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<p>The five-year survival rate of patients diagnosed with oral squamous cell carcinoma (OSCC) is less than 60%, mainly because of tumor metastasis and recurrence. The metastasis of cancer from the primary site is a complex process known as epithelial-mesenchymal transition (EMT). In this study, we examined the function of ITPR3 in EMT in OSCC. OSCC cells were infected with sh-ITPR3 lentivirus, and the effect of ITPR3 knockdown was assessed. An in vivo model was constructed by subcutaneous injection of SCC15 cells into nude mice to detect the effect of ITPR3 on OSCC tumor growth. The upstream mechanism of elevated ITPR3 expression was analyzed using bioinformatics. ITPR3 and GABPB1 were overexpressed in OSCC tissue and cells. ITPR3 knockdown inhibited epithelial-mesenchymal transition (EMT) and tumor growth in vivo. GABPB1 activated ITPR3 transcription by binding to its promoter. ITPR3-mediated calcium ion release activated the expression of the oncogenic factor RELB and the phosphorylation of ERK within OSCC cells. Knockdown of GABPB1 inhibited OSCC progression, which was negated by ITPR3 overexpression. In summary, this study elucidates that GABPB1 activates ITPR3 transcription, thereby inducing EMT in OSCC.</p>

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GABPB1 activates transcription of ITPR3 and EMT in OSCC progression

  • 期刊论文

  • 发表日期：

    2026年2月10日

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  • Jun Liu,
  • Chaoyue Zhao,
  • Song Yang,
  • Jichen Li

摘要

The five-year survival rate of patients diagnosed with oral squamous cell carcinoma (OSCC) is less than 60%, mainly because of tumor metastasis and recurrence. The metastasis of cancer from the primary site is a complex process known as epithelial-mesenchymal transition (EMT). In this study, we examined the function of ITPR3 in EMT in OSCC. OSCC cells were infected with sh-ITPR3 lentivirus, and the effect of ITPR3 knockdown was assessed. An in vivo model was constructed by subcutaneous injection of SCC15 cells into nude mice to detect the effect of ITPR3 on OSCC tumor growth. The upstream mechanism of elevated ITPR3 expression was analyzed using bioinformatics. ITPR3 and GABPB1 were overexpressed in OSCC tissue and cells. ITPR3 knockdown inhibited epithelial-mesenchymal transition (EMT) and tumor growth in vivo. GABPB1 activated ITPR3 transcription by binding to its promoter. ITPR3-mediated calcium ion release activated the expression of the oncogenic factor RELB and the phosphorylation of ERK within OSCC cells. Knockdown of GABPB1 inhibited OSCC progression, which was negated by ITPR3 overexpression. In summary, this study elucidates that GABPB1 activates ITPR3 transcription, thereby inducing EMT in OSCC.