Open Access

High expression of Sam68 contributes to metastasis by regulating vimentin expression and a motile phenotype in oral squamous cell carcinoma

  • Authors:
    • Takuya Komiyama
    • Takeshi Kuroshima
    • Takehito Sugasawa
    • Shin-Ichiro Fujita
    • Yuta Ikami
    • Hideaki Hirai
    • Fumihiko Tsushima
    • Yasuyuki Michi
    • Kou Kayamori
    • Fumihiro Higashino
    • Hiroyuki Harada
  • View Affiliations

  • Published online on: September 7, 2022     https://doi.org/10.3892/or.2022.8398
  • Article Number: 183
  • Copyright: © Komiyama et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The present study aimed to investigate the clinical and biological significance of Src‑associated in mitosis 68 kDa (Sam68) in oral squamous cell carcinoma (OSCC). Immunohistochemical analysis was performed on tissue samples obtained from 77 patients with OSCC. Univariate analysis revealed that the high expression of Sam68 was significantly correlated with advanced pathological T stage (P=0.01), positive lymphovascular invasion (P=0.01), and pathological cervical lymph node metastasis (P<0.01). Moreover, multivariate analysis demonstrated that the high expression of Sam68 was an independent predictive factor for cervical lymph node metastasis (odds ratio, 4.39; 95% confidence interval, 1.49‑14.23; P<0.01). These results indicated that high Sam68 expression contributed to tumor progression, especially cervical lymph node metastasis, in OSCC. mRNA sequencing was also performed to assess the changes in the transcriptome between OSCC cells with Sam68 knockdown and control cells with the aim of elucidating the biological roles of Sam68. Gene Ontology enrichment analysis revealed that downregulated differentially expressed genes (DEGs) were concentrated in some biological processes related to epithelial‑mesenchymal transition. Among these DEGs, it was established that vimentin was particularly downregulated in these cells. It was also confirmed that Sam68 knockdown reduced the motility of OSCC cells. Furthermore, the immunohistochemical study of vimentin identified the association between vimentin expression and Sam68 expression as well as cervical lymph node metastasis. In conclusion, the present study suggested that the high expression of Sam68 may contribute to metastasis by regulating vimentin expression and a motile mesenchymal phenotype in OSCC.
View Figures
View References

Related Articles

Journal Cover

October-2022
Volume 48 Issue 4

Print ISSN: 1021-335X
Online ISSN:1791-2431

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Komiyama T, Kuroshima T, Sugasawa T, Fujita S, Ikami Y, Hirai H, Tsushima F, Michi Y, Kayamori K, Higashino F, Higashino F, et al: High expression of Sam68 contributes to metastasis by regulating vimentin expression and a motile phenotype in oral squamous cell carcinoma. Oncol Rep 48: 183, 2022
APA
Komiyama, T., Kuroshima, T., Sugasawa, T., Fujita, S., Ikami, Y., Hirai, H. ... Harada, H. (2022). High expression of Sam68 contributes to metastasis by regulating vimentin expression and a motile phenotype in oral squamous cell carcinoma. Oncology Reports, 48, 183. https://doi.org/10.3892/or.2022.8398
MLA
Komiyama, T., Kuroshima, T., Sugasawa, T., Fujita, S., Ikami, Y., Hirai, H., Tsushima, F., Michi, Y., Kayamori, K., Higashino, F., Harada, H."High expression of Sam68 contributes to metastasis by regulating vimentin expression and a motile phenotype in oral squamous cell carcinoma". Oncology Reports 48.4 (2022): 183.
Chicago
Komiyama, T., Kuroshima, T., Sugasawa, T., Fujita, S., Ikami, Y., Hirai, H., Tsushima, F., Michi, Y., Kayamori, K., Higashino, F., Harada, H."High expression of Sam68 contributes to metastasis by regulating vimentin expression and a motile phenotype in oral squamous cell carcinoma". Oncology Reports 48, no. 4 (2022): 183. https://doi.org/10.3892/or.2022.8398