Abstract
Objective We aimed to observe the impact of ginkgolic acid (GA) on the proliferation and metastasis ability of ovarian cancer (OCa) cells and to further explore whether GA affects the malignant progress of OCa via regulating the lncRNA MALAT1/JAK2 axis. Methods OCa cells SKOV3 and CAOV3 were administered with 1 ng/ml GA, 5 ng/ml GA, 10 ng/ml GA, 20 ng/ml GA, and DSMO as control, respectively. The cell proliferation and migration ability of the abovementioned cells in each group were measured by CCK-8 test and Transwell experiments. The expression levels of lncRNA MALAT1 and JAK2 protein were examined by qRT-PCR and western blot, respectively. Subsequently, in OCa cells treated with GA, lncRNA MALAT1 overexpression vector was transfected to continue to detect the proliferation activity and migration ability of each treatment group. Finally, the regulation of GA on activity of lncRNA MALAT1/JAK2 axis in OCa cells was further explored in nude mice. Results Our data showed that the proliferation inhibition rate of cells at each ginkgolic acid concentration was higher than that of the control group (P < 0.05), suggesting that GA has an inhibitory influence on the proliferation of OCa cells, in a dose-dependent way. GA was able to inhibit the proliferation rate and migration ability of OCa cells. Administration of ginkgolic acid downregulated the levels of lncRNA MALAT1 and JAK2 protein. Overexpression of lncRNA MALAT1 partially reversed the inhibited OCa proliferative capacity caused by GA treatment. Consistent with the results observed in vitro, we also found that the OCa tumor weight and volume of nude mice injected with lncRNA MALAT1 overexpression vector were enhanced and JAK2 protein level increased remarkably in comparison to the ginkgolic acid group. Conclusions In summary, GA may exert its inhibitory effect on the proliferative and migratory capacities of OCa cells through suppressing the activity of lncRNA MALAT1/JAK2 axis.
Highlights
Gynecological malignancy as the main cause of tumor occurrence and death in women globally mainly includes ovarian tumor, uterine tumor, fallopian tube tumor, vulvar tumor, and vaginal tumor, among which ovarian and uterus tumor are the most common [1, 2]. e incidence of OCa ranks second in female reproductive system malignancies, among which epithelial OCa is the most common histological type, accounting for about 90% of the total number of cases, and its mortality ranks first in gynecological tumors [3, 4]. e latest statistics from the National Cancer Institute show that the mortality rate of ovarian cancer has not changed significantly, and the 5-year survival rate is only 45.6%
To test the mechanism by which ginkgolic acid (GA) inhibits the malignant progression of OCa, we examined the expression of lncRNA MALAT1 and JAK2 protein in OCa cells after GA treatment
We found a reduction in both the mRNA expression of lncRNA MALAT1 (Figure 2(a)) and the protein level of JAK2 (Figure 2(b))
Summary
E incidence of OCa ranks second in female reproductive system malignancies, among which epithelial OCa is the most common histological type, accounting for about 90% of the total number of cases, and its mortality ranks first in gynecological tumors [3, 4]. Tumor reduction surgery combined with platinum-based chemotherapy is the classic treatment for epithelial ovarian cancer. It has been clinically implemented for decades and is recognized as the most effective treatment for ovarian cancer worldwide; this classic approach has little effect on patients with platinum-resistant and recurrent ovarian cancer [7, 8]. Diagnosis, and treatment of OCa are key factors affecting the prognosis of OCa. us, it is necessary to further explore the mechanism
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