selected miRNAs (miR-183, miR-200a, miR-876-3p and miR-939) was found to be indirect. MiR-29a and miR-330-5p are also deregulated in human pancreatic cancer cell lines and tissues and in pancreatic tissues of Kras(G12D) mice. In vitro, miR-29a and miR-330-5p inhibit cell proliferation, cell migration, cell invasion and sensitize pancreatic cancer cells to gemcitabine. In vivo intra-tumoral injection of these two miRNAs in xenografted pancreatic tumors led to reduced tumor growth. Altogether, we have identified miR-29a and miR-330-5p as two new tumor suppressive miRNAs that inhibit the expression of MUC1 oncogenic mucin in pancreatic cancer cells.

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Section: Discussionmentioning

confidence: 77%

Micro-RNAs miR-29a and miR-330-5p function as tumor suppressors by targeting the MUC1 mucin in pancreatic cancer cells

Tréhoux

Lahdaoui

Delpu

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…Among others, this led to the identification of CEACAM genes, which encode membrane-bound members of the immunoglobulin superfamily, overexpressed in many cancers and associated with adhesion and invasion [22,23]. In addition, CEACAM6 was reported to attenuate the adenovirus infection in cancer cells by antagonizing intracellular trafficking [24].…”

Section: Discussionmentioning

confidence: 99%

Enhanced Replication of Hepatitis E Virus Strain 47832c in an A549-Derived Subclonal Cell Line

Schemmerer

Apelt

Trojnar

et al. 2016

Viruses

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Hepatitis E virus (HEV) is a human pathogen with increasing importance. The lack of efficient cell culture systems hampers systematic studies on its replication cycle, virus neutralization and inactivation. Here, several cell lines were inoculated with the HEV genotype 3c strain 47832c, previously isolated from a chronically infected transplant patient. At 14 days after inoculation the highest HEV genome copy numbers were found in A549 cells, followed by PLC/PRF/5 cells, whereas HepG2/C3A, Huh-7 Lunet BLR and MRC-5 cells only weakly supported virus replication. Inoculation of A549-derived subclone cell lines resulted in most cases in reduced HEV replication. However, the subclone A549/D3 was susceptible to lower virus concentrations and resulted in higher virus yields as compared to parental A549 cells. Transcriptome analysis indicated a downregulation of genes for carcinoembryonic antigen-related cell adhesion molecules (CEACAM) 5 and 6, and an upregulation of the syndecan 2 (SDC2) gene in A549/D3 cells compared to A549 cells. However, treatment of A549/D3 cells or A549 cells with CEACAM- or syndecan 2-specific antisera did not influence HEV replication. The results show that cells supporting more efficient HEV replication can be selected from the A549 cell line. The specific mechanisms responsible for the enhanced replication remain unknown.

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“…By contrast, CEACAM6 expression is up-regulated in many epithelial malignancies, including pancreatic, colorectal, breast, gastric, and lung adenocarcinomas, and its overexpression is associated with poor clinical outcomes [10][11][12][13][14][15][16][17]. In pancreatic cancer cells, overexpression of CEACAM6 is associated with anoikis resistance, metastasis, and gemcitabine resistance [11,21,23,24]. Furthermore, overexpression of the protein is correlated with reduced survival and the development of metastasis in colorectal cancer patients [9,14,25], and is a significant predictor of recurrence in breast cancer [26].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, miR-29a has a tumor suppressive role in restricting the activity of DNA damage responsive kinases such as Cdc7 in lung cancer cells [37]. Recently, Chen et al reported that CEACAM6 directly impacts the epithelial-mesenchymal transition, migration, invasion, and metastasis of pancreatic cancer cells, and showed that miR-29a/b/c can regulate CEACAM6 at the post-transcriptional level in pancreatic cancer [24]. Therefore, miR-29a may act as a tumor suppressor in lung adenocarcinoma and pancreatic cancer by inhibiting the expression of CEACAM6.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐29a suppresses the growth, migration, and invasion of lung adenocarcinoma cells by targeting carcinoembryonic antigen‐related cell adhesion molecule 6

et al. 2014

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Edited by Tamas Dalmay Keywords:Carcinoembryonic antigen-related cell adhesion molecule 6 Lung adenocarcinoma MicroRNA 29a a b s t r a c t Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is an important regulator of cell adhesion, invasion, and metastasis. The aim of this study was to evaluate the functional roles of CEACAM6 in lung adenocarcinoma and to identify miRNAs that inhibit the growth, migration, and invasion of lung adenocarcinoma cells by targeting CEACAM6. CEACAM6 expression is associated with poor prognosis of patients with lung adenocarcinoma, and CEACAM6 has important functional roles in controlling the growth, migration, and invasion of lung adenocarcinoma cells in vitro and in vivo. Furthermore, miR-29a can suppress the growth, migration, and invasion of lung adenocarcinoma cells by targeting CEACAM6. Therefore, miR-29a/CEACAM6 axis represents a potential therapeutic target for treatment of lung adenocarcinoma.

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CEACAM6 induces epithelial-mesenchymal transition and mediates invasion and metastasis in pancreatic cancer

Cited by 16 publications

References 0 publications

Micro-RNAs miR-29a and miR-330-5p function as tumor suppressors by targeting the MUC1 mucin in pancreatic cancer cells

Micro-RNAs miR-29a and miR-330-5p function as tumor suppressors by targeting the MUC1 mucin in pancreatic cancer cells

Enhanced Replication of Hepatitis E Virus Strain 47832c in an A549-Derived Subclonal Cell Line

MicroRNA‐29a suppresses the growth, migration, and invasion of lung adenocarcinoma cells by targeting carcinoembryonic antigen‐related cell adhesion molecule 6

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