Monotherapy with poly ADP-ribose polymerase (PARP) inhibitors (PARPi) leads to a limited objective response rate in cervical cancer patients with homologous recombination (HR) repair-deficiency, urgently requiring more studies to improve the therapeutic efficacy of PARPi during cervical cancer progression. In the study, we attempted to explore the effects of co-treatments with PARPi rucaparib phosphate (Ruc-P) and PI3Kα inhibitor CNX-1351 on cervical cancer growth in vivo and in vitro. Our results showed that CNX-1351 significantly facilitated the anti-cancer role of Ruc-P in cervical cancer, as proved by the remarkably decreased cell proliferation. In addition, G2/M cell cycle arrest and apoptosis were considerably induced by CNX-1351 and Ruc-P combinational treatments compared with the drug alone-treated group. Furthermore, the capacity of Ruc-P to trigger DNA damage was dramatically promoted in cervical cancer cells co-treated with CNX-1351 and Ruc-P, accompanied with elevated expression of γ-H2AX. Importantly, we found that Ruc-P markedly down-regulated the expression of HR markers, including breast cancer 1/2 (BRCA1/2) and RAD51, along with evidently decreased HR repair efficacy, which was, notably, further promoted in cervical cancer cells co-incubated with CNX-1351. Consistently, our in vivo findings confirmed that CNX-1351 administration markedly improved the function of Ruc-P via co-treatments to reduce tumor growth in a xenograft mouse model with cervical cancer. Together, all these results provided new insights into the combinational blockage of PARP and PI3K signals on the suppression of cervical cancer, which was more efficient than either drug alone, and thus could be considered as a promising therapeutic strategy in future.