Abstract

Objective To study the expression and mechanism of trihistidine nucleotide binding protein 1 in esophageal carcinoma. Methods The Eca-109 esophageal cancer cell line was cultured in laboratory. The Hint1 vector was expressed by pLVX-IRES-ZsCreen1 lentivirus. After 293T cells were purified and concentrated, the Eca-109 cells were infected to obtain Eca-109 Hint1 group cells. To detect the expression of green fluorescent protein (CFP) in two groups, to detect whether the transfection was successful or not, to detect the expression of Hint1 protein by Western blotting method, detection of invasiveness in different groups of cells by Transwell invasion assay, to detect the cell cycle by flow cytometry, and to detect the cell growth by methyl thiazol tetrazolium (MTT) method. Results The average expression rate of fluorescent protein in Eca-109 Hint1 group was (68.26±3.12)% (t=8.250, P<0.01). These results indicated that the transfection of human esophageal cancer cells infected with Hint1 vector virus was successful. The expression of Hint1 in Eca-109 Hint1 group was (1.86±0.02), and that of Hint1 in Eca-109 group was (0.61±0.01) by Western blot assay (t=5.529, P<0.05). The invasiveness of Eca-109Hint1+ group was (49.36±3.02), while that of Eca-109 group was (114.11±10.01). The invasiveness of Eca-109Hint1+ group was significantly lower than that of Eca-109 group (t=8.988, P<0.05). The cell cycle of Eca-109 group was (50.31±0.41), and that of Eca-109 Hint1 group was (41.24±0.62). On the third day of culture, the absorbance of cells in Eca-109 Hint1 group was (0.82±0.01) and that in Eca-109 group was (0.57±0.02). The results showed that the absorbance value of Eca-109 Hint1 group was significantly higher than that of Eca-109 group (t=6.527, P<0.05). Conclusion The expression of tri-histidine nucleotides binding protein-1 in esophageal carcinoma resulted in the increase of cell cycle and cell viability, which could inhibit the growth of esophageal cancer cells. Key words: Trihistidine nucleotide binding protein 1; Esophageal carcinoma; Cell expression and inhibition

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.