Suppression of OSCC malignancy by oral glands derived-PIP identified by iTRAQ combined with 2D LC-MS/MS
| Autor: | Qibo Wang, Zhichao Dou, Chunmiao Jiang, Xiao Liang, Wenhao Ren, Ling Gao, Xinyu Quan, Yuting Wang, Xiaoming Xing, Yuan Zhi, Shaoming Li, Keqian Zhi |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Cell cycle checkpoint Physiology Clinical Biochemistry Proteomics 03 medical and health sciences 0302 clinical medicine Western blot Original Research Articles medicine Original Research Article Clonogenic assay Protein kinase B medicine.diagnostic_test Cell growth Chemistry Cell Biology PIP stomatognathic diseases 030104 developmental biology iTRAQ 030220 oncology & carcinogenesis Cancer research Immunohistochemistry OSCC |
| Zdroj: | Journal of Cellular Physiology |
| ISSN: | 1097-4652 |
| Popis: | Oral squamous cell carcinoma (OSCC) is the most common malignancy in head and neck cancer and a global cause of cancer‐related death. Due to the poor survival rates associated with OSCC, there is a growing need to develop novel technologies and predictive biomarkers to improve disease diagnosis. The identification of new cellular targets in OSCC tumors will benefit such developments. In this study, isobaric tags for relative and absolute quantitation (iTRAQ)‐based proteomics analysis combined with 2‐dimensional liquid chromatography and tandem mass spectrometry (2D LC‐MS/MS) were used to identify differentially expressed proteins (DEPs) between tumor and normal tissues. Of the DEPs detected, the most significantly downregulated protein in OSCC tissue was prolactin‐inducible protein (PIP). Clonogenic and 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) experiments showed that the proliferation capacity of OSCC cells overexpressing PIP decreased due to cell cycle arrest at the G0/G1 checkpoint. Wound‐healing and transwell assay further showed that PIP overexpression also reduced the migration and invasion of OSCC cells. Immunohistochemistry (IHC) was used to analyze the expression in OSCC, indicating that PIP may be secreted by glandular cells and have an inhibitory effect on OSCC cells to produce. In western blot analysis, silencing studies confirmed that PIP mediates these effects through the AKT/mitogen‐activated protein kinase (MAPK) signaling axis in OSCC cells. Taken together, this study reveals PIP as a key mediator of OSCC cell growth, migration, and invasion through its effect on AKT/MAPK signaling. |
| Databáze: | OpenAIRE |
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