Screening for novel protein targets of indomethacin in HCT116 human colon cancer cells using proteomics

Cheng,Yan‑Li; Zhang,Gui‑Ying; Li,Cui; Lin,Jing

doi:10.3892/ol.2013.1560

Screening for novel protein targets of indomethacin in HCT116 human colon cancer cells using proteomics

Authors:
- Yan‑Li Cheng
- Gui‑Ying Zhang
- Cui Li
- Jing Lin
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Affiliations: Department of Gastroenterology, The First Hospital of Tsinghua University, Beijing 100016, P.R. China, Department of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China, Medical Research Center, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China
Published online on: September 3, 2013 https://doi.org/10.3892/ol.2013.1560
Pages: 1222-1228

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Abstract

Non‑steroidal anti‑inflammatory drugs, such as indomethacin (IN), inhibit colorectal cancer (CRC) growth through cyclooxygenase (COX)‑independent mechanisms, however, the precise biological mechanisms are not completely understood. The aim of the present study was to investigate new molecular factors potentially associated with IN in HCT116 human CRC cells, which do not express COX, using a proteomic approach. The total proteins from the IN‑treated and untreated groups were separated by immobilized pH gradient‑based two‑dimensional gel electrophoresis. The differentially‑expressed proteins were identified by peptide mass fingerprint (PMF) based on matrix‑assisted laser desorption/ionization time of flight mass spectrometry. The PMF maps were searched in the SWISS‑PROT/TrEMBL database using the PeptIdent software. Between the IN‑treated and untreated groups, a total of 45 differential protein spots were detected and 15 differentially‑expressed proteins were identified by PMF. IN downregulated Wnt1‑inducible signaling pathway protein 1, Bcl‑2‑related protein A1 and mitogen‑activated protein kinase, inhibited HCT116 cell growth and induced apoptosis. In conclusion, IN may exert its effects on CRC to induce HCT116 cell apoptosis and suppress growth through COX‑independent pathways.

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