Abstract
BackgroundThe metastasis of oral cancer is one of the main causes of death. However, the mechanisms underlying oral cancer metastasis have not been completely elucidated. Fermitin family member 1 (FERMT1) plays an -oncogene role in many cancers; however, the role of FERMT1 in oral squamous cell cancer (OSCC) remains unclear.MethodsIn this study, OSCC cells were treated with 5 ng/ml recombinant human Transforming growth factor-β1 (TGF-β1) protein. FERMT1 expression was measured in OSCC cell lines by RT-qPCR and western blotting. The effect of FERMT1 knockdown on the migration and invasion of OSCC cells was evaluated by Transwell assay. The epithelial-mesenchymal transition (EMT) and PI3K/AKT signaling pathway-related mRNA expression and protein levels were assessed by RT-qPCR and western blotting.ResultsWe found that FERMT1 expression was elevated in TGF-β1-induced OSCC cell lines, and knockdown of FERMT1 inhibited the migration and invasion in TGF-β1-induced OSCC cells. FERMT1 silencing inhibited vimentin, N-cadherin, matrix metalloproteinase 9 (MMP-9) expression and promoted E-cadherin expression, suggesting that FERMT1 silencing inhibited EMT in TGF-β1-induced OSCC cells. Furthermore, FERMT1 silencing inactivated the PI3K/AKT signaling pathway in TGF-β1-induced OSCC cells. Activation of the PI3K/AKT signaling pathway reversed the effect of FERMT1 silencing on OSCC cell migration, invasion, and EMT.ConclusionsFERMT1 silencing inhibits the migration, invasion, and EMT of OSCC cells via inactivation of the PI3K/AKT signaling pathway, suggesting that FERMT1 is a novel and potential therapeutic target for anti-metastatic strategies for OSCC.
Highlights
The metastasis of oral cancer is one of the main causes of death
Reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR) Total RNA was extracted from Transforming growth factor-β1 (TGF-β1)-treated Tca8113 and SCC15 cells using the TRIzol® reagent (Invitrogen; Thermo Fisher Scientific, Inc., Foster City, CA, USA), reversed transcription using the PrimeScript RT Reagent kit, and Fermitin family member 1 (FERMT1) expression was measured by RT-qPCR using SYBR Premix Ex Taq reagent (Takara, Dalian, China)
FERMT1 mRNA expression and protein level was significantly enhanced in the in TGF-β1-induced Human oral keratinocytes (HOK), CAL-27, Tca8113, and SCC15
Summary
The metastasis of oral cancer is one of the main causes of death. Fermitin family member 1 (FERMT1) plays an -oncogene role in many cancers; the role of FERMT1 in oral squamous cell cancer (OSCC) remains unclear. In. China, the overall crude incidence rate for oral cancer was 2.93/100,000 in 2011 [2]. Alcohol drinking, human papilloma virus, serum excess and deficient levels of Cu or Zn, and betel quid (BQ) chewing play key roles in the development of oral cancer [3,4,5,6,7]. The mortality rate of oral cancer remains high, and the primary cause is tumor metastasis [8, 9]. Knowing what genes can inhibit oral cancer metastasis and EMT can help the development of therapeutic targets.
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