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

Abstract

Pancreatic cancer is a disease with an extremely poor prognosis. The acquisition of invasion properties in pancreatic cancer is accompanied by the process of epithelial-mesenchymal transition (EMT). Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is emerging as an important determinant of the malignant phenotype in a range of cancers, including pancreatic cancer. Therefore, the aim of this study was to evaluate the potential involvement of CEACAM6 in the invasion and metastasis of pancreatic cancer cells via EMT regulation. The results of our study showed a positive association between CEACAM6 expression and poor prognosis of pancreatic cancer, differentiation and lymph node metastasis. Elevated levels of CEACAM6 in pancreatic cancer cells promoted EMT, migration and invasion in vitro and metastasis in animal models, whereas shRNA-mediated CEACAM6 knockdown had the opposite effect. Furthermore, we demonstrated that miR-29a/b/c specific for CEACAM6 could regulate its expression at the post-transcriptional level. Collectively, our findings identified CEACAM6, which is regulated by miR-29a/b/c, as an important positive regulator of EMT in pancreatic cancer offering an explanation for how elevated levels of CEACAM6 are likely to contribute to the highly metastatic phenotype of pancreatic cancer.

Diagnostic performance of CD66c in lung adenocarcinoma-associated malignant pleural effusion: comparison with CEA, CA 19-9, and CYFRA 21-1

“…23,24,[40][41][42] CD66c plays a significant role in cell migration, invasion, and adhesion, which are key steps in the metastatic cascade. 43 The mechanism resulting in CD66c overexpression in lung cancer is not yet clear. 24 Recently, Chen et al revealed that elevated CD66c could promote pancreatic cancer progression and metastasis by epithelial-mesenchymal transition via the ZEB1/ZEB2 pathway.…”

Partial Portal Vein Arterialization Attenuates Acute Bile Duct Injury Induced by Hepatic Dearterialization in a Rat Model

“…Immunohistochemical analysis was performed as previously described [23]. The primary antibody used was mouse monoclonal antihypoxia inducible factor-1 α (anti-HIF-1 α , Sigma, St. Louis, MO, USA) and antialpha smooth muscle actin (anti- α -SMA, Abcam, Cambridge, MA, USA).…”

“…Quantitative real-time polymerase chain reaction (qRT-PCR) was performed as previously described [23]. Briefly, total RNA was extracted from 50 mg liver tissue using the TRIzol reagent (Invitrogen, Shanghai, China), and cDNA was synthesized using the PrimeScript RT kit (Takara, Dalian, China).…”

“…Total liver protein was prepared as previously reported [23]. The protein concentration was determined using a BCA kit.…”

Ginsenoside Rg1 attenuates invasion and migration by inhibiting transforming growth factor-β1-induced epithelial to mesenchymal transition in HepG2 cells

“…Previous studies have demonstrated that EMT is involved in cancer invasion and metastasis, which are key processes in cancer progression and metastasis (20,21). Thus, in the present study, the effect of TGF-β1 on invasion and migration in HepG2 cells were assessed using transwell and wound-healing assays.…”