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Involvement of RNase 7 in the malignant potential of oral squamous cell carcinoma cells

Authors :
Puja Neopane
Jun Sato
Tetsuro Morikawa
Masato Saitoh
Koki Yoshida
Durga Paudel
Yoshihito Kurashige
Osamu Uehara
Yoshihiro Abiko
Source :
Oncology Reports. 44:1216-1223
Publication Year :
2020
Publisher :
Spandidos Publications, 2020.

Abstract

RNase 7 is involved in the innate immunity of the oral epithelium. Variations in the expression levels of RNase 7 have been reported in cutaneous squamous cell carcinoma, but not in oral squamous cell carcinoma (OSCC). The present study investigated the expression levels of RNase 7 in OSCC and its role in the malignant potential of these cells. The localization of RNase 7 in OSCC tissue sections was determined via immunohistochemistry. Positive staining for RNase 7 was observed around the epithelial pearls and spinous cells of the OSCC tissues. Four different types of OSCC cell lines (OSC‑19, BSC‑OF, SAS, and HSC‑2) and a normal keratinocyte (HaCaT) were used. The mRNA and protein expression levels of RNase 7 were significantly higher in the OSCC cells compared to the HaCaT cells. Based on our hypothesis that high levels of RNase 7 expression may be involved in the malignant potential of OSCC cells, the effect of RNase 7 knockdown on both proliferation and invasion were evaluated by transfecting the cells with siRNA. Cell numbers, cell invasion, and MMP 9 expression levels were significantly higher in the siRNA‑BSC‑OF, ‑SAS, and ‑HSC‑2 cells compared to the BSC‑OF, SAS, and HSC‑2 cells. The extent of differentiation of the siRNA‑OSCC cells was examined using the differentiation and undifferentiation markers involucrin (INV) and K14, respectively. The expression level of K14 was significantly higher in the siRNA‑OSCC cells compared to the OSCC cells. Alternatively, HSC‑2 and SAS cells demonstrated higher expression levels of INV compared to the siRNA‑HSC‑2 and ‑SAS cells. These findings indicate that RNase 7 may contribute to the suppression of the malignant potential of OSCC.

Details

ISSN :
17912431 and 1021335X
Volume :
44
Database :
OpenAIRE
Journal :
Oncology Reports
Accession number :
edsair.doi.dedup.....38b9468baae2c1a1a3ddbccb1a9f6061