Objective To investigate the role and regulatory mechanism of lncRNAs PCAT-1 in the sensitivity of cervical cancer cells to DDP. Methods The expressions of PCAT-1 in human cervical cancer cell lines (HeLa and SiHa) and DDP-resistant cell lines (HeLa/DDP and SiHa/DDP) were analyzed by real-time PCR. After PCAT-1 silencing and overexpression in HeLa/DDP and SiHa/DDP cells, CCK-8 and flow cytometry were used to detect cell viability ability and cell cycle, respectively. Western blot was used to detect the protein expression of STAT3 and PTEN. Results The DDP resistance index of HeLa/DDP cells to HeLa cells was 4.49, while that of SiHa/DDP cells to SiHa cells was 6.87. The expression levels of PCAT-1 in HeLa/DDP and SiHa/DDP cells were significantly higher than those in HeLa and SiHa cells, respectively (P < 0.05). The overexpression of PCAT-1 reduced the sensitivity of HeLa/DDP and SiHa/DDP cells to DDP, enhanced the proportion of S phase in cell cycle, and decreased the proportion of G₀-G₁ and G₂-M phases (P < 0.05). The silencing of PCAT-1 increased the sensitivity of HeLa/DDP and SiHa/DDP cells to DDP, decreased the proportion of S phase in the cell cycle, and enhanced the proportion of G₀-G₁ and G₂-M phase (P < 0.05). Overexpression of PCAT-1 promoted STAT3 protein expression but inhibited PTEN protein expression in HeLa/DDP and SiHa/DDP cells (P < 0.05). The silencing of PCAT-1 inhibited STAT3 protein expression but promoted PTEN protein expression in HeLa/DDP and SiHa/DDP cells (P < 0.05). Conclusion PCAT-1 is upregulated in HeLa/DDP and SiHa/DDP cells. PCAT-1 reduces the sensitivity of HeLa/DDP and SiHa/DDP cells to DDP by upregulating the expression of STAT3 and downregulating the expression of PTEN.