Carboxy‑terminal domain phosphatase 1 silencing results in the inhibition of tumor formation ability in gastric cancer cells
- Authors:
- Hongbing Fu
- Dejun Yang
- Changming Wang
- Jiapeng Xu
- Weimin Wang
- Ronglin Yan
- Qingping Cai
View Affiliations
Affiliations: Department of Gastrointestinal Surgery, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China
- Published online on: September 10, 2015 https://doi.org/10.3892/ol.2015.3693
-
Pages:
2947-2952
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Abstract
Gastric cancer (GC), one of the most malignant types of cancer, is the second greatest cause of cancer‑associated mortality worldwide. Novel therapeutic targets for GC treatment are therefore urgently required. Carboxy‑terminal domain phosphatase 1 (CTDP1) has a crucial role in the regulation of gene expression. However, to the best of our knowledge, the role of CTDP1 in GC has not previously been explored. In the present study, reverse transcription‑quantitative polymerase chain reaction analysis was used to detect CTDP1 messenger RNA expression in various GC cell lines. CTDP1 was subsequently silenced in GC cells by lentivirus‑mediated small interfering RNA (siRNA) infection, and the effects of CTDP1 inhibition on cell proliferation were evaluated by cell number counting, cell cycle analysis with propidium iodide staining and fluorescence‑activated cell sorting (FACS) analysis, apoptotic rate with Annexin V staining and FACS analysis, as well as colony formation assay in GC cells. The results revealed that CTDP1 was highly expressed in certain GC cell lines and lentivirus‑mediated siRNA infection was able to effectively silence CTDP1 expression in GC cells. CTDP1 inhibition decreased cell proliferation, arrested the cell cycle at G0/G1 phase and increased cell apoptosis in GC cells. Furthermore, the colony formation ability of GC cells was also suppressed by silencing CTDP1. Taken together these results indicated that CTDP1 has a significant role in the tumor formation ability of GC cells and is a novel and promising therapeutic target for the treatment of GC.
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