J Cancer 2018; 9(22):4242-4249. doi:10.7150/jca.26095
Long Non-coding RNA LINC01234 Regulates Proliferation, Invasion and Apoptosis in Esophageal Cancer Cells
1. Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing, China.
2. National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, and State Key Laboratory for Infectious Disease Prevention and Control, Beijing, China.
3. Hubei Key Laboratory of Medical Information Analysis & Tumor Diagnosis and Treatment, Hubei, China.
4. School of Economics and Management, North China Electric Power University, Beijing, China.
Ghaffar M, Khodahemmati S, Li J, Shahzad M, Wang M, Wang Y, Li C, Chen S, Zeng Y. Long Non-coding RNA LINC01234 Regulates Proliferation, Invasion and Apoptosis in Esophageal Cancer Cells. J Cancer 2018; 9(22):4242-4249. doi:10.7150/jca.26095. Available from http://www.jcancer.org/v09p4242.htm
Esophageal cancer is one of the leading malignancies globally and long non-coding RNAs (lncRNAs) have been proved to have an important role in different malignancies including esophageal cancer. However their role in disease progression is still not clear. The objective of the study was to investigate the expression and role of LINC01234 in progression of esophageal cancer cells. LncRNA LINC01234 was found to be upregulated in esophageal cancer cells by chip sequencing. The expression level of LINC01234 was detected from different esophageal cancer cell lines by qRT-PCR. After this, the LINC01234 knockdown effects on cell proliferation, migration, invasion, and apoptosis were evaluated by cell proliferation assay, wound healing assay, invasion assay, and flow cytometric analysis in vitro. Expression of lncRNA LINC01234 was found to be markedly upregulated in the CEC2 cell line. Furthermore, cell proliferation, migration and invasion were significantly (P < 0.05) suppressed as compared to negative control while apoptotic rate was also found increased as a result of the knockdown of LINC01234. Significantly upregulated expression of LINC01234 in CEC2 cells and downregulated expression after knockdown is observed. The impact of LINC01234 knockdown on cell migration, invasion, proliferation and apoptosis indicated that LINC01234 may represent a new marker and a potential therapeutic target for esophageal cancer.
Keywords: LINC01234, esophageal cancer, cell proliferation, invasion, long noncoding RNA, flow cytometry