Effect of human papillomavirus 16 oncoproteins on oncostatin M upregulation in oral squamous cell carcinoma.

Authors:
Jureeporn Chuerduangphui
Jureeporn Chuerduangphui
Khon Kaen University
Chamsai Pientong
Chamsai Pientong
Khon Kaen University
Thailand
Ponlatham Chaiyarit
Ponlatham Chaiyarit
Khon Kaen University
Thailand
Natcha Patarapadungkit
Natcha Patarapadungkit
Khon Kaen University
Apinya Chotiyano
Apinya Chotiyano
Khon Kaen Hospital
Bunkerd Kongyingyoes
Bunkerd Kongyingyoes
Khon Kaen University
Thailand
Supannee Promthet
Supannee Promthet
Khon Kaen University
Thailand
Piyawut Swangphon
Piyawut Swangphon
Khon Kaen University
Thailand

Med Oncol 2016 Aug 27;33(8):83. Epub 2016 Jun 27.

Department of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.

Human papillomavirus (HPV) infection modulates several host cytokines contributing to cancer development. Oncostatin M (OSM), an IL-6 family cytokine, acts to promote cell senescence and inhibit growth. Its dysregulation promotes cell survival, cell proliferation and metastasis in various malignancies. The effect of HPV on OSM dysregulation has not been investigated. To elucidate this, immunohistochemistry was used on formalin-fixed, paraffin-embedded oral squamous cell carcinoma (OSCC) tissues: HPV-positive (50) and HPV-negative (50) cases. Immortalized human cervical keratinocytes expressing HPV16E6 (HCK1T, Tet-On system) were used to demonstrate the role of HPV16E6 in OSM expression. In addition, a vector containing HPV16E6/E7 was transiently transfected into oral cancer cell lines. Cell viability, cell-cycle progression and cell migration were evaluated using flow cytometry and a wound healing assay, respectively. The results showed various intensities of OSM expression in OSCC. Interestingly, the median percentages of strongly stained cells were significantly higher in HPV-positive OSCCs than in HPV-negative OSCCs. To explore the role of HPV oncoproteins on OSM expression, the expression of HPV16E6 in the HCK1T Tet-On condition was induced by doxycycline and HPV16E6 was found to significantly upregulate levels of OSM mRNA and protein, with concomitant upregulation of c-Myc. In addition, the levels of OSM mRNA and protein in E6/E7 transiently transfected oral cancer cells also gradually increased in a time-dependent manner and these transfected cells showed greater viability and higher migration rates and cell-cycle progression than controls. This result demonstrates that HPV16 oncoproteins upregulate OSM and play an important role to promote OSCC development.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12032-016-0800-6DOI Listing

Still can't find the full text of the article?

We can help you send a request to the authors directly.
August 2016
33 Reads
2.060 Impact Factor

Article Mentions


Provided by Crossref Event Data
crossref
Crossref: Crossref
June 20, 2019, 8:00 pm EST

Publication Analysis

Top Keywords

osm expression
12
osm mrna
8
squamous cell
8
cell
8
cell carcinoma
8
human papillomavirus
8
transiently transfected
8
oral cancer
8
levels osm
8
oral squamous
8
mrna protein
8
hck1t tet-on
8
hpv16e6 hck1t
8
transfected oral
8
osm
8
cell-cycle progression
8
cytometry wound
4
intensities osm
4
wound healing
4
assay intensities
4

Similar Publications