Esophageal Cancer Migration Research Articles

MiR-30b inhibits cancer cell growth, migration, and invasion by targeting homeobox A1 in esophageal cancer

Emerging evidence has shown that microRNAs (miRNAs) play important roles in tumor development and progression. In particular, miR-30b is thought to be closely related to the migration, invasion, proliferation, communication, and drug resistance of tumor cells. However, the potential value of miR-30b in human esophageal cancer (EC) remains unclear. In this study, we investigated the biological functions of miR-30b and its potential role in EC. The results indicated that the expression levels of miR-30b were decreased in EC tissues and were correlated with invasion classification (P < 0.01), lymph node metastasis (P < 0.01), and pathological stage (P < 0.05). Log-rank tests demonstrated that low expression of miR-30bwas strongly correlated with poor overall survival in patients with EC (P < 0.05). Moreover, overexpression of miR-30b markedly inhibited the growth, migration, and invasion of ECA109 and TE-1 cells by directly downregulating homeobox A1 (HOXA1). When HOXA1 was reintroduced into miR-30b-transfected ECA109 or TE-1 cells, the inhibitory effects of miR-30b on EC cell growth, migration, and invasion were markedly reversed. In conclusion, our findings demonstrated that miR-30b could inhibit tumor cell growth, migration, and invasion by directly targeting HOXA1 in EC cells.

Transglutaminase 3 protein modulates human esophageal cancer cell growth by targeting the NF-κB signaling pathway.

It has recently been found that the expression of the transglutaminase 3 (TGM3) is significantly reduced in esophageal cancer (EC). However, the potential of TGM3 as a useful biomarker or as a molecular target for EC diagnosis and treatment is unclear. The aim of the present study was to explore the role of the TGM3 in EC. The expression level of TGM3 were measured by real-time polymerase chain reaction and western blot analysis in EC cell lines, including SKGT-4, KYSE-510, OE33, OE21 and the normal esophageal epithelial cell line HEEC; fifty-eight pairs of tissues samples were also measured. through exogenous expression of TGM3 in EC cells it was found that the expression of TGM3 is closely associated with tumor cell growth and apoptosis. TGM3 was found downregulated in EC and closely associated with tumor proliferation and migration. In addition, overexpression of TGM3 apparently induces EC cell proliferation, migration, invasion and promotes cell apoptosis invitro. Subsequent experiments identified the NF-κB signaling pathway as direct target of TGM3. Our data collectively demonstrate that TGM3 can be a candidate tumor suppressor that is able to induce EC cell proliferation and migration by downregulating the NF-κB signaling pathway, indicating that TGM3 may serve as a useful biomarker and therapeutic target for EC treatment.