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Cervical cancer is one of the most common types of gynecological tumors. Lysophosphatidic acid (LPA), as a bioactive lipid medium, plays an important role in numerous physiological and pathophysiological processes, including the stimulation of cell migration and tumor cell invasion. LPA is increased in the plasma of patients with cervical cancer. Doxorubicin hydrochloride (DOX) is used as a first-line drug in the treatment of cervical cancer in clinics, however, the effect and molecular mechanism of LPA on DOX-induced apoptosis in cervical cancer cells remain unclear. Therefore, the present study aimed to explore the effect and underlying molecular mechanism of LPA on DOX-induced apoptosis in cervical cancer cells. HeLa cells were treated as a control group or with LPA (10 µmol/l), DOX (4 µmol/l) or LPA (10 µmol/l) + DOX (4 µmol/l) for 24 h. Using transmission electron microscopy the results demonstrated that LPA reduced cell death and the degree of chromatin aggregation in DOX-induced HeLa cells. Reverse transcription-quantitative PCR demonstrated that LPA significantly downregulated caspase-3 mRNA expression levels in DOX-induced HeLa cells. Moreover, western blotting demonstrated that LPA significantly reduced caspase-3 and cleaved caspase-3 protein expression levels in DOX-induced HeLa, C33A and SiHa cells. Furthermore, flow cytometry demonstrated that LPA may prevent apoptosis in DOX-induced HeLa cells (P<0.05).Using dichloro-dihydro-fluorescein diacetate assay, it was demonstrated that LPA significantly reduced the intracellular ROS levels induced by DOX. In summary, the present study indicated that LPA may protect HeLa cells from apoptosis induced by DOX. These findings have provided experimental evidence that LPA may be a potential therapeutic target for the treatment of cervical cancer.

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Background: Interleukin 1 beta (IL-1β) is considered to be a mediator of infectious, inflammatory and autoimmune diseases, and the kinetics of its production is relevant to understanding the pathogenesis of these diseases. Lysophosphatidic acid (LPA), the structurally simplest bioactive phospholipid, is necessary for homeostasis in various physiological and pathophysiological processes and plays a pivotal role in wound healing. Skin trauma can not only weaken the barrier function, but also cause pain and infection. Chronic wounds are characterized by impaired healing and uncontrolled inflammation that damages the protection of the immune system. The aim of this study is to investigate whether inflammatory factor IL-1β has an effect on LPA in the wound healing model. Results: In this study, the kinetics of IL-1β gene expression was studied in vivo and in vitro with a wound healing model by quantitative real-time polymerase chain reaction (qRT-PCR) through LPA treatment. As a result, we found that LPA up-regulated inflammatory factor IL-1β in HaCaT cell and skin wound healing. The pro-inflammatory cytokines IL-1β mRNA had higher expression in LPA-treated mice group 3 days after the treatment. In vitro, after the treatment with LPA (20 μM) for 6, 12, and 24 hours, IL-1β mRNA expression increased by 61.16%, 129.39%, and 117.07%, respectively. Conclusion: These results strongly suggest that IL-1β may regulate LPA-accelerated skin wound healing. IL-1β has significant efficacy, and our observations are of interest to the development of drugs targeting LPA in skin therapy.