Knockdown of ISOC1 suppresses cell proliferation in pancreatic cancer in vitro
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- Published online on: February 28, 2019 https://doi.org/10.3892/ol.2019.10082
- Pages: 4263-4270
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Copyright: © Cheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Pancreatic cancer is a deadly disease that is frequently associated with mortality at the time of diagnosis due to rapid metastasis, which makes it unsuitable for operative surgery, and resistant to chemotherapy and radiation therapy. Isochorismatase domain‑containing protein 1 (ISOC1) has putative isochorismatase activity, and is positively regulated by estrogen in human breast cancer. However, its role in pancreatic cancer has yet to be fully elucidated. Analysis from datasets downloaded from The Cancer Genome Atlas and Genotype‑Tissue Expression databases indicated that the ISOC1 mRNA expression level was increased in pancreatic cancer tissues, compared with normal pancreatic tissues. In the present study, it was determined that the human pancreatic cancer cell lines SW 1990, PANC‑1 and AsPC‑1 had increased expression levels of ISOC1 mRNA, compared with human pancreatic ductal epithelial cells. Additionally, two of the pancreatic cancer cell lines, SW 1990 and PANC‑1, transfected with lentivirus‑delivered short hairpin RNA, to knockdown the expression of ISOC1, were established. Cell counting and MTT assays indicated that knockdown of ISOC1 decreased the ability of cell growth and proliferation in pancreatic cancer cells. Furthermore, Annexin V staining and caspase‑3/7 activity assays demonstrated that inhibition of ISOC1 promoted cell apoptosis via elevation of the expression of caspase‑3/7. Furthermore, inhibition of ISOC1 impaired the cell migration and invasive capability of the cells. In conclusion, ISOC1 exerts a role in pancreatic cancer cell growth and apoptosis, and may have a role in pancreatic cancer tumorigenesis.
