Wang Liang, Wang Yu, Xu Lei
Department of Dermatology, The First Affiliated Hospital of Harbin Medical University, 23 Post Street, Nangang District, Harbin, Heilongjiang, 150001, China.
Arch Dermatol Res. 2025 Mar 12;317(1):559. doi: 10.1007/s00403-025-03964-y.
Long non-coding RNA (lncRNA) TINCR has been shown to play a crucial regulatory role in various tumors. However, its specific mechanism of action in cutaneous squamous cell carcinoma (CSCC) remains unclear. This study aimed to explore the role of lncRNA TINCR in CSCC. We utilized overexpression techniques to study the effects of TINCR on CSCC cells. Methylation-specific PCR (MSP) and RNA immunoprecipitation (RIP) assays were used to assess the impact of TINCR on the methylation of the promoter regions of the Myc and TERC genes, and its interaction with DNA methyltransferase 1 (DNMT1). The results showed that overexpression of TINCR significantly promoted methylation in the promoter regions of Myc (N-MYC, L-MYC, and c-MYC) and TERC genes, inhibiting the proliferation, migration, and invasion of CSCC cells. MSP and RIP experiments further confirmed that TINCR binds to DNMT1, enhancing the methylation levels of the promoter regions of Myc and TERC genes. These findings suggest that lncRNA TINCR may serve as a potential therapeutic target for CSCC by regulating the methylation of key oncogenes. These findings provide new insights into the molecular mechanisms of CSCC and highlight the therapeutic potential of targeting TINCR.
长链非编码RNA（lncRNA）TINCR已被证明在多种肿瘤中发挥关键的调节作用。然而，其在皮肤鳞状细胞癌（CSCC）中的具体作用机制仍不清楚。本研究旨在探讨lncRNA TINCR在CSCC中的作用。我们利用过表达技术研究TINCR对CSCC细胞的影响。采用甲基化特异性PCR（MSP）和RNA免疫沉淀（RIP）试验评估TINCR对Myc和TERC基因启动子区域甲基化的影响及其与DNA甲基转移酶1（DNMT1）的相互作用。结果表明，TINCR的过表达显著促进了Myc（N-MYC、L-MYC和c-MYC）和TERC基因启动子区域的甲基化，抑制了CSCC细胞的增殖、迁移和侵袭。MSP和RIP实验进一步证实TINCR与DNMT1结合，提高了Myc和TERC基因启动子区域的甲基化水平。这些发现表明，lncRNA TINCR可能通过调节关键癌基因的甲基化作为CSCC的潜在治疗靶点。这些发现为CSCC的分子机制提供了新的见解，并突出了靶向TINCR的治疗潜力。
