G-四链体 (G4) 是在富含鸟嘌呤的端粒末端形成的结构，并由与特定位点结合的分子稳定。 TMPyP4 和百里醌 (TQ) 是与 G4 结合的小分子，因其作为端粒酶抑制剂的作用而受到关注。本研究的目的是评估端粒酶抑制剂对细胞增殖、衰老和死亡的影响。两种细胞系，LC-HK2（非小细胞肺癌 - NSCLC）和 RPE-1（hTERT 永生化），用 TMPyP4 (5 μM) 和 TQ (10 μM) 处理。两种抑制剂都会降低端粒酶活性。 TMPyP4 增加了与细胞死亡相关的膜损伤的细胞百分比，并降低了细胞处于 S 期的频率。 TMPyP4 降低细胞粘附能力并改变粘着斑模式。 TQ 以浓度依赖性方式发挥作用，增加衰老细胞的频率并诱导细胞周期停滞在 G1 期。因此，目前的结果表明，TMPyP4和TQ虽然充当端粒酶抑制剂，但对细胞中的其他信号传导途径和过程具有更广泛的影响，并且彼此不同。然而，它们同时作用于恶性细胞和永生化细胞，在考虑其抗癌潜力之前还需要进一步研究。

G-quadruplexes (G4) are structures formed at the ends of telomeres rich in guanines and stabilized by molecules that bind to specific sites. TMPyP4 and thymoquinone (TQ) are small molecules that bind to G4 and have drawn attention because of their role as telomerase inhibitors. The aim of this study was to evaluate the effects of telomerase inhibitors on cellular proliferation, senescence, and death. Two cell lines, LC-HK2 (non-small cell lung cancer - NSCLC) and RPE-1 (hTERT-immortalized), were treated with TMPyP4 (5 μM) and TQ (10 μM). Both inhibitors decreased telomerase activity. TMPyP4 increased the percentage of cells with membrane damage associated with cell death and decreased the frequency of cells in the S-phase. TMPyP4 reduced cell adhesion ability and modified the pattern of focal adhesion. TQ acted in a concentration-dependent manner, increasing the frequency of senescent cells and inducing cell cycle arrest in G1 phase. Thus, the present results showed that TMPyP4 and TQ, although acting as telomerase inhibitors, had a broader effect on other signaling pathways and processes in cells, differing from each other. However, they act both on malignant and immortalized cells, and further studies are needed before their anti-cancer potential can be considered.