Aims: Ovarian cancer (OC) is the most lethal disease in women. Despite the improvement of therapeutic responses, about 70% of OC patients with stage III-IV faced chemoresistance and relapsed within 3 years. Our previous study found that the paclitaxel (PTX)-resistant acquisition was related to the disorders of signal transducer and activator of transcription 1 (STAT1) expression and lncRNAs. The current study focuses on the mechanisms of PTX resistance and launches a prediction model for therapeutic responses in OC patients. Methods: qRT-PCR, Western blot, immunofluorescence, immunohistochemistry, CCK-8, colony formation, spheroid formation, and dual-luciferase assays were used. The xenograft mouse model was applied for the in vivo study. Bioinformatics and clinical correlation data were analyzed using online databases. The RNA-seq technique was used to identify differentially expressed PTX-resistant lncRNAs. Results: Transcriptome sequencing and experimental verification demonstrated the decrease of STAT1 in PTX-resistant OC cells. Gain-of-function and loss-of-function experiments indicated that STAT1 enhanced PTX sensitivity and inhibited tumor formation in vitro and in vivo by triggering the apoptotic pathway. The RNA-seq defined differentially excessed-lncRNAs between PTX-resistant and PTX-sensitive OC cells. Combined with the analysis of immune-related lncRNAs from the public database, 9 PTX-resistant immune-related lncRNAs (DEir) were discovered. Single-cell RNA sequencing (scRNA-seq) data of OC confirmed the relevance of DEir-lncRNAs in immune responsiveness. Patients with a high prediction score were more prone to evade immunotherapy and chemotherapy. Conclusions: These findings provide a potential application for reversing PTX resistance and the novel prediction model for predicting immunotherapeutic and chemotherapeutic responses in OC patients.