The authors initially performed reverse transcription‑quantitative polymerase chain reaction to determine the expression profile of KDM5A in ovarian cancer tissues and adjacent normal tissue. Compared with adjacent normal tissue, it was identified that KDM5A was highly expressed in ovarian cancer tissues. Moreover, human ovarian cell lines also confirmed that KDM5A was highly expressed in ovarian cancer. KDM5A was especially highly expressed in SKOV3/paclitaxel (PTX) cells, which are resistant to PTX. Previous studies demonstrated that chemoresistance in cancer cells facilitates epithelial‑to‑mesenchymal transition (EMT). Following this, whether KDM5A influenced EMT and metastasis was investigated. The expression of KDM5A and N‑cadherin were obviously higher in SKOV3/PTX cells than in SKOV3 cells. The expression of E‑cadherin was decreased and the expression of N‑cadherin was increased following ectopic expression of KDM5A, while the expression of E‑cadherin was increased and the expression of N‑cadherin was decreased following KDM5A depletion. Transwell and wound healing assays were used to explore the function of KMD5A in metastasis. The present results indicated that KDM5A facilitated EMT and metastasis in ovarian cells. Moreover, it was identified that P‑glycoprotein was increased while KDM5A was expressed ectopically in SKOV3 cells. Following fluorescence‑activated cell sorting flow cytometry analysis and CCK‑8 assay all revealed that KDM5A regulated the PTX sensitivity in SKOV3 and SKOV3/PTX cells. In brief, KDM5A is a crucial oncogene that is significantly upregulated in ovarian cancer. Its expression is closely correlated with cancer cell proliferation, EMT and metastasis. KDM5A suppresses ovarian cancer cell apoptosis under PTX treatment.

MiR‐145 has been shown to suppress cell invasiveness and proliferation in endometriosis, whereas prostate cancer‐associated transcript 1 (PCAT1) was reported to act as a sponge of miR‐145 with one single‐nucleotide polymorphism (SNP), rs710886, located in the chromosomal segment of PCAT1. Therefore, this study aimed to explore the association between rs710886 SNP and the risk of endometriosis, as well as the effect of this SNP on the activation of the signaling pathway downstream of PCAT1. Real‐time polymerase chain reaction (PCR) was performed to observe the expression of miR‐145 in transfected cells, while Matrigel invasion chamber assays and MTT assay were conducted to examine the invasiveness/proliferation among different cell groups. Moreover, bioinformatics tools, luciferase assays, real‐time PCR, and Western blot analysis were used to measure the expression of these target genes in the presence of miR‐145. Finally, a statistical analysis was conducted to compare the genotypes of rs710886 SNP between fertile healthy women and infertile women with endometriosis. PCAT1 small interfering RNA (siRNA) evidently increased the expression of miR‐145 but reduced the invasiveness/proliferation of cells. P‐PCAT1 exhibited an opposite effect as that of PCAT1 siRNA, indicating PCAT1 could promote the proliferation and invasiveness of endometriosis stem cells via inhibiting the expression of miR‐145. Meanwhile, FASCIN1, SOX2, MSI2, SERPINE1, and JAM‐A were identified as target genes of miR‐145 via computational analysis and luciferase assays. Finally, a significant genetic effect was observed in both the dominant (AG+GG vs AA) and recessive models (GG vs AG+AA), indicating the presence of an association between the genotype of SNP rs710886 and the risk of endometriosis. SNP rs710886 A>G could lower the expression of PCAT1, thus leading to the overexpression of miR‐145. Highly expressed miR‐145 would inhibit the invasiveness and proliferation of endometriosis stem cells via targeting specific genes, thus decreasing the risk of endometriosis.