4.5 Article

High expression of Rab31 confers a poor prognosis and enhances cell proliferation and invasion in oral squamous cell carcinoma

期刊

ONCOLOGY REPORTS
卷 45, 期 3, 页码 1182-1192

出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/or.2021.7940

关键词

Rab31; oral squamous cell carcinoma; prognosis; proliferation; invasion

类别

资金

  1. National Natural Science foundation Project [81570949]
  2. Excellent Subject Leader Plan of Shanghai Municipal Commission of Health and Family Planning [2017BR019]
  3. Youth Project of Shanghai Municipal Commission of Health and Family Planning [20164Y0067]
  4. Science and Technology Commission of Shanghai Municipality, Natural Science Grant [19ZR1430000]
  5. Hospital Innovation Project [CK2019004]

向作者/读者索取更多资源

The dysregulation of Rab proteins has been implicated in various cancers, with Rab31 playing a role in the development and progression of cancer, particularly in oral squamous cell carcinoma (OSCC). High expression of Rab31 was associated with poor prognosis in OSCC patients. Knocking down Rab31 suppressed cell proliferation, induced apoptosis, and inhibited invasion, potentially through the regulation of gene expression.
Dysregulation of Rab proteins has been observed in various types of cancer. Ectopic expression of Rab31, a member of the Rab protein family, is involved in cancer development and progression. However, the specific role and potential molecular mechanism underlying the functions of Rab31 remain largely unknown. Therefore, the current study aimed to investigate the functions of Rab31 in the development of cancer. Human oral squamous cell carcinoma (OSCC) samples were examined to determine the expression profile of Rab31 and its association with the clinicopathological characteristics of patients with OSCC. Knockdown of Rab31 expression with short hairpin RNA was performed to analyze the functions of Rab31 in vitro and in vivo. The expression of Rab31 was significantly elevated in human OSCC samples compared with that in normal oral mucosal epithelial tissues, and high expression levels were associated with high pathological grades. Furthermore, positive expression of Rab31 was associated with a poor prognosis in patients with OSCC. In addition, knockdown of Rab31 expression suppressed OSCC cell proliferation and induced apoptosis compared with those in the control-transfected cells, which may have been caused by downregulated cyclin D1 and survivin expression and upregulated B-cell lymphoma 2 expression. The invasive ability of OSCC cells was also abrogated by Rab31 silencing compared with that in the control-transfected cells, which was associated with downregulated N-cadherin and matrix metalloproteinase-9 expression levels and upregulated levels of E-cadherin expression. Furthermore, silencing Rab31 in OSCC cell lines, when compared with the control-transfected cells, significantly reduced tumor growth and inhibited the expression of survivin, Ki-67 and N-cadherin in vivo. By contrast, the expression levels of E-cadherin were increased. Taken together, the results of the present study supported important roles for Rab31 in regulating OSCC cell proliferation, apoptosis and invasion and may facilitate the identification of a new therapeutic target for the treatment of OSCC.

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